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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">INTRODUCTION</span></p><p class="elsevierStylePara">Chronic kidney disease &#40;CKD&#41; is a major public health problem&#46; According to the results of the EPIRCE &#40;Epidemiology of Chronic Renal Failure in Spain&#41; study&#44; designed to obtain information about the prevalence of CKD in Spain&#44; promoted by the Spanish Society of Nephrology &#40;S&#46;E&#46;N&#46;&#41; with the support of the Ministry of Health and Consumption&#44; 9&#46;24&#37; of the adult population has some degree of CKD&#46;<span class="elsevierStyleSup">1 </span>6&#46;83&#37; of the population has a glomerular filtration rate &#40;GFR&#41; of less than 60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; with this percentage being 20&#46;6&#37; in those over 64 years of age&#46; As well as high prevalence&#44; CKD is associated with high cardiovascular morbidity and mortality and very significant costs&#46; In Spain&#44; the annual cost of treatment in the most advanced stages of CKD is estimated to be more than 800 million euros&#46;<span class="elsevierStyleSup">2</span></p><p class="elsevierStylePara">Conveying in one document both CKD detection strategies and risk situations in which there is a high likelihood of progression to end-stage renal disease or higher morbidity and mortality will undoubtedly help identify individuals who are at higher risk of renal progression or cardiovascular complications at an early stage&#46; Likewise&#44; establishing strategies for preventing and managing CKD and its complications by Primary Care&#44; as well as criteria for the appropriate referral of patients to Nephrology comprise the aspects covered in this document&#46; Its purpose is&#44; therefore&#44; to prevent&#44; detect&#44; refer to the specialist and manage CKD&#44; with the aim of improving kidney health and prognosis in our patients&#46;</p><p class="elsevierStylePara">This consensus document arises from the need to revise and update the previous document developed in 2007 by S&#46;E&#46;N&#46;-SEMFyC &#40;Spanish Society of Family and Community Medicine&#41; on CKD&#44;<span class="elsevierStyleSup">3 </span>after an extensive review of the most recent literature and the latest clinical practice recommendations&#46; The methodology used herein was based on a critical review of the main clinical guidelines on CKD and on the occasional support of the few randomised studies in CKD patients&#46;</p><p class="elsevierStylePara">We considered it appropriate to involve in its drafting scientific societies whose objectives include care for kidney patients and&#44; we therefore developed the consensus between the ten signatory societies&#46; Each of them appointed its representatives &#40;who appear as authors&#41; in the drafting of the document&#44; which was subsequently submitted for approval by their respective boards of directors&#46; The document was displayed on the webpages of ten societies and was open to possible suggestions by their members&#46; These suggestions were incorporated into the final complete text and were also sent for display on the respective webpages of the signatory societies&#46;</p><p class="elsevierStylePara">This document is an abridged summary of the original document&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">CHRONIC KIDNEY DISEASE&#58; DEFINITION AND EPIDEMIOLOGY</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">All of the guidelines consulted&#44;<span class="elsevierStyleSup">4&#44;5</span> including the current 2012 KDIGO &#40;Kidney Disease Improving Global Outcomes&#41; guidelines&#44; published in January 2013&#44;<span class="elsevierStyleSup">6</span> confirmed the definition of CKD &#40;independently of the clinical diagnosis&#41; as the presence&#44; for at least THREE MONTHS&#44; of&#58;</p><p class="elsevierStylePara">-&#160;&#160;&#160;&#160;&#160;&#160; an eGFR &#40;estimated glomerular filtration rate&#41; less than 60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#46;</p><p class="elsevierStylePara">-&#160;&#160;&#160;&#160;&#160;&#160; Or renal lesion&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Renal lesion </span>may be revealed directly from histological abnormalities in the renal biopsy or indirectly through the presence of <span class="elsevierStyleBold">albuminuria</span> or <span class="elsevierStyleBold">urinary sediment </span>abnormalities or by using <span class="elsevierStyleBold">imaging </span>techniques&#46;</p><p class="elsevierStylePara">In Spain&#44; it is estimated that 9&#46;24&#37; of the adult population suffers from some degree of CKD&#44; with 6&#46;83&#37; of the general population having stages 3-5 CKD&#46; CKD prevalence is increasing due to an ageing population&#44; the increased prevalence of risk factors such as cardiovascular disease and diabetes mellitus &#40;DM&#41;&#44; high blood pressure &#40;HBP&#41; or obesity and&#44; obviously&#44; due to its early diagnosis&#46; It is estimated that renal replacement therapy consumes 2&#46;5&#37; of the National Health System&#8217;s budget and more than 4&#37; of that of Specialist Care&#46;<span class="elsevierStyleSup">2</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Chronic kidney disease risk factors</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The continuous conceptual CKD model<span class="elsevierStyleSup">7</span> includes risk factors for each phase&#44; which are classified into susceptibility&#44; initiating&#44; progression and end-stage factors &#40;Table 1&#41;&#46; Some risk factors may be included in the susceptibility&#44; initiating and progression factor categories&#44; such as HBP&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Chronic kidney disease screening</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">CKD screening in risk populations should be carried out by assessing the eGFR and albuminuria at least once a year&#46; The diagnosis must not be based on one SINGLE eGFR and&#47;or albuminuria test and must ALWAYS be confirmed&#46;</p><p class="elsevierStylePara">We recommend CKD screening in patients with HBP&#44; type 2 DM or established cardiovascular disease&#46; Likewise&#44; its screening is advised in individuals older than 60 years of age&#44; those who are obese &#40;body mass index &#91;BMI&#93; &#62;35kg&#47;m<span class="elsevierStyleSup">2</span>&#41;&#44; with type 1 DM for more than five years&#44; patients with first degree relatives who have kidney disease or hereditary kidney diseases&#44; patients with urinary tract obstruction diseases&#44; patients on prolonged treatment with nephrotoxic drugs &#40;including non-steroidal anti-inflammatory drugs &#91;NSAIDs&#93;&#41;&#44; patients with other cardiovascular disease risk factors &#40;hyperlipidaemia&#44; metabolic syndrome&#44; smokers&#41;&#44; those with a history of acute renal failure and those with chronic infections&#44; autoimmune diseases and neoplasia associated with CKD&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">DIAGNOSIS OF CHRONIC KIDNEY DISEASE</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Estimation of the glomerular filtration rate</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Serum creatinine concentration should not be used as the only test for assessing renal function&#44; with GFR being the best tool for doing so&#46; Calculating the GFR from creatinine clearance &#40;measurement of creatinine concentration in serum and 24-hour urine&#41; has a series of disadvantages&#44; such as overestimation of the GFR and the problem posed by collecting 24-hour urine both for the patient and for laboratories&#46; Measuring creatinine clearance by collecting 24-hour urine does not improve GFR estimation from equations except in certain circumstances&#46;</p><p class="elsevierStylePara">We recommend estimating the GFR using equations obtained by measuring serum creatinine concentration&#44; age&#44; sex and ethnicity&#46; These equations are more accurate than an isolated measurement of serum creatinine&#46; The equations most used are those of the Modification of Diet in Renal Disease study &#40;MDRD-4 or MDRD-IDMS&#41;&#44;<span class="elsevierStyleSup">8</span> in accordance with whether the method used by the laboratory to measure serum creatinine is <span class="elsevierStyleBold">traceable </span>or not &#40;Table 2&#41; in the isotope dilution mass spectrometry &#40;IDMS&#41; reference measurement procedure&#44; with the latter being recommended&#46;</p><p class="elsevierStylePara">The CKD-EPI &#40;Chronic Kidney Disease-Epidemiology Collaboration&#41; equation&#44;<span class="elsevierStyleSup">9</span> also using standardised creatinine methods&#44; has advantages over MDRD-IDMS&#44; given that it is more accurate and improves the predictive capacity of the GFR &#40;particularly between values of 60 and 90ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#41;&#44; as well as improving the prediction of overall and cardiovascular mortality and the risk of developing ESRD&#46;<span class="elsevierStyleSup">10 </span>As such&#44; it is considered that CKD-EPI should replace the previous formulas &#40;Table 3&#41;&#46; The new 2012 KDIGO guidelines consider the use of alternative formulas to be acceptable if they have been shown to improve accuracy when compared with the CKD-EPI formula&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara">This equation has demonstrated that it is superior to other GFR estimation equations based on the serum concentration of creatinine &#40;MDRD&#41;&#44; cystatin C or the combination of both&#46;<span class="elsevierStyleSup">10-13</span></p><p class="elsevierStylePara">Although the Cockcroft-Gault &#40;C-G&#41; equation<span class="elsevierStyleSup">14</span> has classically been used in the adjustment of drug doses and has been a reference for assessing hyperfiltration states&#44; it should be advised against&#46; This equation has not been reformulated for creatinine values obtained using appropriate procedures and cannot be re-expressed for the current methods of measuring creatinine&#44; and as such&#44; it should not be used&#46; The CKD-EPI or MDRD-IDMS equations may be used for this purpose&#44; since they are based on standardised creatinine measurement procedures&#46; The GFR obtained by MDRD or CKD-EPI is useful for drug dose adjustment&#44; since it correlates better than that obtained by C-G for values below 60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; which are the most likely to require a dose adjustment and are available in the clinical laboratory reports&#44; unlike C-G&#46;<span class="elsevierStyleSup">10&#44;11&#44;15&#44;16</span></p><p class="elsevierStylePara">The values obtained using the MDRD or CKD-EPI equations are adjusted for a body surface area &#40;BSA&#41; of 1&#46;73m<span class="elsevierStyleSup">2</span>&#46;<span class="elsevierStyleSup"> </span>However&#44; when there is a need to use the formula or adjust particularly toxic drugs or those with a low therapeutic index in patients with major deviations in BSA&#44; GFR values should not be standardised to 1&#46;73m<span class="elsevierStyleSup">2</span>&#46;<span class="elsevierStyleSup"> </span>In these cases&#44; it is only necessary to multiply the laboratory result expressed in ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2 </span>by the patient&#8217;s real BSA ratio divided by 1&#46;73m<span class="elsevierStyleSup">2 </span>&#40;GFR x BSA&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#41;&#46;</p><p class="elsevierStylePara">In general&#44; the use of equations for estimating the GFR &#40;MDRD and CKD-EPI&#41; is inadequate in a series of clinical situations&#44; especially in individuals with an extreme body weight &#40;BMI &#60;19kg&#47;m<span class="elsevierStyleSup">2 </span>or 35kg&#47;m<span class="elsevierStyleSup">2</span>&#41;&#44; those with special diets or malnutrition&#44; muscle mass disorders&#44; amputations&#44; patients &#60;18 years of age&#44; those with liver disease&#44; pregnant women&#44; individuals with acute renal failure and in the study of potential kidney donors&#46; In these cases&#44; for an adequate measurement of renal function&#44; we would require 24-hour urine collection in order to calculate renal clearance&#46;<span class="elsevierStyleSup">3</span></p><p class="elsevierStylePara">Until present&#44; no clinical practice guidelines have included the use of cystatin C or the GFR estimated from it as a CKD screening parameter&#44; but the new 2012 KDIGO guidelines<span class="elsevierStyleSup">6 </span>suggest measuring cystatin C in adults with a GFR between 45 and 59ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44;<span class="elsevierStyleSup"> </span>without other renal lesion markers&#44; if diagnostic confirmation of CKD is required&#46; The recently published CKD-EPI equation for cystatin C should therefore be used&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Assessment of renal lesion</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Albuminuria &#40;urinary excretion of albumin&#41;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Albuminuria is&#44; along with GFR&#44; the basis for CKD diagnosis and staging&#46; The persistent presence of high protein or albumin concentrations in urine is not only a sign of renal lesion&#44; but is also often a sign of &#8220;systemic damage&#8221; beyond the kidney&#46; Different studies have demonstrated the importance of proteinuria in the pathogeny of CKD <span class="elsevierStyleBold">progression</span>&#44; as well as the link between albuminuria and renal <span class="elsevierStyleBold">prognosis</span> and <span class="elsevierStyleBold">mortality</span> in various populations <span class="elsevierStyleBold">independently </span>of the GFR and other classic cardiovascular disease risk factors&#46;</p><p class="elsevierStylePara">We recommend not using terms such as micro- or macroalbuminuria and employing the term albuminuria or urinary albumin excretion and the absolute value of the albumin&#47;creatinine ratio &#40;ACR&#41; in urine&#44; preferably in the first urine of the morning&#46; The ACR is a more sensitive marker than proteinuria in the context of CKD secondary to DM&#44; HBP or glomerular disease&#44; which are more common causes of CKD in adults&#46;</p><p class="elsevierStylePara">In the case of patients with CKD diagnosis and significant proteinuria &#40;for example&#44; an ACR &#62;300-500mg&#47;g&#41;&#44; monitoring could be carried out using the protein&#47;creatinine ratio in urine since it is a more economical test and because&#44; as proteinuria increases&#44; particularly in nephrotic proteinuria&#44; the ACR is less sensitive&#46; The use of the protein&#47;creatinine ratio in urine is also recommended in patients who have suspected interstitial disease and nephrotoxicity due to antiretrovirals&#44; since in both situations&#44; proteinuria mainly involves low molecular weight proteins that are different from albumin&#46; In order to determine albuminuria in a patient&#44; two high values in three samples obtained over a 3 to 6 month period are necessary&#46;</p><p class="elsevierStylePara">The value and persistence of albuminuria are closely related to renal and survival prognosis in CKD patients&#44; but we must also consider that albuminuria is a major independent marker of overall cardiovascular risk &#40;endothelial dysfunction&#44; arterial remodelling&#41;&#44; and not only of chronic kidney disease&#46; The presence of albuminuria alone&#44; without any other sign of renal damage&#44; is called into question by various authors as being specific to CKD&#44; since it may be detected in other diseases &#40;e&#46;g&#46; obesity&#44; smoking&#44; dermatitis and arthritis&#41;&#46;</p><p class="elsevierStylePara">We must remember that determining proteinuria includes not only the quantification of albuminuria&#44; but also the quantification of low molecular weight proteins&#44; such as proteins of tubular origin or immunoglobulin light chains&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Urinary sediment abnormalities</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The presence of haematuria and&#47;or leukocyturia in the urinary sediment for more than three months&#44; once a urological cause or urinary infection have been ruled out &#40;including urinary tuberculosis&#41;&#44; may also be an indication of CKD&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">X-ray pathological images</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Renal ultrasound firstly allows to rule out the presence of an <span class="elsevierStyleBold">obstructive </span>urinary tract pathology&#44; but also to identifiy structural abnormalities that indicate the presence of renal damage&#46; Simple isolated renal cysts alone are NOT criteria for renal damage&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Histological abnormalities</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The indication of biopsies is part of the specialist field in Nephrology&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">New chronic kidney disease staging</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Recently&#44; from the results of different clinical studies that include normal individuals&#44; those at risk of developing CKD and CKD patients&#44; the international organisation KDIGO<span class="elsevierStyleSup">6 </span>has established a new CKD prognostic classification based on eGFR and albuminuria stages&#46; This classification is divided into six risk categories according to the eGFR &#40;G1-G5&#41;&#44; which include three risk categories according to ACR concentration&#58; <span class="elsevierStyleBold">A1</span> for optimal or normal-high values &#40;&#60;30mg&#47;g or &#60;3mg&#47;mmol&#41;&#44; <span class="elsevierStyleBold">A2</span> for moderately high values &#40;30-299mg&#47;g or 3-29mg&#47;mmol&#41;&#44; and <span class="elsevierStyleBold">A3</span> for very high values &#40;&#8805;300mg&#47;g or &#8805;30mg&#47;mmol&#41;&#44; respectively &#40;Table 4&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">DEFINITION OF CHRONIC KIDNEY DISEASE PROGRESSION</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The mean annual GFR decrease is very variable and is higher in patients with significant proteinuria&#44; DM or HBP&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Key points</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">1&#46; </span>Normal renal progression rate&#58; 0&#46;7-1ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span> per year from 40 years of age&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">2&#46; </span>We can consider that a patient has renal progression&#58; with a GFR &#62;5ml&#47;min&#47;year or &#62;10ml&#47;min in five years&#46;<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">3&#46; </span>Progression must be defined on the basis of two <span class="elsevierStyleBold">aspects</span>&#58;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">-&#160;Progression to a higher renal function deterioration category </span>&#40;&#60;30&#44; 30-299&#44; &#62;300mg&#47;g&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">-&#160;Percentage of change with respect to the baseline situation</span> &#40;&#62;25&#37; deterioration in the GFR&#41; or a more than 50&#37; increase in the ACR&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">4&#46;&#160;For assessing renal progression&#44; we recommend albuminuria and baseline GFR estimation</span>&#44; as well as the identification of renal progression factors&#46; This will indicate the frequency of successive laboratory tests&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">5&#46;&#160;</span>To ensure the accuracy of renal deterioration rate measurement&#44; the aforementioned guidelines advise carrying out two <span class="elsevierStyleBold">measurements of eGFR within a period of no less than three months </span>and ruling out a decrease due to acute renal failure or the start of treatment with drugs that affect glomerular haemodynamics &#40;angiotensin converting enzyme inhibitors &#91;ACEI&#93;&#44; angiotensin II receptor blockers &#91;ARBs&#93;&#44; NSAIDs&#44; diuretics&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">6&#46;&#160;In</span><span class="elsevierStyleBold"> patients with a new diagnosis of CKD</span> &#40;for the first time&#41;&#44; GFR estimation must be repeated within a period of no less than three months&#44; in order to rule out acute renal deterioration due to exogenous factors &#40;diarrhoea&#44; vomiting&#44; depletion due to diuretics or any drug that affects glomerular haemodynamics&#44; such as ACEI&#44; ARBs or direct renin inhibitors&#41;&#46; It may be repeated within less than three months where the clinical situation indicates&#46; <span class="elsevierStyleBold">In patients with known </span>CKD&#44; it is suggested to measure the eGFR and the ACR once a year if they have a low risk of progression&#44; and more frequently if there is a high risk of progression&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">PREDICTORS OF PROGRESSION</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The factors of renal progression are displayed in Table 5&#46;<span class="elsevierStyleSup">5&#44;17-28</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">CRITERIA FOR REFERRAL TO NEPHROLOGY &#40;Figure 1&#41;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Referral to Nephrology will be carried out taking into account the CKD stage&#44; the speed of renal failure progression&#44; the degree of albuminuria&#44; warning signs&#44; associated comorbidities and the patient&#8217;s functional situation&#46;<span class="elsevierStyleSup">3&#44;5&#44;29</span></p><p class="elsevierStylePara">Generally speaking&#44; <span class="elsevierStyleBold">patients who have an eGFR &#60;30ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2 </span>should be referred to the Nephrology specialist </span>&#40;except those &#62;80 years of age without renal progression and albuminuria &#60;300mg&#47;g&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">According to glomerular filtration rate&#58;</span></p><p class="elsevierStylePara">- All patients with an eGFR &#60;30ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; except patients &#62;80 years of age without renal progression&#46;</p><p class="elsevierStylePara">- Patients &#62;80 years of age and with an eGFR &#60;20ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; if their general condition advises it&#44; can be referred for a nephrological assessment and agree on treatment&#46; It is recommended for the candidate patient to be referred to Nephrology at least one year prior to the start of renal replacement therapy&#46; Although this period is not easy to calculate&#44; renal progression &#40;see point 5&#41; may be used as a guideline&#46; The objective is to avoid a patient who is a candidate for renal replacement therapy requiring non-scheduled dialysis&#46;</p><p class="elsevierStylePara">Patients &#60;70 years of age with an eGFR between 30 and 45ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span> should be monitored more frequently &#40;every 3-6 months&#41; and only be referred to Nephrology in the case of albuminuria progression in two consecutive tests or when the ACR ratio is around 300mg&#47;g&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">- According to albuminuria&#58;</span> ACR ratio &#62;300mg&#47;g&#44; equivalent to proteinuria &#62;300mg&#47;24 hours&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Other reasons&#58;</span></p><p class="elsevierStylePara">- Acute deterioration of renal function &#40;&#62;25&#37; decrease in the eGFR&#41; in less than a month&#44; having excluded exogenous factors &#40;diarrhoea&#44; vomiting&#44; depletion due to diuretics during treatment with ACEI&#44; ARBs or direct renin inhibitors&#41;&#46;</p><p class="elsevierStylePara">- Patients who have renal progression &#40;&#62;5ml&#47;min&#47;year&#41; &#40;see definition above&#41;&#46;</p><p class="elsevierStylePara">- CKD and HBP refractory to treatment &#40;&#62;140&#47;90mmHg&#41; with three drugs at full dose&#44; one of them being a diuretic&#46;</p><p class="elsevierStylePara">- Abnormalities in potassium &#40;&#62;5&#46;5mEq&#47;l or &#60;3&#46;5mEq&#47;l without the patient receiving diuretics&#41;&#46;</p><p class="elsevierStylePara">- Anaemia&#58; haemoglobin &#91;Hb&#93;&#160;&#60;10&#46;5g&#47;dl with CKD in spite of correcting iron deficiency &#40;transferrin saturation index &#91;TSI&#93; &#62;20&#37; and ferritin &#62;100&#41;&#46;</p><p class="elsevierStylePara">- Warning signs&#58;</p><p class="elsevierStylePara">&#160; &#160;- Non-urological haematuria associated with proteinuria&#46;</p><p class="elsevierStylePara">&#160; &#160; - Decrease of &#62;25&#37; in the eGFR in less than one month or a &#62;25&#37; increase in plasma creatinine in less than one month&#44; ruling out exogenous factors &#40;diarrhoea&#44; vomiting&#44; depletion due to diuretics during treatment with ACEI&#44; ARBs or direct renin inhibitors&#41;&#46;</p><p class="elsevierStylePara">There may be Primary Care or joint follow-up&#44; according to the cases&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Elderly patients &#40;&#62;80 years of age&#41;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Given that CKD progression is very uncommon in the elderly population&#44; we can accept that patients older than 80 years of age with stable renal function or with a slow deterioration of the latter &#40;&#60;5ml&#47;min&#47;year&#41; without proteinuria or anaemia or warning signs can be followed up conservatively in Primary Care&#46;<span class="elsevierStyleSup">30&#44;31</span></p><p class="elsevierStylePara">Likewise&#44; elderly patients with stage 5 CKD who are not expected to live for long &#40;&#60;6 months&#41;&#44; who have a poor functional situation &#40;dependence in daily activities&#44; dementia&#44; etc&#46;&#41; or severe associated comorbidity or who do not accept dialysis may be suitable for palliative treatment either in Primary Care or shared with Nephrology&#46;<span class="elsevierStyleSup">32</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Diabetic patients</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Patients will be referred to Nephrology with the aforementioned criteria in mind&#44; and furthermore&#44; the following patients must be referred&#58;</p><p class="elsevierStylePara">- Those with albuminuria&#58; a &#40;confirmed&#41; ACR &#62;300mg&#47;g&#44; despite suitable treatment and blood pressure &#40;BP&#41; monitoring&#46;</p><p class="elsevierStylePara">- An increase in albuminuria despite suitable treatment&#46;</p><p class="elsevierStylePara">- Refractory HBP &#40;three drugs at full dose and absence of control&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Indications for a request for ultrasound in Primary Care</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Either for patient follow-up in Primary Care or for their referral to Nephrology&#44; the request for an ultrasound in the diagnostic study of CKD is considered to be relevant&#46; It is indicated in&#58;</p><p class="elsevierStylePara">- Progressive CKD &#40;decrease in the eGFR &#62;5ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span> in one year&#41;&#46;</p><p class="elsevierStylePara">-&#160;Macroscopic haematuria or persistent albuminuria&#46;</p><p class="elsevierStylePara">-&#160;Symptoms of urinary tract obstruction&#46;</p><p class="elsevierStylePara">-&#160;Age &#62;15 years and a family history of polycystic kidney disease&#46;</p><p class="elsevierStylePara">-&#160;Stage 4 or 5&#46; Assess associated comorbidities beforehand&#46;</p><p class="elsevierStylePara">-&#160;CKD with proteinuria&#46;</p><p class="elsevierStylePara">-&#160;Recurrent urinary infections with renal involvement&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">MONITORING AND FOLLOW-UP OF CHRONIC KIDNEY DISEASE PATIENTS</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The frequency of monitoring and visits of CKD patients is displayed in Table 6&#46; In any case&#44; it is necessary to individualise these general criteria&#46;</p><p class="elsevierStylePara">For each check-up in Primary Care&#44; we recommend&#58;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226; Monitoring BP and adjusting treatment&#46;</span> BP objective &#60;140&#47;90mmHg&#46; In patients with proteinuria &#40;ACR &#62;300mg&#47;g&#41;&#44; we recommend around 130&#47;80mmHg&#46; In elderly patients&#44; this measurement will be carefully individualised&#46;<span class="elsevierStyleSup">33</span> Avoid low blood pressure in elderly patients with significant atheromatous disease&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Monitoring anaemia&#58; if the patient has stage 3-5 CKD and Hb &#60;10&#46;5g&#47;dl &#40;once iron deficiency has been ruled out&#58; TSI &#62;20&#37; and ferritin &#62;100ng&#47;ml&#41;</span>&#44; estimate referral or advance it in Nephrology in order to assess treatment with erythropoiesis-stimulating factors&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Reviewing medication</span> and adjusting the dose in accordance with the GFR&#46; In stages 3-5 CKD&#44; avoid using NSAIDs&#44; oral anti-diabetic drugs eliminated in the kidneys and iodinated contrasts&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Reviewing dietary habits</span> and guiding the patient on the type of diet to follow according to the GFR&#58;</p><p class="elsevierStylePara">&#160; &#160;- Stages 1-3 CKD&#58; a low sodium diet is only recommended in the case of HBP&#46;</p><p class="elsevierStylePara">&#160; &#160;- Stages 4-5 CKD&#58; dietary recommendations for sodium&#44; phosphorus and potassium&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Laboratory tests in each check-up from stage 3 CKD&#42;</span> &#40;the minimum advised is in bold&#41;&#58;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160; &#160;-&#160;Complete blood count&#46;</span></p><p class="elsevierStylePara">&#160; -&#160;Blood biochemical analysis&#58; <span class="elsevierStyleBold">glucose&#44; creatinine</span>&#44; urea&#44; <span class="elsevierStyleBold">Na</span>&#44; <span class="elsevierStyleBold">K</span>&#44; Ca&#44; P&#44; albumin and cholesterol&#46; <span class="elsevierStyleBold">GFR estimated using MDRD or CKD-EPI&#46;</span></p><p class="elsevierStylePara">&#160; &#160;-&#160;Urinary biochemical analysis &#40;single urine sample&#44; first in the morning&#41;&#58; <span class="elsevierStyleBold">ACR</span>&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160; &#160;-&#160;Urinary sediment&#46;</span></p><p class="elsevierStylePara">The extractions should be combined so that they do not have to be repeated&#46; The patient will be provided with a report or&#44; failing that&#44; a copy of the tests&#46; If the Nephrology check-ups are carried out once a month&#44; it is not necessary to repeat the tests in Primary Care&#46;</p><p class="elsevierStylePara">Table 7 displays the objectives of monitoring and follow-up of CKD patients according to the stage&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">PREVENTION OF NEPHROTOXICITY</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Once the patient has been diagnosed with CKD&#44; the most important thing is to avoid its evolution&#44; and as such&#44; we must be aware that there are drugs used in daily practice&#44; and more specifically&#44; in these patients&#44; that may cause this disease to worsen&#46; Moreover&#44; the indiscriminate use of intravenous contrast agents without prior preparation may cause contrast-induced nephropathy&#46; As such&#44; it is necessary to avoid using nephrotoxins and minimise the effect and use of intravenous contrasts&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Avoid nephrotoxins and take precautions with drugs that may alter glomerular haemodynamics</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">1&#46;</span> Avoid <span class="elsevierStyleBold">hyperkalaemia </span>associated with drugs&#46; Particular caution must be taken with the association of a potassium-sparing diuretic &#40;spironolactone&#44; amiloride&#44; eplerenone&#41; to another potassium-retaining drug &#40;ACEI&#44; ARBs&#44; direct renin inhibitors&#44; NSAIDs&#44; beta blockers&#41;&#46; In these cases&#44; frequent monitoring of serum potassium is essential&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">2&#46;&#160;</span>Avoid using drugs that may cause rapid volume depletion and tubular damage&#44; particularly in situations of dehydration&#44; as well as those with a direct negative effect on the tubule &#40;aminoglycosides&#44; tacrolimus&#44; cyclosporin A&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">3&#46;&#160;</span>We must particularly emphasise <span class="elsevierStyleBold">avoiding the unnecessary use of NSAIDs</span>&#44; due to the risk of renal function deterioration&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">4&#46;&#160;</span>Adjust drugs to the GFR&#44; particularly in elderly and diabetic individuals&#46; In these patients&#44; metformin &#40;it should not be administered when the eGFR is &#60;30ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#41;&#44; oral anti-diabetic drugs eliminated via the kidney&#44; new anticoagulants&#44; nephrotoxic antibiotics and some heparins must be used with caution&#46; Many drugs produce direct nephrotoxicity and their detrimental effect worsens when combined with those that interfere with glomerular haemodynamics&#46; It is very important to avoid them in risk situations or adjust their dose in accordance with the eGFR &#40;aminoglycosides&#44; vancomycin&#44; aciclovir&#44; tenofovir&#44; amphotericin&#44; etc&#46;&#41;&#46; The list of drugs for adjusting the dose can be consulted on the following webpage&#58; http&#58;&#47;&#47;nefrologiadigital&#46;revistanefrologia&#46;com&#47;modules&#46;php&#63;name&#61;libro&#38;op&#61;viewCap&#38;idpublication&#61;1&#38;idedition&#61;13&#38;idcapitulo&#61;109&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Minimise the use of intravenous contrasts</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Contrast-induced nephropathy is defined as a deterioration in renal function manifested as a relative 25&#37; increase in creatinine or an absolute increase in creatinine of 0&#46;5mg&#47;dl with respect to baseline&#44; which occurs during the first three days following administration of the contrast&#44; not due to any other mechanism&#46; It occurs due to direct toxicity in tubular cells&#46;<span class="elsevierStyleSup">34</span></p><p class="elsevierStylePara">The most important aspect for preventing nephropathy by contrast is to detect it in patients at risk of developing it &#40;old age&#44; heart failure&#44; DM&#44; previous renal failure&#44; dehydration&#44; acute myocardial infarction&#44; shock&#44; contrast volume&#44; anaemia&#44; low blood pressure&#44; the use of nephrotoxins and high doses of diuretics&#44; taking care with drugs that alter glomerular haemodynamics and avoiding low blood pressure&#41;&#46; The best treatment is prevention&#44; avoiding risk situations&#46; We recommend discontinuing diuretics at least 4-6 days before administering the contrast&#44; as well as correct hydration using intravenous fluid therapy and oral hydration&#46; Some drugs may be potentially toxic after contrast administration&#44; such as metformin&#46; However&#44; there is currently not sufficient evidence to discontinue metformin in patients with previously normal renal function who are administered a &#8220;moderate&#8221; amount of contrast&#44;<span class="elsevierStyleSup">35 </span>although some authors suggest this&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">ATTITUDES&#44; LIFESTYLE AND TREATMENT</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Physical exercise</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">As a general rule&#44; it is recommended to carry out 30-60 minutes of moderate exercise 4 to 7 days a week&#46; When the kidney disease is established&#44; the exercise must be adapted to the physical ability of each patient&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Diet</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Dietary recommendations must be individualised in order to avoid patients being overweight or obese&#44; but also in accordance with their renal function and the existence of other risk factors in which some specific restriction is indicated&#46;</p><p class="elsevierStylePara">&#8226; Stages 1-3 CKD&#58; low salt diets are only recommended for HBP and&#47;or heart failure&#46;</p><p class="elsevierStylePara">&#8226;&#160;Stages 4-5 CKD&#58; dietary recommendations on sodium&#44; phosphorus&#44; potassium and proteins&#46;</p><p class="elsevierStylePara">The energy requirements are similar to those of the general population&#46; The information available suggests that protein restriction delays progression of kidney failure and should start to be applied when the GFR falls below 30ml&#47;min&#44; except in cases of proteinuria due to hyperfiltration&#44; where it must be established long before&#44; even with normal renal function&#46; Protein content must be adjusted to 0&#46;8g&#47;kg&#47;day &#40;at least half must be animal proteins of a high biological value&#41;&#44; but with a fat-based high-calorie content &#40;mono and polyunsaturated&#41; and carbohydrates&#44; if there is not carbohydrate intolerance or dyslipidaemia that require additional adjustments&#46; The appropriate protein intake in CKD patients is 0&#46;8g&#47;kg&#44; 50&#37; of which must be of high biological value&#44; that is&#44; of animal origin&#59; the remaining 50&#37; must be complemented with proteins contained in the rest of the foods included in the diet &#40;vegetable origin&#41;&#46; The use of high-protein diets&#44; as well as drugs that cause weight reduction&#44; may have adverse effects in CKD&#46;<span class="elsevierStyleSup">36</span></p><p class="elsevierStylePara">The daily consumption of salt must be less than 6g &#40;the equivalent of 2&#46;4g of sodium&#41;&#46; In initial phases of kidney disease&#44; a stricter salt restriction will only be applied to patients with HBP&#46; The diet must be complemented with potassium and phosphorus restriction and vitamin D intake&#46;</p><p class="elsevierStylePara">In CKD patients on haemodialysis &#40;HD&#41;&#44; protein intake may be increased by up to 1&#46;2g&#47;kg in order to achieve an adequate protein balance&#44; avoid calorie-energy exhaustion and attain an adequate nutritional status&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Alcohol</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Moderate alcohol intake is not considered to be harmful&#44; as with the general population&#44; that is&#44; around 12 to 14g of alcohol &#40;around 300cc of beer or 150cc of wine&#41;&#46; But we must bear in mind not only the calories present in alcohol&#44; but also the quantity of liquid and the sugar&#44; potassium&#44; phosphorus and sodium content&#44; which must be limited in many patients in accordance with associated risk factors and the degree of renal failure that they may cause&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">SPECIFIC OBJECTIVES OF TREATMENT</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">High blood pressure in chronic kidney disease&#58; treatment objectives<span class="elsevierStyleSup">5&#44;33&#44;37</span></span></p><p class="elsevierStylePara">&#8226;&#160;In CKD patients&#44; the objective of anti-hypertensive treatment is threefold&#58; to reduce BP&#44; to reduce the risk of cardiovascular complications and to slow down CKD progression&#46;</p><p class="elsevierStylePara">&#8226;&#160;In patients with CKD and an ACR &#60;30mg&#47;g&#44; the recommended BP control target is &#8804;140&#47;90mmHg&#46; If the ACR is &#8805;30mg&#47;g&#44; a stricter target is suggested&#44; with BP &#8804;130&#47;80mmHg&#44; both in patients with and those without DM&#46;</p><p class="elsevierStylePara">&#8226;&#160;The drugs of first choice are those that block the renin-angiotensin system actions&#44; either ACEI or ARBs&#46;</p><p class="elsevierStylePara">&#8226;&#160;The use of anti-hypertensive drug combinations is recommended to achieve the control objectives&#46; This combination must include a thiazide or loop diuretic depending on the severity of CKD&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Hyperglycaemia management in chronic kidney disease</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Management objectives</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">How is metabolic control assessed&#63;&#160;</p><p class="elsevierStylePara">Glycated haemoglobin A<span class="elsevierStyleInf">1C</span> &#40;HbA<span class="elsevierStyleInf">1C</span>&#41; is the reference parameter for assessing metabolic control in patients with chronic renal failure &#40;CRF&#41; and we must bear in mind factors that limit its usefulness as a glycaemic control marker&#44; such as transfusions and treatment with erythropoietin&#46;<span class="elsevierStyleSup">38-43</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Objectives of glycaemic control</p><p class="elsevierStylePara">The guidelines recommend that in patients with short-term DM and without a decrease in life expectancy&#44; the target must be HbA<span class="elsevierStyleInf">1C</span> &#60;7 &#40;&#60;53mmol&#47;mol&#41;&#46;<span class="elsevierStyleSup">44</span></p><p class="elsevierStylePara">By contrast&#44; for patients with long-term DM with a previous history of poor glycaemic control or with a condition that decreases life expectancy&#44; the control target must be individualised&#44; avoiding therapeutic strategies that involve an unacceptable increase in the risk of hypoglycaemia&#46;</p><p class="elsevierStylePara">There is no evidence that indicate what the optimal HbA<span class="elsevierStyleInf">1C </span>level is for dialysis patients&#46;</p><p class="elsevierStylePara">It is necessary to bear in mind that the risk of severe hypoglycaemia in patients with renal failure on intensive treatment is very high and is increased by a decreased intake&#44; a change in meal times and the presence of autonomic neuropathy&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Oral anti-diabetic drugs<span class="elsevierStyleSup">44</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Secretagogues&#160;</p><p class="elsevierStylePara">Sulfonylureas &#40;SU&#41; are not the first choice drug in renal failure&#46;</p><p class="elsevierStylePara">Glibenclamide and glimepiride are metabolised in the liver to weaker metabolites&#44; but are eliminated in urine&#44; and as such&#44; even in low doses&#44; their use is not recommended in patients with CRF&#46;</p><p class="elsevierStylePara">Glipizide is metabolised to inactive metabolites and&#44; consequently&#44; it would be the only SU that could be administered in CRF&#44; but its use is not permitted with a low GFR &#40;CCr &#60;30ml&#47;m&#41;&#46;</p><p class="elsevierStylePara">Repaglinide is metabolised in the liver and less than 10&#37; is eliminated via the kidneys&#46; Nevertheless&#44; a low dose of treatment &#40;0&#46;5mg&#41; should initially be administered&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Metformin&#160;</p><p class="elsevierStylePara">Metformin is mainly eliminated in urine without being metabolised&#46; In its data sheet&#44; its use is not recommended with an eGFR &#60;60ml&#47;min&#44; but this recommendation is not usually followed in normal clinical practice&#46; With an eGFR &#60;45ml&#47;min&#44; it is recommended to monitor glycaemia and renal function frequently and not administer it with an eGFR &#60;30ml&#47;min&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Alpha-glucosidase inhibitors</p><p class="elsevierStylePara">Both acarbose and miglitol and their metabolites accumulate in renal failure and their use is therefore not recommended&#46;<span class="elsevierStyleSup">45</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Glitazones&#160;</p><p class="elsevierStylePara">Glitazones are metabolised in the liver and less than 2&#37; is eliminated in urine&#46; There is therefore no accumulation of active metabolites in renal failure&#46; However&#44; given that their use increases the risk of oedema&#44; heart failure and osteoporosis&#44; it is limited in these patients and contraindicated in those on dialysis&#46;&#160;</p><p class="elsevierStylePara">Dipeptidyl peptidase-4 inhibitors&#160;</p><p class="elsevierStylePara">When there is an eGFR greater than 50ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span><span class="elsevierStyleInf">&#44;</span> no gliptine requires adjustment&#46; Sitagliptin&#44; vildagliptin and saxagliptin require a dose adjustment whenever the GFR is less than 50ml&#47;minute&#46;</p><p class="elsevierStylePara">Sitagliptin must be used at doses of 50mg and 25mg whenever the GFR is between 50 and 30ml&#47;minute and less than 30ml&#47;minute&#44; respectively&#46;</p><p class="elsevierStylePara">Vildagliptin must be used at doses of 50mg whenever the GFR is less than 50ml&#47;minute&#44; including in ESRD requiring dialysis&#46;</p><p class="elsevierStylePara">Saxagliptin must be used at doses of 2&#46;5mg in patients with a GFR of less than 50ml&#47;minute&#46; Saxagliptin is not indicated in patients with ESRD or those on dialysis&#46;</p><p class="elsevierStylePara">Linagliptin does not require dose adjustment in any stage of CKD&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Glucagon-like peptide-1 analogues&#160;</p><p class="elsevierStylePara">Liraglutide is only indicated in patients with an eGFR &#62;60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#46; Experience with liraglutide and exenatide in this field is very limited&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Insulin&#160;</p><p class="elsevierStylePara">Insulin requirements are very variable and as such&#44; individualisation of treatment is essential&#46; We can indicate the following initial rules that must be adapted to each patient through glucose control&#58;</p><p class="elsevierStylePara">&#8226;&#160;CCr &#62;50&#58; does not require a dose adjustment&#46;</p><p class="elsevierStylePara">&#8226;&#160;CCr 50-10&#58; will require a 75&#37; reduction of the previous insulin dose&#46;</p><p class="elsevierStylePara">&#8226;&#160;CCr &#60;10&#58; will require a 50&#37; reduction of the previous insulin dose&#46;</p><p class="elsevierStylePara">The insulin regimen will be adapted to the control target and may be a conventional therapy or an intensive treatment&#44; although we should remember that the basal-bolus regimen has a lower rate of hypoglycaemia&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Objectives and management of dyslipidaemia&#160;</span></p><p class="elsevierStylePara">One of the factors that increase renal damage and accelerate renal function deterioration is dyslipidaemia&#44; independently of its arteriosclerosis-promoting effect&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Risk stratification</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">In accordance with the latest European guidelines&#44; CKD individuals must be considered to be patients with high or very high cardiovascular risk&#44; without the need to apply risk scales&#46; As such&#44; CKD patients with a GFR &#60;60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2 </span>are classified as having a very high cardiovascular risk&#46;<span class="elsevierStyleSup">46</span></p><p class="elsevierStylePara">Dyslipidaemia screening must be performed systematically&#46; Although LDL &#40;low-density lipoprotein&#41; cholesterol is the main risk predictor&#44; non-HDL &#40;high-density lipoprotein&#41; cholesterol may be better&#44; as is the case in diabetics or metabolic syndrome patients&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Evidence on the benefit of treating dyslipidaemia on chronic kidney disease</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Data obtained by <span class="elsevierStyleItalic">post hoc</span> analysis support the ability of statins to reduce cardiovascular complications in patients with stages 2 and 3 CKD&#46;<span class="elsevierStyleSup">47&#44;48</span></p><p class="elsevierStylePara">The results in stages 4 and 5 or in HD are not as clear&#46;<span class="elsevierStyleSup">49&#44;50</span> However&#44; in the SHARP &#40;Study of Heart and Renal Protection&#41; study&#44; a 17&#37; reduction in cardiovascular events was observed in patients with stages 3&#44; 4 and 5 CKD treated with simvastatin-ezetimibe compared with placebo&#46;<span class="elsevierStyleSup">51</span> This reduction was not observed in patients treated with dialysis&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Lifestyle recommendations</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Diet is the main determinant of cholesterol levels&#46; The basic advice is therefore dietary&#46; It is recommended that 30&#37; or less of the total calories come from fatty foods and that less than 10&#37; be saturated fats&#46; It is advised that no more than 300mg&#47;day of cholesterol be consumed&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Lipid-lowering drugs and chronic kidney disease</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Statins</p><p class="elsevierStylePara">It is not necessary to adjust statin dose&#44; except in very advanced stages of CKD<span class="elsevierStyleSup">3-5</span> and only for those that are eliminated via the kidney&#46; They are the treatment of choice&#46; CKD&#44; as well as old age&#44; female sex&#44; a low BMI&#44; liver dysfunction&#44; alcohol consumption&#44; systemic diseases and hypothyroidism&#44; increase the risk of side effects&#44; however&#44; these are not common&#46;</p><p class="elsevierStylePara">Drugs that are eliminated via the liver are the drugs of choice &#40;fluvastatin&#44; atorvastatin&#44; pitavastatin and ezetimibe&#41;&#46; Statins metabolised via CYP3A4 &#40;atorvastatin&#44; lovastatin&#44; simvastatin&#41; may increase side effects by enhancing pharmacological interactions when they are administered with certain inducing drugs &#40;phenytoin&#44; phenobarbital&#44; barbiturates&#44; rifampicin&#44; dexamethasone&#44; cyclophosphamide&#44; carbamazepine&#44; omeprazole&#41; or inhibitors&#46;</p><p class="elsevierStylePara">For kidney transplant patients&#44; certain interactions must be borne in mind&#44; particularly with cyclosporine and statins&#44; such as atorvastatin&#44; lovastatin and simvastatin&#44; since they may increase their levels and the risk of myopathy&#46; Fluvastatin&#44; pravastatin&#44; pitavastatin and rosuvastatin are less likely to interact&#46; Although tacrolimus is also metabolised by CYP3A4&#44; it seems that there is less risk of it interacting with statins&#46; In these patients&#44; statins must be introduced at low doses&#44; titrated with caution and the interactions must be monitored&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Fibrates&#160;</p><p class="elsevierStylePara">Most guidelines recommend gemfibrozil as the fibrate of choice and they recommend avoiding the others&#46; The risk of myopathy increases more than five times when it is combined with a statin and this is greater in CKD&#46; The association with statins may cause acute renal failure due to rhabdomyolysis&#46; If this combination is necessary&#44; fenofibrate must be used and strict monitoring must be carried out&#46; The normal dose of gemfibrozil is 600mg&#47;day and it can be used in patients with a GFR of between 15 and 59ml&#47;min&#46; Its use is not advised if the GFR is &#60;15ml&#47;min&#46; However&#44; given the lack of evidence on the cardiovascular benefit of hypertriglyceridaemia treatment with fibrates and their potential side effects&#44; treatment with fibrates is not recommended in CKD&#44; particularly in combination with statins&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Ezetimibe&#160;</p><p class="elsevierStylePara">Its efficacy along with simvastatin has been demonstrated in CKD patients in the SHARP study&#46;<span class="elsevierStyleSup">51</span> A dose adjustment is not necessary for renal failure&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Control objectives</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">CKD is a coronary heart disease risk equivalent&#59; therefore&#44; the objectives are the same as in patients with ischaemic heart disease&#46;</p><p class="elsevierStylePara">The therapeutic objective in CKD patients &#40;GFR &#60;60ml&#47;m&#41; is LDL cholesterol &#60;70mg&#47;dl or a 50&#37; reduction if the previous objective is not achievable&#46;<span class="elsevierStyleSup">16 </span>However&#44; recently the KDIGO guidelines for treating dyslipidaemia in CKD recommend therapy with statins for all adults &#62;50 years of age&#44; independently of LDL cholesterol levels&#46; Based on the SHARP study and in the <span class="elsevierStyleItalic">post hoc </span>analysis of clinical trials with statins compared with a placebo that studied CKD patients&#44; a strategy for &#8220;treating cardiovascular risk&#8221; has been established&#46; Likewise&#44; initiating treatment with statins in stage 5 CKD patients not on dialysis is not recommended&#46;<span class="elsevierStyleSup">52</span></p><p class="elsevierStylePara">After the creation of this document&#44; the new international guidelines on dyslipidaemia management in CKD &#40;Kidney Int Suppl 2013&#59; 3&#40;3&#41;&#58; 259-305&#41; were published&#44; which suggest not pursuing objectives&#44; but rather a strategy of &#8220;action&#8221;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Smoking</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Smoking is one of the factors directly involved in kidney disease progression and data have been published that link this habit to renal function deterioration in the general population &#40;the MRFIT study&#44;<span class="elsevierStyleSup">53 </span>the study by Briganti et al&#46;<span class="elsevierStyleSup">56</span>&#41; and in diabetics&#46;<span class="elsevierStyleSup">57-60</span></p><p class="elsevierStylePara">Therefore&#44; in all patients with CKD &#40;as with the general population&#41;&#44; we must ask patients about their tobacco consumption in all consultations that we perform &#40;both in primary and in specialised care&#41;&#46; Empathetic but firm and motivated advice should be given to smokers to encourage them to quit smoking&#44; and emphasis must be put on the individual benefits and the help available to achieve it &#40;systematic minimal intervention&#44; cognitive-behavioural techniques&#44; pharmacological treatment&#44; etc&#46;&#41;&#46;</p><p class="elsevierStylePara">In kidney disease patients&#44; nicotine replacement therapy &#40;patches&#44; chewing gum&#44; sweets&#41; seems to be safe&#44; as well as their combination with lower doses than normal of bupropion &#40;150mg&#47;24h&#41; in advanced stages of the disease&#46; Varenicline use at normal doses seems safe and&#44; as with bupropion&#44; it can be used at half the dose &#40;1mg&#47;24h&#41; of that of patients with moderately decreased renal function and in the general population&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Obesity</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">There are few specially designed clinical trials in this regard&#44; but there are data that support that the reduction of weight and intake of fat may decrease the risk of CKD&#46;<span class="elsevierStyleSup">61 </span></p><p class="elsevierStylePara">Treatment of obesity in CKD patients must be non-pharmacological and consist of physical exercise and a low-calorie diet&#44; in accordance with the recommendations of the corresponding section of these guidelines&#46;</p><p class="elsevierStylePara">The only drug authorised in Spain for treating obesity&#44; orlistat&#44; is indicated in individuals with a BMI higher than 30kg&#47;m<span class="elsevierStyleSup">2</span>&#46; It has interactions with many drugs and has not been studied in CKD patients&#44; and as such&#44; its use does not appear to be advisable in them&#46; The use of drugs to reduce appetite is not indicated in CKD patients&#46;<span class="elsevierStyleSup"> </span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Hyperuricaemia</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Hyperuricaemia is defined as the increase of uric acid levels above their solubility level in plasma&#46; This occurs in males with uric acid values greater than 7mg&#47;dl and in females&#44; due to the oestrogenic effect&#44; with values greater than 6mg&#47;dl&#46; Hyperuricaemia may be asymptomatic or cause diseases such as uric nephrolithiasis&#44; nephropathy due to uric acid&#44; tophaceous gout&#44; acute gouty arthritis and asymptomatic hyperuricaemia&#46; An increased cardiovascular risk has been reported with uric acid values in the high normal limit&#44; above 5&#46;2mg&#47;dl&#46;<span class="elsevierStyleSup">62&#44;63</span></p><p class="elsevierStylePara">It has been demonstrated that allopurinol and other xanthine oxidase inhibitors have effects on the circulatory system that are independent of uric acid concentration&#46;<span class="elsevierStyleSup">64-66</span></p><p class="elsevierStylePara">The clinical guidelines do not recommend treating asymptomatic hyperuricaemia&#44; since this would only be supported by two randomised clinical trials&#46;<span class="elsevierStyleSup">67&#44;68 </span>Another drug&#44; febuxostat&#44; has recently become available for treating hyperuricaemia in patients with a history of gout or uric arthritis&#46; In those with symptomatic hyperuricaemia and mild to moderate renal failure&#44; febuxostat administration has demonstrated greater efficacy and a similar safety to allopurinol&#44; without the need to adjust the dose&#46;<span class="elsevierStyleSup">69</span></p><p class="elsevierStylePara">Colchicine is indicated for treating acute gout attacks&#46; In patients with a GFR between 30 and 50ml&#47;min&#44; the dose must be reduced&#46; If the GFR is less than 30ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; colchicine use is contraindicated&#46; In the event of an acute gout crisis in these patients with a reduced eGFR&#44; intramuscular tetracosactrin &#40;Nuvacthen depot<span class="elsevierStyleSup">&#174;</span>&#41; may be administered for three days or corticosteroids in doses of 2-30mg&#47;day with a rapid reduction until they are discontinued after 5-7 days&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Anaemia</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The main cause of anaemia in CKD patients is the inadequate production of endogenous erythropoietin&#44; a hormone that acts on the differentiation and maturation of red blood cell precursors&#46; In CKD patients&#44; anaemia is defined as a situation in which Hb concentration in blood is two standard deviations below the mean Hb concentration of the general population&#44; corrected for age and sex&#46;<span class="elsevierStyleSup">70 </span>The lower limit of Hb levels from which anaemia is considered to exist in females is 11&#46;5g&#47;l&#44;<span class="elsevierStyleSup">71 </span>according to the S&#46;E&#46;N&#46; and 12g&#47;l according to the World Health Organization &#40;WHO&#41;&#44; the Kidney Disease Outcomes Quality Initiative &#40;KDOQI&#41; and the European Renal Best Practice &#40;ERBP&#41;&#46;<span class="elsevierStyleSup">72 </span>The lower limit of Hb values in males younger than 70 according to the S&#46;E&#46;N&#46;&#44; KDOQI and ERBP is 13&#46;5g&#47;l and 13g&#47;l according to the WHO&#46; For males older than 70 years of age&#44; the S&#46;E&#46;N&#46; and the WHO set the lower Hb limits at 12g&#47;l and the KDOQI and ERBP set it at 13&#46;5g&#47;l&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Diagnosis of anaemia and iron and erythropoiesis-stimulating agent administration assessment and criteria</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Characteristics of anaemia in chronic kidney disease</p><p class="elsevierStylePara">Anaemia associated with CKD is usually normocytic and normochromic in origin and is related to a decrease in erythropoietin production by peritubular cells&#44; low bone marrow response&#44; an increased production of hepcidin and a decrease in the availability of iron for erythropoiesis&#46;<span class="elsevierStyleSup">73</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">When to start the study of anaemia in chronic kidney disease</p><p class="elsevierStylePara">&#8226;&#160;When Hb is &#60;11g&#47;dl in premenopausal females and prepubertal patients&#46;</p><p class="elsevierStylePara">&#8226;&#160;When Hb is &#60;12g&#47;dl in adult males and postmenopausal females&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">How to study anaemia in chronic kidney disease&#44; laboratory requests</p><p class="elsevierStylePara">&#8226;&#160;Haematocrit &#40;Ht&#41;-Hb&#46;</p><p class="elsevierStylePara">&#8226;&#160;Haemocytometer readings&#58; mean corpuscular volume &#40;MCV&#41;&#44; mean corpuscular Hb &#40;MCH&#41;&#44; mean corpuscular Hb concentration &#40;MCHC&#41;&#46;</p><p class="elsevierStylePara">Reticulocytes&#46;</p><p class="elsevierStylePara">&#8226;&#160;Iron parameters&#58; serum iron&#44; ferritin&#44; transferrin&#44; TSI&#46;</p><p class="elsevierStylePara">&#8226;&#160;Rule out intestinal blood losses &#40;if microcytic hypochromic anaemia or suspicion of digestive bleeding&#41;&#46;</p><p class="elsevierStylePara">&#8226;&#160;In patients with stage 5 CKD on HD&#44; samples are taken immediately before dialysis&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Haemoglobin targets</p><p class="elsevierStylePara">In adult CKD patients&#44; Hb control targets between 10 and 12g&#47;dl must be aimed for and symptoms and comorbidity must be assessed&#46; If in patients with stages 3B to 5 CKD Hb &#60;10&#46;5g&#47;dl is found&#44; they should be referred to Nephrology if they were not being followed-up or they should be reviewed at an early stage&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Iron metabolism required before the start of treatment with erythropoiesis-stimulating agents</p><p class="elsevierStylePara">Sufficient caution should be taken to achieve and maintain target Ht&#47;Hb&#58;</p><p class="elsevierStylePara">&#8226;&#160;TSI &#8805;20&#37; and &#60;50&#37;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">During treatment with erythropoiesis-stimulating agents &#40;ESA&#41;&#44; iron metabolism should be studied every three months&#44; if the patient receives intravenous Fe&#46;</p><p class="elsevierStylePara">In patients with ESA without intravenous Fe&#44; the monitoring should be monthly until Hb has stabilised between 10 and 12g&#47;dl&#46;</p><p class="elsevierStylePara">In diabetic patients&#44; it is recommended to not start treatment with ESA until Hb &#60;10g&#47;dl has been achieved&#44; if the patient has a history of stroke&#46;</p><p class="elsevierStylePara">In patients not treated with EPO&#44; the target must be TSI &#8805;20&#37; and Ferritin &#8805;100ng&#47;ml&#46; Patients must be monitored every 3-6 months&#46;</p><p class="elsevierStylePara">The test must be carried out 15 days after the last dose of intravenous Fe is administered&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Intravenous iron administration regimen</p><p class="elsevierStylePara">It is administered with the purpose of preventing deficiency and maintaining iron reserves in order that the target Ht&#47;Hb is achieved and maintained&#46; The administration must be carried out in the hospital&#46; With certain joint protocols&#44; some intravenous Fe may be administered in the health centre under medical supervision&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Oral iron administration regimen</p><p class="elsevierStylePara">&#8226;&#160;Adults&#58; 200mg&#47;day&#46;</p><p class="elsevierStylePara">&#8226;&#160;Children&#58; 2-3mg&#47;kg&#47;day&#46;</p><p class="elsevierStylePara">In pre-dialysis&#44; home dialysis and PD adults who do not achieve adequate iron reserves with Fe by the oral route&#44; a 100mg infusion of Fe dextran or 500-1000mg of intravenous Fe carboxymaltose should be administered and this process should be repeated as necessary in accordance with the iron parameters&#46; Another option is intravenous iron sucrose &#40;maximum 200mg&#47;dose&#41;&#46;</p><p class="elsevierStylePara">It is considered unlikely for HD patients to achieve the target with oral Fe&#44; and as such&#44; intravenous iron will be required&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Route of erythropoiesis-stimulating agent administration&#160;</p><p class="elsevierStylePara">Subcutaneous administration is indicated in HD&#44; PD and home dialysis patients&#44; with the injection location being rotated&#46;</p><p class="elsevierStylePara">The intraperitoneal route would be possible when doses are administered to the empty abdomen or with a low amount of peritoneal fluid&#46; Higher doses may be required using this route&#46;</p><p class="elsevierStylePara">The intravenous route would be indicated in the case of high doses &#40;volume&#41; or recurrent ecchymosis at the site of injection&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">EPO dose and adjustment&#160;</p><p class="elsevierStylePara">It is prescribed by Nephrology services&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Transfusions in chronic kidney disease patients</p><p class="elsevierStylePara">&#8226;&#160;In patients with functional anaemia&#46;</p><p class="elsevierStylePara">&#8226;&#160;In patients who are resistant to EPO with chronic blood loss&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Potential adverse side effects of treatment with erythropoiesis-stimulating agents</p><p class="elsevierStylePara">HBP&#44; seizures&#44; arteriovenous fistula thrombosis&#44; increase in blood viscosity&#46; Treatment with ESA when there is Hb &#62;13g&#47;dl has been associated with high levels of cardiovascular disease&#44; although without an increase in mortality&#46;<span class="elsevierStyleSup">74</span></p><p class="elsevierStylePara">Anaemia control in CKD patients must incorporate educational programmes for patients that include information about the health issue&#44; professional support and lifestyle guidance&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Detection of mineral and bone metabolism disorders</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Calcium and phosphorus metabolism disorders in CKD are associated with various complications that are beyond simple bone involvement and include other systems&#44; particularly the cardiovascular system &#40;for example&#44; calcifications&#41;&#46; The earliest clinical manifestation is an increase in the parathyroid hormone &#40;PTH&#41;&#44; caused by active vitamin D deficiency &#40;calcitriol&#41;&#44; phosphate retention &#40;with or without hyperphosphataemia&#41; and&#47;or marked hyperphosphataemia&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Detection and treatment objectives</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">&#8226;&#160;Avoid hyperphosphataemia&#46;</p><p class="elsevierStylePara">&#8226;&#160;Maintain normal levels of calcium and phosphorus&#46;</p><p class="elsevierStylePara">&#8226;&#160;Avoid the onset and progression of secondary hyperparathyroidism&#46;</p><p class="elsevierStylePara">According to the 2003 K-DOQI&#44; 2007 S&#46;E&#46;N&#46; and 2011 S&#46;E&#46;N&#46; guidelines&#44;<span class="elsevierStyleSup">75-77 </span>the therapeutic objective is variable in different stages of CKD&#44; but it may be summarised by saying that we should aim to maintain calcium&#44; phosphate and PTH within the normal limits&#46; In stage 4&#44; it is even advised to maintain PTH values slightly higher than normal values&#46; The guidelines also recommend measuring calcidiol &#40;25-OH-vitamin D&#41; in order to diagnose the deficiency or insufficiency of vitamin D&#46; These levels should ideally be greater than 20-30ng&#47;m &#40;50-75nmol&#47;l&#41;&#46;</p><p class="elsevierStylePara">A small degree of stable hyperparathyroidism is not a concern&#44; but progressive hyperparathyroidism&#44; with PTH values that are two or three times higher than the reference value&#44; require consultation with Nephrology specialists&#46; Nephrologists should also be consulted for patients with high levels of phosphate that are greater than 5mg&#47;dl &#40;1&#46;40mmol&#47;l&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Treatment</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Treatment will be carried out through diet&#44; phosphate binders&#44; native or active vitamin D&#44; and&#47;or selective activation of vitamin D receptors&#46; Calcimimetics may be used in dialysis patients&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Drugs for adequate maintenance of mineral metabolism</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Phosphate binders</p><p class="elsevierStylePara">These are administered with meals&#46; Binders with calcium include calcium carbonate&#44; calcium acetate or its combination with magnesium&#46; Binders without calcium or aluminium include sevelamer and lanthanum carbonate&#46; Aluminium compounds are excellent binders&#44; but are not recommended over long periods&#44; given that they may induce aluminium intoxication in CKD patients&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Treatment of vitamin D deficiency</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Cholecalciferol &#40;D3&#41;&#58; Belenguer<span class="elsevierStyleSup">&#174;</span> or Kern<span class="elsevierStyleSup">&#174;</span></span><span class="elsevierStyleBold">vitamin D3 </span>&#40;cholecalciferol&#44; 800IU &#61; 12 drops&#44; 50&#160;000IU &#61; 25ml&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Calcifediol &#40;25-OH-vitamin D&#41;&#58; Hidroferol<span class="elsevierStyleSup">&#174;</span></span> 0&#46;266mg &#40;calcifediol 16&#160;000&#160;IU&#41;&#46;</p><p class="elsevierStylePara">The purpose of fortnightly or monthly calcifediol administration in vials is to normalise calcidiol levels &#40;25-OH &#62;20-30ng&#47;ml&#41; independently or not of a decrease in PTH&#46; It should be managed with the utmost care and it is necessary to measure calcium and phosphorus in its control&#44; since in patients with advanced CKD&#44; it may increase them&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Treatment of secondary hyperparathyroidism</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Calcitriol and vitamin D analogues&#58;</span> renal hydroxylation is not required to obtain the active form&#46; These include <span class="elsevierStyleBold">Rocaltrol<span class="elsevierStyleItalic"><span class="elsevierStyleSup">&#174;</span></span></span> &#40;calcitriol&#59; 1&#44;25-&#40;OH&#41;<span class="elsevierStyleInf">2</span>-D<span class="elsevierStyleInf">3</span>&#41; and&#160;<span class="elsevierStyleBold">Etalpha<span class="elsevierStyleItalic"><span class="elsevierStyleSup">&#174;</span></span></span> &#40;alfacalcidol&#59; 1&#945;-&#40;OH&#41;-D<span class="elsevierStyleInf">3</span>&#41;&#46; Alfacalcidol requires activation in the liver&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Selective vitamin D receptor activators&#58;</span><span class="elsevierStyleBold">Zemplar<span class="elsevierStyleItalic"><span class="elsevierStyleSup">&#174;</span></span></span> &#40;paricalcitol&#41;&#58; there is a lower likelihood of hypercalcaemia and hyperphosphataemia&#44; and it seems to induce fewer vascular calcifications&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Calcimimetics&#58;</span><span class="elsevierStyleBold">Mimpara<span class="elsevierStyleItalic"><span class="elsevierStyleSup">&#174;</span></span></span> &#40;cinacalcet&#41;&#58; indicated in the treatment of hyperparathyroidism in dialysis and in primary hyperparathyroidism&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Detection and treatment of acidosis</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">A situation of metabolic acidosis not compensated with venous bicarbonate &#60;15mmol&#47;l will require intravenous treatment in the hospital&#46; Mild metabolic acidosis &#40;bicarbonate between 15 and 20mmol&#47;l&#41; may require the administration of oral bicarbonate&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Other attitudes</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Preparation for renal replacement therapy and start time</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The optimal initiation of renal replacement therapy &#40;RRT&#41; is that which is planned&#46; The lack of planning unnecessarily increases the use of catheters in HD&#44; causing higher morbidity&#44; infections and increased hospitalisation&#46;</p><p class="elsevierStylePara">A referral of the patient to the nephrologist at the appropriate time means that the patient will receive the best information on the possible RRT techniques&#58; PD&#44; HD and home HD&#44; as well as the possibility of an early or living donor renal transplantation&#44; if this were available&#46; This adequate referral decreases complications&#44; particularly infectious and cardiovascular complications and has a significant impact on survival&#46;</p><p class="elsevierStylePara">RRT is considered when the GFR is &#60;15ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span> or earlier if there are signs or symptoms of uraemia or a difficulty in controlling hydration &#40;carried out frequently in diabetic patients&#41;&#44; HBP that is difficult to control or a deterioration of nutritional status&#46;</p><p class="elsevierStylePara">In general&#44; dialysis is introduced whenever the GFR is between 8 and 10ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span> and it is essential with a GFR &#60;6ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; even in the absence of symptoms of uraemia&#46; In high-risk patients&#44; we insist that the early introduction of dialysis should be considered and it should be personalised&#46;</p><p class="elsevierStylePara">It is necessary to bear in mind that the patient may be suitably studied and prepared for a potential living donor renal transplantation &#40;if this is possible&#41; before dialysis is initiated&#46; Likewise&#44; they can be studied and placed on the waiting list for a deceased donor renal transplantation&#44; where possible&#44; before starting dialysis&#46; This is what we call early renal transplantation&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Follow-up</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Patients with stages 4-5 CKD should be monitored preferably by the nephrologist&#44; in close collaboration with the Primary Care doctor and the nursing staff&#46;</p><p class="elsevierStylePara">The frequency of visits must be established every three months in stage 4 CKD and every month in pre-dialysis stage 5 CKD&#46; This frequency may be modified according to the doctor&#8217;s opinion&#46;</p><p class="elsevierStylePara">In each visit&#44; it is advisable to provide detailed information about the laboratory test&#44; changes to treatment&#44; its justification and&#44; where appropriate&#44; a prognostic assessment&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Roles of the Primary Care doctor in addressing and following up chronic kidney disease determined by the stage of disease</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">&#8226;&#160;Follow-up of elderly patients&#44; with a stable GFR&#44; who due to age&#44; quality of life or other reasons&#44; do not receive RRT&#44; ESA and&#47;or medication for secondary hyperparathyroidism&#46;</p><p class="elsevierStylePara">&#8226;&#160;Control of cardiovascular risk factors&#46;</p><p class="elsevierStylePara">&#8226;&#160;Monitoring of CKD progression factors&#46;</p><p class="elsevierStylePara">&#8226;&#160;Monitoring of nephrotoxicity in order to avoid iatrogeny in any process&#46;</p><p class="elsevierStylePara">&#8226;&#160;Special attention must be paid to&#58;</p><p class="elsevierStylePara">&#160; &#160;-&#160;Avoiding NSAID use&#44; whenever possible&#46;</p><p class="elsevierStylePara">&#160; &#160;-&#160;Avoiding hyperkalaemia associated with the use of drugs&#46;</p><p class="elsevierStylePara">&#160; &#160;-&#160;Avoiding&#47;adjusting the use of oral anti-diabetics in accordance with the eGFR&#46;</p><p class="elsevierStylePara">&#160; &#160; -&#160;Avoiding&#44; insofar as possible&#44; use of iodine contrasts and adjusting all drugs to the patient&#8217;s eGFR&#46;</p><p class="elsevierStylePara">&#8226;&#160;Participation in therapeutic compliance and referral to Nephrology in the case of acute deterioration of renal function or complications&#46;</p><p class="elsevierStylePara">&#8226;&#160;Vaccination&#58; hepatitis B virus&#44; pneumococcus&#44; flu&#44; etc&#46;</p><p class="elsevierStylePara">&#8226;&#160;Collaboration in palliative activities&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Keys for managing haemodialysis&#47;peritoneal dialysis patients in Primary Care</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">&#8226;&#160;Facilitation of the disease adaptation process in accordance with age&#44; the family situation&#44; educational and work conditions&#44; the form of occurrence and development of the disease&#44; trust in the healthcare system&#44; etc&#46;</p><p class="elsevierStylePara">&#8226;&#160;Knowledge by the GP of the different options and implementation of the latter &#40;frequency&#44; location where it is performed&#44; potential complications according to the alternative chosen&#41;&#46;</p><p class="elsevierStylePara">&#8226;&#160;Good relationship and communication channel with the reference Nephrology Service&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Keys for managing kidney transplant patients</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The same applies as in the previous case but with a very intense interaction with the nephrologist&#44; for special requirements related to immunosuppression&#44; pharmacological interactions and vaccinations&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Keys for follow-up of terminal uraemia at home&#46; Palliative treatment</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The objective of home management of terminal uraemia is to facilitate the wellbeing of uraemic patients who cannot undergo dialysis&#44; minimising the physical&#44; family and healthcare impact of their condition and optimising the resources of our National Health System&#46; This requires close coordination between Nephrology and Primary Care&#46; In health areas where there are home support teams&#44; whether they are dependent on Primary Care or Specialist Care&#44; their inclusion in the therapeutic team could be very useful&#46;</p><p class="elsevierStylePara">The individualisation of the decision with the agreement of the patient&#44; family and professionals is recommended&#46; It is useful for the decision to be made at an early stage&#44; since it allows follow-up to be organised before a very significant deterioration has occurred in the patient&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Acknowledgements</span></p><p class="elsevierStylePara">We would like to thank Esteve and Abbvie laboratories for their logistical support in the project&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56728&#95;en&#95;t1&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56728_en_t1.jpg" alt="Chronic kidney disease risk factors"></img></a></p><p class="elsevierStylePara">Table 1&#46; Chronic kidney disease risk factors</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56729&#95;en&#95;t2&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56729_en_t2.jpg" alt="Equations to use in methods for measuring creatinine without traceability to IDMS &#40;non-standardised&#41;"></img></a></p><p class="elsevierStylePara">Table 2&#46; Equations to use in methods for measuring creatinine without traceability to IDMS &#40;non-standardised&#41;</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56730&#95;en&#95;t3&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56730_en_t3.jpg" alt="Equations to use in methods for measuring creatinine with traceability to IDMS &#40;standardised&#41;"></img></a></p><p class="elsevierStylePara">Table 3&#46; Equations to use in methods for measuring creatinine with traceability to IDMS &#40;standardised&#41;</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56731&#95;en&#95;t4&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56731_en_t4.jpg" alt="Prognosis of chronic kidney disease by estimated glomerular filtration rate and albuminuria &#40;6&#41;"></img></a></p><p class="elsevierStylePara">Table 4&#46; Prognosis of chronic kidney disease by estimated glomerular filtration rate and albuminuria &#40;6&#41;</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56732&#95;en&#95;t5&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56732_en_t5.jpg" alt="Predictors of chronic kidney disease progression"></img></a></p><p class="elsevierStylePara">Table 5&#46; Predictors of chronic kidney disease progression</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56737&#95;en&#95;t6&#95;copy1&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56737_en_t6_copy1.jpg" alt="Frequency of monitoring visits &#40;number of annual visits&#41;"></img></a></p><p class="elsevierStylePara">Table 6&#46; Frequency of monitoring visits &#40;number of annual visits&#41;</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56738&#95;en&#95;t7&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56738_en_t7.jpg" alt="Objectives by specialty in chronic kidney disease patient follow-up "></img></a></p><p class="elsevierStylePara">Table 7&#46; Objectives by specialty in chronic kidney disease patient follow-up </p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56739&#95;en&#95;f1&#95;copy1&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56739_en_f1_copy1.jpg" alt="Algorithm of referral to Nephrology&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Algorithm of referral to Nephrology&#46;</p>"
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Consensus document for the detection and management of chronic kidney disease
Documento de consenso para la detección y manejo de la enfermedad renal crónica
Grupo de Redactores, Grupo de redactores, Alberto Martínez-Castelaob, José L. Górriz-Teruelb, Jordi Bover-Sanjuánb, Julián Segura-de la Morenac, Jesús Cebolladad, Javier Escaladae, Enric Esmatjesf, Lorenzo Fácilag, Javier Gamarrah, Silvia Gràciai, Julio Hernánd-Morenoh, José L. Llisterri-Caroj, Pilar Mazóng, Rosario Montañési, Francisco Morales-Olivac, Manuel Muñoz-Torrese, Pedro de Pablos-Velascof, Ana de Santiagoj..., Marta Sánchez-Celayak, Carmen Suárezd, Salvador TranchekVer más
b Sociedad Española de Nefrología (S.E.N.),
c Sociedad Española de Hipertensión Arterial-Liga Lucha Contra la HTA (SEH-LELHA),
d Sociedad Española de Medicina Interna (SEMI),
e Sociedad Española de Endocrinología y Nutrición (SEEN),
f Sociedad Española de Diabetes (SED),
g Sociedad Española de Cardiología (SEC),
h Sociedad Española de Médicos Generalistas (AP) (SEMG),
i Sociedad Española de Química Clínica (SEQC),
j Sociedad Española de Medicina Rural y Generalista (AP) (SEMERGEN),
k Sociedad Española de Medicina de Familia y Comunitaria (AP) (SEMFyC),
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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">INTRODUCTION</span></p><p class="elsevierStylePara">Chronic kidney disease &#40;CKD&#41; is a major public health problem&#46; According to the results of the EPIRCE &#40;Epidemiology of Chronic Renal Failure in Spain&#41; study&#44; designed to obtain information about the prevalence of CKD in Spain&#44; promoted by the Spanish Society of Nephrology &#40;S&#46;E&#46;N&#46;&#41; with the support of the Ministry of Health and Consumption&#44; 9&#46;24&#37; of the adult population has some degree of CKD&#46;<span class="elsevierStyleSup">1 </span>6&#46;83&#37; of the population has a glomerular filtration rate &#40;GFR&#41; of less than 60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; with this percentage being 20&#46;6&#37; in those over 64 years of age&#46; As well as high prevalence&#44; CKD is associated with high cardiovascular morbidity and mortality and very significant costs&#46; In Spain&#44; the annual cost of treatment in the most advanced stages of CKD is estimated to be more than 800 million euros&#46;<span class="elsevierStyleSup">2</span></p><p class="elsevierStylePara">Conveying in one document both CKD detection strategies and risk situations in which there is a high likelihood of progression to end-stage renal disease or higher morbidity and mortality will undoubtedly help identify individuals who are at higher risk of renal progression or cardiovascular complications at an early stage&#46; Likewise&#44; establishing strategies for preventing and managing CKD and its complications by Primary Care&#44; as well as criteria for the appropriate referral of patients to Nephrology comprise the aspects covered in this document&#46; Its purpose is&#44; therefore&#44; to prevent&#44; detect&#44; refer to the specialist and manage CKD&#44; with the aim of improving kidney health and prognosis in our patients&#46;</p><p class="elsevierStylePara">This consensus document arises from the need to revise and update the previous document developed in 2007 by S&#46;E&#46;N&#46;-SEMFyC &#40;Spanish Society of Family and Community Medicine&#41; on CKD&#44;<span class="elsevierStyleSup">3 </span>after an extensive review of the most recent literature and the latest clinical practice recommendations&#46; The methodology used herein was based on a critical review of the main clinical guidelines on CKD and on the occasional support of the few randomised studies in CKD patients&#46;</p><p class="elsevierStylePara">We considered it appropriate to involve in its drafting scientific societies whose objectives include care for kidney patients and&#44; we therefore developed the consensus between the ten signatory societies&#46; Each of them appointed its representatives &#40;who appear as authors&#41; in the drafting of the document&#44; which was subsequently submitted for approval by their respective boards of directors&#46; The document was displayed on the webpages of ten societies and was open to possible suggestions by their members&#46; These suggestions were incorporated into the final complete text and were also sent for display on the respective webpages of the signatory societies&#46;</p><p class="elsevierStylePara">This document is an abridged summary of the original document&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">CHRONIC KIDNEY DISEASE&#58; DEFINITION AND EPIDEMIOLOGY</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">All of the guidelines consulted&#44;<span class="elsevierStyleSup">4&#44;5</span> including the current 2012 KDIGO &#40;Kidney Disease Improving Global Outcomes&#41; guidelines&#44; published in January 2013&#44;<span class="elsevierStyleSup">6</span> confirmed the definition of CKD &#40;independently of the clinical diagnosis&#41; as the presence&#44; for at least THREE MONTHS&#44; of&#58;</p><p class="elsevierStylePara">-&#160;&#160;&#160;&#160;&#160;&#160; an eGFR &#40;estimated glomerular filtration rate&#41; less than 60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#46;</p><p class="elsevierStylePara">-&#160;&#160;&#160;&#160;&#160;&#160; Or renal lesion&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Renal lesion </span>may be revealed directly from histological abnormalities in the renal biopsy or indirectly through the presence of <span class="elsevierStyleBold">albuminuria</span> or <span class="elsevierStyleBold">urinary sediment </span>abnormalities or by using <span class="elsevierStyleBold">imaging </span>techniques&#46;</p><p class="elsevierStylePara">In Spain&#44; it is estimated that 9&#46;24&#37; of the adult population suffers from some degree of CKD&#44; with 6&#46;83&#37; of the general population having stages 3-5 CKD&#46; CKD prevalence is increasing due to an ageing population&#44; the increased prevalence of risk factors such as cardiovascular disease and diabetes mellitus &#40;DM&#41;&#44; high blood pressure &#40;HBP&#41; or obesity and&#44; obviously&#44; due to its early diagnosis&#46; It is estimated that renal replacement therapy consumes 2&#46;5&#37; of the National Health System&#8217;s budget and more than 4&#37; of that of Specialist Care&#46;<span class="elsevierStyleSup">2</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Chronic kidney disease risk factors</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The continuous conceptual CKD model<span class="elsevierStyleSup">7</span> includes risk factors for each phase&#44; which are classified into susceptibility&#44; initiating&#44; progression and end-stage factors &#40;Table 1&#41;&#46; Some risk factors may be included in the susceptibility&#44; initiating and progression factor categories&#44; such as HBP&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Chronic kidney disease screening</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">CKD screening in risk populations should be carried out by assessing the eGFR and albuminuria at least once a year&#46; The diagnosis must not be based on one SINGLE eGFR and&#47;or albuminuria test and must ALWAYS be confirmed&#46;</p><p class="elsevierStylePara">We recommend CKD screening in patients with HBP&#44; type 2 DM or established cardiovascular disease&#46; Likewise&#44; its screening is advised in individuals older than 60 years of age&#44; those who are obese &#40;body mass index &#91;BMI&#93; &#62;35kg&#47;m<span class="elsevierStyleSup">2</span>&#41;&#44; with type 1 DM for more than five years&#44; patients with first degree relatives who have kidney disease or hereditary kidney diseases&#44; patients with urinary tract obstruction diseases&#44; patients on prolonged treatment with nephrotoxic drugs &#40;including non-steroidal anti-inflammatory drugs &#91;NSAIDs&#93;&#41;&#44; patients with other cardiovascular disease risk factors &#40;hyperlipidaemia&#44; metabolic syndrome&#44; smokers&#41;&#44; those with a history of acute renal failure and those with chronic infections&#44; autoimmune diseases and neoplasia associated with CKD&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">DIAGNOSIS OF CHRONIC KIDNEY DISEASE</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Estimation of the glomerular filtration rate</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Serum creatinine concentration should not be used as the only test for assessing renal function&#44; with GFR being the best tool for doing so&#46; Calculating the GFR from creatinine clearance &#40;measurement of creatinine concentration in serum and 24-hour urine&#41; has a series of disadvantages&#44; such as overestimation of the GFR and the problem posed by collecting 24-hour urine both for the patient and for laboratories&#46; Measuring creatinine clearance by collecting 24-hour urine does not improve GFR estimation from equations except in certain circumstances&#46;</p><p class="elsevierStylePara">We recommend estimating the GFR using equations obtained by measuring serum creatinine concentration&#44; age&#44; sex and ethnicity&#46; These equations are more accurate than an isolated measurement of serum creatinine&#46; The equations most used are those of the Modification of Diet in Renal Disease study &#40;MDRD-4 or MDRD-IDMS&#41;&#44;<span class="elsevierStyleSup">8</span> in accordance with whether the method used by the laboratory to measure serum creatinine is <span class="elsevierStyleBold">traceable </span>or not &#40;Table 2&#41; in the isotope dilution mass spectrometry &#40;IDMS&#41; reference measurement procedure&#44; with the latter being recommended&#46;</p><p class="elsevierStylePara">The CKD-EPI &#40;Chronic Kidney Disease-Epidemiology Collaboration&#41; equation&#44;<span class="elsevierStyleSup">9</span> also using standardised creatinine methods&#44; has advantages over MDRD-IDMS&#44; given that it is more accurate and improves the predictive capacity of the GFR &#40;particularly between values of 60 and 90ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#41;&#44; as well as improving the prediction of overall and cardiovascular mortality and the risk of developing ESRD&#46;<span class="elsevierStyleSup">10 </span>As such&#44; it is considered that CKD-EPI should replace the previous formulas &#40;Table 3&#41;&#46; The new 2012 KDIGO guidelines consider the use of alternative formulas to be acceptable if they have been shown to improve accuracy when compared with the CKD-EPI formula&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara">This equation has demonstrated that it is superior to other GFR estimation equations based on the serum concentration of creatinine &#40;MDRD&#41;&#44; cystatin C or the combination of both&#46;<span class="elsevierStyleSup">10-13</span></p><p class="elsevierStylePara">Although the Cockcroft-Gault &#40;C-G&#41; equation<span class="elsevierStyleSup">14</span> has classically been used in the adjustment of drug doses and has been a reference for assessing hyperfiltration states&#44; it should be advised against&#46; This equation has not been reformulated for creatinine values obtained using appropriate procedures and cannot be re-expressed for the current methods of measuring creatinine&#44; and as such&#44; it should not be used&#46; The CKD-EPI or MDRD-IDMS equations may be used for this purpose&#44; since they are based on standardised creatinine measurement procedures&#46; The GFR obtained by MDRD or CKD-EPI is useful for drug dose adjustment&#44; since it correlates better than that obtained by C-G for values below 60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; which are the most likely to require a dose adjustment and are available in the clinical laboratory reports&#44; unlike C-G&#46;<span class="elsevierStyleSup">10&#44;11&#44;15&#44;16</span></p><p class="elsevierStylePara">The values obtained using the MDRD or CKD-EPI equations are adjusted for a body surface area &#40;BSA&#41; of 1&#46;73m<span class="elsevierStyleSup">2</span>&#46;<span class="elsevierStyleSup"> </span>However&#44; when there is a need to use the formula or adjust particularly toxic drugs or those with a low therapeutic index in patients with major deviations in BSA&#44; GFR values should not be standardised to 1&#46;73m<span class="elsevierStyleSup">2</span>&#46;<span class="elsevierStyleSup"> </span>In these cases&#44; it is only necessary to multiply the laboratory result expressed in ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2 </span>by the patient&#8217;s real BSA ratio divided by 1&#46;73m<span class="elsevierStyleSup">2 </span>&#40;GFR x BSA&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#41;&#46;</p><p class="elsevierStylePara">In general&#44; the use of equations for estimating the GFR &#40;MDRD and CKD-EPI&#41; is inadequate in a series of clinical situations&#44; especially in individuals with an extreme body weight &#40;BMI &#60;19kg&#47;m<span class="elsevierStyleSup">2 </span>or 35kg&#47;m<span class="elsevierStyleSup">2</span>&#41;&#44; those with special diets or malnutrition&#44; muscle mass disorders&#44; amputations&#44; patients &#60;18 years of age&#44; those with liver disease&#44; pregnant women&#44; individuals with acute renal failure and in the study of potential kidney donors&#46; In these cases&#44; for an adequate measurement of renal function&#44; we would require 24-hour urine collection in order to calculate renal clearance&#46;<span class="elsevierStyleSup">3</span></p><p class="elsevierStylePara">Until present&#44; no clinical practice guidelines have included the use of cystatin C or the GFR estimated from it as a CKD screening parameter&#44; but the new 2012 KDIGO guidelines<span class="elsevierStyleSup">6 </span>suggest measuring cystatin C in adults with a GFR between 45 and 59ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44;<span class="elsevierStyleSup"> </span>without other renal lesion markers&#44; if diagnostic confirmation of CKD is required&#46; The recently published CKD-EPI equation for cystatin C should therefore be used&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Assessment of renal lesion</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Albuminuria &#40;urinary excretion of albumin&#41;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Albuminuria is&#44; along with GFR&#44; the basis for CKD diagnosis and staging&#46; The persistent presence of high protein or albumin concentrations in urine is not only a sign of renal lesion&#44; but is also often a sign of &#8220;systemic damage&#8221; beyond the kidney&#46; Different studies have demonstrated the importance of proteinuria in the pathogeny of CKD <span class="elsevierStyleBold">progression</span>&#44; as well as the link between albuminuria and renal <span class="elsevierStyleBold">prognosis</span> and <span class="elsevierStyleBold">mortality</span> in various populations <span class="elsevierStyleBold">independently </span>of the GFR and other classic cardiovascular disease risk factors&#46;</p><p class="elsevierStylePara">We recommend not using terms such as micro- or macroalbuminuria and employing the term albuminuria or urinary albumin excretion and the absolute value of the albumin&#47;creatinine ratio &#40;ACR&#41; in urine&#44; preferably in the first urine of the morning&#46; The ACR is a more sensitive marker than proteinuria in the context of CKD secondary to DM&#44; HBP or glomerular disease&#44; which are more common causes of CKD in adults&#46;</p><p class="elsevierStylePara">In the case of patients with CKD diagnosis and significant proteinuria &#40;for example&#44; an ACR &#62;300-500mg&#47;g&#41;&#44; monitoring could be carried out using the protein&#47;creatinine ratio in urine since it is a more economical test and because&#44; as proteinuria increases&#44; particularly in nephrotic proteinuria&#44; the ACR is less sensitive&#46; The use of the protein&#47;creatinine ratio in urine is also recommended in patients who have suspected interstitial disease and nephrotoxicity due to antiretrovirals&#44; since in both situations&#44; proteinuria mainly involves low molecular weight proteins that are different from albumin&#46; In order to determine albuminuria in a patient&#44; two high values in three samples obtained over a 3 to 6 month period are necessary&#46;</p><p class="elsevierStylePara">The value and persistence of albuminuria are closely related to renal and survival prognosis in CKD patients&#44; but we must also consider that albuminuria is a major independent marker of overall cardiovascular risk &#40;endothelial dysfunction&#44; arterial remodelling&#41;&#44; and not only of chronic kidney disease&#46; The presence of albuminuria alone&#44; without any other sign of renal damage&#44; is called into question by various authors as being specific to CKD&#44; since it may be detected in other diseases &#40;e&#46;g&#46; obesity&#44; smoking&#44; dermatitis and arthritis&#41;&#46;</p><p class="elsevierStylePara">We must remember that determining proteinuria includes not only the quantification of albuminuria&#44; but also the quantification of low molecular weight proteins&#44; such as proteins of tubular origin or immunoglobulin light chains&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Urinary sediment abnormalities</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The presence of haematuria and&#47;or leukocyturia in the urinary sediment for more than three months&#44; once a urological cause or urinary infection have been ruled out &#40;including urinary tuberculosis&#41;&#44; may also be an indication of CKD&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">X-ray pathological images</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Renal ultrasound firstly allows to rule out the presence of an <span class="elsevierStyleBold">obstructive </span>urinary tract pathology&#44; but also to identifiy structural abnormalities that indicate the presence of renal damage&#46; Simple isolated renal cysts alone are NOT criteria for renal damage&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Histological abnormalities</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The indication of biopsies is part of the specialist field in Nephrology&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">New chronic kidney disease staging</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Recently&#44; from the results of different clinical studies that include normal individuals&#44; those at risk of developing CKD and CKD patients&#44; the international organisation KDIGO<span class="elsevierStyleSup">6 </span>has established a new CKD prognostic classification based on eGFR and albuminuria stages&#46; This classification is divided into six risk categories according to the eGFR &#40;G1-G5&#41;&#44; which include three risk categories according to ACR concentration&#58; <span class="elsevierStyleBold">A1</span> for optimal or normal-high values &#40;&#60;30mg&#47;g or &#60;3mg&#47;mmol&#41;&#44; <span class="elsevierStyleBold">A2</span> for moderately high values &#40;30-299mg&#47;g or 3-29mg&#47;mmol&#41;&#44; and <span class="elsevierStyleBold">A3</span> for very high values &#40;&#8805;300mg&#47;g or &#8805;30mg&#47;mmol&#41;&#44; respectively &#40;Table 4&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">DEFINITION OF CHRONIC KIDNEY DISEASE PROGRESSION</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The mean annual GFR decrease is very variable and is higher in patients with significant proteinuria&#44; DM or HBP&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Key points</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">1&#46; </span>Normal renal progression rate&#58; 0&#46;7-1ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span> per year from 40 years of age&#46;<span class="elsevierStyleSup">6</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">2&#46; </span>We can consider that a patient has renal progression&#58; with a GFR &#62;5ml&#47;min&#47;year or &#62;10ml&#47;min in five years&#46;<span class="elsevierStyleSup">1</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">3&#46; </span>Progression must be defined on the basis of two <span class="elsevierStyleBold">aspects</span>&#58;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">-&#160;Progression to a higher renal function deterioration category </span>&#40;&#60;30&#44; 30-299&#44; &#62;300mg&#47;g&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">-&#160;Percentage of change with respect to the baseline situation</span> &#40;&#62;25&#37; deterioration in the GFR&#41; or a more than 50&#37; increase in the ACR&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">4&#46;&#160;For assessing renal progression&#44; we recommend albuminuria and baseline GFR estimation</span>&#44; as well as the identification of renal progression factors&#46; This will indicate the frequency of successive laboratory tests&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">5&#46;&#160;</span>To ensure the accuracy of renal deterioration rate measurement&#44; the aforementioned guidelines advise carrying out two <span class="elsevierStyleBold">measurements of eGFR within a period of no less than three months </span>and ruling out a decrease due to acute renal failure or the start of treatment with drugs that affect glomerular haemodynamics &#40;angiotensin converting enzyme inhibitors &#91;ACEI&#93;&#44; angiotensin II receptor blockers &#91;ARBs&#93;&#44; NSAIDs&#44; diuretics&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">6&#46;&#160;In</span><span class="elsevierStyleBold"> patients with a new diagnosis of CKD</span> &#40;for the first time&#41;&#44; GFR estimation must be repeated within a period of no less than three months&#44; in order to rule out acute renal deterioration due to exogenous factors &#40;diarrhoea&#44; vomiting&#44; depletion due to diuretics or any drug that affects glomerular haemodynamics&#44; such as ACEI&#44; ARBs or direct renin inhibitors&#41;&#46; It may be repeated within less than three months where the clinical situation indicates&#46; <span class="elsevierStyleBold">In patients with known </span>CKD&#44; it is suggested to measure the eGFR and the ACR once a year if they have a low risk of progression&#44; and more frequently if there is a high risk of progression&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">PREDICTORS OF PROGRESSION</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The factors of renal progression are displayed in Table 5&#46;<span class="elsevierStyleSup">5&#44;17-28</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">CRITERIA FOR REFERRAL TO NEPHROLOGY &#40;Figure 1&#41;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Referral to Nephrology will be carried out taking into account the CKD stage&#44; the speed of renal failure progression&#44; the degree of albuminuria&#44; warning signs&#44; associated comorbidities and the patient&#8217;s functional situation&#46;<span class="elsevierStyleSup">3&#44;5&#44;29</span></p><p class="elsevierStylePara">Generally speaking&#44; <span class="elsevierStyleBold">patients who have an eGFR &#60;30ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2 </span>should be referred to the Nephrology specialist </span>&#40;except those &#62;80 years of age without renal progression and albuminuria &#60;300mg&#47;g&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">According to glomerular filtration rate&#58;</span></p><p class="elsevierStylePara">- All patients with an eGFR &#60;30ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; except patients &#62;80 years of age without renal progression&#46;</p><p class="elsevierStylePara">- Patients &#62;80 years of age and with an eGFR &#60;20ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; if their general condition advises it&#44; can be referred for a nephrological assessment and agree on treatment&#46; It is recommended for the candidate patient to be referred to Nephrology at least one year prior to the start of renal replacement therapy&#46; Although this period is not easy to calculate&#44; renal progression &#40;see point 5&#41; may be used as a guideline&#46; The objective is to avoid a patient who is a candidate for renal replacement therapy requiring non-scheduled dialysis&#46;</p><p class="elsevierStylePara">Patients &#60;70 years of age with an eGFR between 30 and 45ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span> should be monitored more frequently &#40;every 3-6 months&#41; and only be referred to Nephrology in the case of albuminuria progression in two consecutive tests or when the ACR ratio is around 300mg&#47;g&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">- According to albuminuria&#58;</span> ACR ratio &#62;300mg&#47;g&#44; equivalent to proteinuria &#62;300mg&#47;24 hours&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Other reasons&#58;</span></p><p class="elsevierStylePara">- Acute deterioration of renal function &#40;&#62;25&#37; decrease in the eGFR&#41; in less than a month&#44; having excluded exogenous factors &#40;diarrhoea&#44; vomiting&#44; depletion due to diuretics during treatment with ACEI&#44; ARBs or direct renin inhibitors&#41;&#46;</p><p class="elsevierStylePara">- Patients who have renal progression &#40;&#62;5ml&#47;min&#47;year&#41; &#40;see definition above&#41;&#46;</p><p class="elsevierStylePara">- CKD and HBP refractory to treatment &#40;&#62;140&#47;90mmHg&#41; with three drugs at full dose&#44; one of them being a diuretic&#46;</p><p class="elsevierStylePara">- Abnormalities in potassium &#40;&#62;5&#46;5mEq&#47;l or &#60;3&#46;5mEq&#47;l without the patient receiving diuretics&#41;&#46;</p><p class="elsevierStylePara">- Anaemia&#58; haemoglobin &#91;Hb&#93;&#160;&#60;10&#46;5g&#47;dl with CKD in spite of correcting iron deficiency &#40;transferrin saturation index &#91;TSI&#93; &#62;20&#37; and ferritin &#62;100&#41;&#46;</p><p class="elsevierStylePara">- Warning signs&#58;</p><p class="elsevierStylePara">&#160; &#160;- Non-urological haematuria associated with proteinuria&#46;</p><p class="elsevierStylePara">&#160; &#160; - Decrease of &#62;25&#37; in the eGFR in less than one month or a &#62;25&#37; increase in plasma creatinine in less than one month&#44; ruling out exogenous factors &#40;diarrhoea&#44; vomiting&#44; depletion due to diuretics during treatment with ACEI&#44; ARBs or direct renin inhibitors&#41;&#46;</p><p class="elsevierStylePara">There may be Primary Care or joint follow-up&#44; according to the cases&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Elderly patients &#40;&#62;80 years of age&#41;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Given that CKD progression is very uncommon in the elderly population&#44; we can accept that patients older than 80 years of age with stable renal function or with a slow deterioration of the latter &#40;&#60;5ml&#47;min&#47;year&#41; without proteinuria or anaemia or warning signs can be followed up conservatively in Primary Care&#46;<span class="elsevierStyleSup">30&#44;31</span></p><p class="elsevierStylePara">Likewise&#44; elderly patients with stage 5 CKD who are not expected to live for long &#40;&#60;6 months&#41;&#44; who have a poor functional situation &#40;dependence in daily activities&#44; dementia&#44; etc&#46;&#41; or severe associated comorbidity or who do not accept dialysis may be suitable for palliative treatment either in Primary Care or shared with Nephrology&#46;<span class="elsevierStyleSup">32</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Diabetic patients</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Patients will be referred to Nephrology with the aforementioned criteria in mind&#44; and furthermore&#44; the following patients must be referred&#58;</p><p class="elsevierStylePara">- Those with albuminuria&#58; a &#40;confirmed&#41; ACR &#62;300mg&#47;g&#44; despite suitable treatment and blood pressure &#40;BP&#41; monitoring&#46;</p><p class="elsevierStylePara">- An increase in albuminuria despite suitable treatment&#46;</p><p class="elsevierStylePara">- Refractory HBP &#40;three drugs at full dose and absence of control&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Indications for a request for ultrasound in Primary Care</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Either for patient follow-up in Primary Care or for their referral to Nephrology&#44; the request for an ultrasound in the diagnostic study of CKD is considered to be relevant&#46; It is indicated in&#58;</p><p class="elsevierStylePara">- Progressive CKD &#40;decrease in the eGFR &#62;5ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span> in one year&#41;&#46;</p><p class="elsevierStylePara">-&#160;Macroscopic haematuria or persistent albuminuria&#46;</p><p class="elsevierStylePara">-&#160;Symptoms of urinary tract obstruction&#46;</p><p class="elsevierStylePara">-&#160;Age &#62;15 years and a family history of polycystic kidney disease&#46;</p><p class="elsevierStylePara">-&#160;Stage 4 or 5&#46; Assess associated comorbidities beforehand&#46;</p><p class="elsevierStylePara">-&#160;CKD with proteinuria&#46;</p><p class="elsevierStylePara">-&#160;Recurrent urinary infections with renal involvement&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">MONITORING AND FOLLOW-UP OF CHRONIC KIDNEY DISEASE PATIENTS</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The frequency of monitoring and visits of CKD patients is displayed in Table 6&#46; In any case&#44; it is necessary to individualise these general criteria&#46;</p><p class="elsevierStylePara">For each check-up in Primary Care&#44; we recommend&#58;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226; Monitoring BP and adjusting treatment&#46;</span> BP objective &#60;140&#47;90mmHg&#46; In patients with proteinuria &#40;ACR &#62;300mg&#47;g&#41;&#44; we recommend around 130&#47;80mmHg&#46; In elderly patients&#44; this measurement will be carefully individualised&#46;<span class="elsevierStyleSup">33</span> Avoid low blood pressure in elderly patients with significant atheromatous disease&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Monitoring anaemia&#58; if the patient has stage 3-5 CKD and Hb &#60;10&#46;5g&#47;dl &#40;once iron deficiency has been ruled out&#58; TSI &#62;20&#37; and ferritin &#62;100ng&#47;ml&#41;</span>&#44; estimate referral or advance it in Nephrology in order to assess treatment with erythropoiesis-stimulating factors&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Reviewing medication</span> and adjusting the dose in accordance with the GFR&#46; In stages 3-5 CKD&#44; avoid using NSAIDs&#44; oral anti-diabetic drugs eliminated in the kidneys and iodinated contrasts&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Reviewing dietary habits</span> and guiding the patient on the type of diet to follow according to the GFR&#58;</p><p class="elsevierStylePara">&#160; &#160;- Stages 1-3 CKD&#58; a low sodium diet is only recommended in the case of HBP&#46;</p><p class="elsevierStylePara">&#160; &#160;- Stages 4-5 CKD&#58; dietary recommendations for sodium&#44; phosphorus and potassium&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Laboratory tests in each check-up from stage 3 CKD&#42;</span> &#40;the minimum advised is in bold&#41;&#58;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160; &#160;-&#160;Complete blood count&#46;</span></p><p class="elsevierStylePara">&#160; -&#160;Blood biochemical analysis&#58; <span class="elsevierStyleBold">glucose&#44; creatinine</span>&#44; urea&#44; <span class="elsevierStyleBold">Na</span>&#44; <span class="elsevierStyleBold">K</span>&#44; Ca&#44; P&#44; albumin and cholesterol&#46; <span class="elsevierStyleBold">GFR estimated using MDRD or CKD-EPI&#46;</span></p><p class="elsevierStylePara">&#160; &#160;-&#160;Urinary biochemical analysis &#40;single urine sample&#44; first in the morning&#41;&#58; <span class="elsevierStyleBold">ACR</span>&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160; &#160;-&#160;Urinary sediment&#46;</span></p><p class="elsevierStylePara">The extractions should be combined so that they do not have to be repeated&#46; The patient will be provided with a report or&#44; failing that&#44; a copy of the tests&#46; If the Nephrology check-ups are carried out once a month&#44; it is not necessary to repeat the tests in Primary Care&#46;</p><p class="elsevierStylePara">Table 7 displays the objectives of monitoring and follow-up of CKD patients according to the stage&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">PREVENTION OF NEPHROTOXICITY</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Once the patient has been diagnosed with CKD&#44; the most important thing is to avoid its evolution&#44; and as such&#44; we must be aware that there are drugs used in daily practice&#44; and more specifically&#44; in these patients&#44; that may cause this disease to worsen&#46; Moreover&#44; the indiscriminate use of intravenous contrast agents without prior preparation may cause contrast-induced nephropathy&#46; As such&#44; it is necessary to avoid using nephrotoxins and minimise the effect and use of intravenous contrasts&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Avoid nephrotoxins and take precautions with drugs that may alter glomerular haemodynamics</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">1&#46;</span> Avoid <span class="elsevierStyleBold">hyperkalaemia </span>associated with drugs&#46; Particular caution must be taken with the association of a potassium-sparing diuretic &#40;spironolactone&#44; amiloride&#44; eplerenone&#41; to another potassium-retaining drug &#40;ACEI&#44; ARBs&#44; direct renin inhibitors&#44; NSAIDs&#44; beta blockers&#41;&#46; In these cases&#44; frequent monitoring of serum potassium is essential&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">2&#46;&#160;</span>Avoid using drugs that may cause rapid volume depletion and tubular damage&#44; particularly in situations of dehydration&#44; as well as those with a direct negative effect on the tubule &#40;aminoglycosides&#44; tacrolimus&#44; cyclosporin A&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">3&#46;&#160;</span>We must particularly emphasise <span class="elsevierStyleBold">avoiding the unnecessary use of NSAIDs</span>&#44; due to the risk of renal function deterioration&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">4&#46;&#160;</span>Adjust drugs to the GFR&#44; particularly in elderly and diabetic individuals&#46; In these patients&#44; metformin &#40;it should not be administered when the eGFR is &#60;30ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#41;&#44; oral anti-diabetic drugs eliminated via the kidney&#44; new anticoagulants&#44; nephrotoxic antibiotics and some heparins must be used with caution&#46; Many drugs produce direct nephrotoxicity and their detrimental effect worsens when combined with those that interfere with glomerular haemodynamics&#46; It is very important to avoid them in risk situations or adjust their dose in accordance with the eGFR &#40;aminoglycosides&#44; vancomycin&#44; aciclovir&#44; tenofovir&#44; amphotericin&#44; etc&#46;&#41;&#46; The list of drugs for adjusting the dose can be consulted on the following webpage&#58; http&#58;&#47;&#47;nefrologiadigital&#46;revistanefrologia&#46;com&#47;modules&#46;php&#63;name&#61;libro&#38;op&#61;viewCap&#38;idpublication&#61;1&#38;idedition&#61;13&#38;idcapitulo&#61;109&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Minimise the use of intravenous contrasts</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Contrast-induced nephropathy is defined as a deterioration in renal function manifested as a relative 25&#37; increase in creatinine or an absolute increase in creatinine of 0&#46;5mg&#47;dl with respect to baseline&#44; which occurs during the first three days following administration of the contrast&#44; not due to any other mechanism&#46; It occurs due to direct toxicity in tubular cells&#46;<span class="elsevierStyleSup">34</span></p><p class="elsevierStylePara">The most important aspect for preventing nephropathy by contrast is to detect it in patients at risk of developing it &#40;old age&#44; heart failure&#44; DM&#44; previous renal failure&#44; dehydration&#44; acute myocardial infarction&#44; shock&#44; contrast volume&#44; anaemia&#44; low blood pressure&#44; the use of nephrotoxins and high doses of diuretics&#44; taking care with drugs that alter glomerular haemodynamics and avoiding low blood pressure&#41;&#46; The best treatment is prevention&#44; avoiding risk situations&#46; We recommend discontinuing diuretics at least 4-6 days before administering the contrast&#44; as well as correct hydration using intravenous fluid therapy and oral hydration&#46; Some drugs may be potentially toxic after contrast administration&#44; such as metformin&#46; However&#44; there is currently not sufficient evidence to discontinue metformin in patients with previously normal renal function who are administered a &#8220;moderate&#8221; amount of contrast&#44;<span class="elsevierStyleSup">35 </span>although some authors suggest this&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">ATTITUDES&#44; LIFESTYLE AND TREATMENT</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Physical exercise</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">As a general rule&#44; it is recommended to carry out 30-60 minutes of moderate exercise 4 to 7 days a week&#46; When the kidney disease is established&#44; the exercise must be adapted to the physical ability of each patient&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Diet</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Dietary recommendations must be individualised in order to avoid patients being overweight or obese&#44; but also in accordance with their renal function and the existence of other risk factors in which some specific restriction is indicated&#46;</p><p class="elsevierStylePara">&#8226; Stages 1-3 CKD&#58; low salt diets are only recommended for HBP and&#47;or heart failure&#46;</p><p class="elsevierStylePara">&#8226;&#160;Stages 4-5 CKD&#58; dietary recommendations on sodium&#44; phosphorus&#44; potassium and proteins&#46;</p><p class="elsevierStylePara">The energy requirements are similar to those of the general population&#46; The information available suggests that protein restriction delays progression of kidney failure and should start to be applied when the GFR falls below 30ml&#47;min&#44; except in cases of proteinuria due to hyperfiltration&#44; where it must be established long before&#44; even with normal renal function&#46; Protein content must be adjusted to 0&#46;8g&#47;kg&#47;day &#40;at least half must be animal proteins of a high biological value&#41;&#44; but with a fat-based high-calorie content &#40;mono and polyunsaturated&#41; and carbohydrates&#44; if there is not carbohydrate intolerance or dyslipidaemia that require additional adjustments&#46; The appropriate protein intake in CKD patients is 0&#46;8g&#47;kg&#44; 50&#37; of which must be of high biological value&#44; that is&#44; of animal origin&#59; the remaining 50&#37; must be complemented with proteins contained in the rest of the foods included in the diet &#40;vegetable origin&#41;&#46; The use of high-protein diets&#44; as well as drugs that cause weight reduction&#44; may have adverse effects in CKD&#46;<span class="elsevierStyleSup">36</span></p><p class="elsevierStylePara">The daily consumption of salt must be less than 6g &#40;the equivalent of 2&#46;4g of sodium&#41;&#46; In initial phases of kidney disease&#44; a stricter salt restriction will only be applied to patients with HBP&#46; The diet must be complemented with potassium and phosphorus restriction and vitamin D intake&#46;</p><p class="elsevierStylePara">In CKD patients on haemodialysis &#40;HD&#41;&#44; protein intake may be increased by up to 1&#46;2g&#47;kg in order to achieve an adequate protein balance&#44; avoid calorie-energy exhaustion and attain an adequate nutritional status&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Alcohol</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Moderate alcohol intake is not considered to be harmful&#44; as with the general population&#44; that is&#44; around 12 to 14g of alcohol &#40;around 300cc of beer or 150cc of wine&#41;&#46; But we must bear in mind not only the calories present in alcohol&#44; but also the quantity of liquid and the sugar&#44; potassium&#44; phosphorus and sodium content&#44; which must be limited in many patients in accordance with associated risk factors and the degree of renal failure that they may cause&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">SPECIFIC OBJECTIVES OF TREATMENT</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">High blood pressure in chronic kidney disease&#58; treatment objectives<span class="elsevierStyleSup">5&#44;33&#44;37</span></span></p><p class="elsevierStylePara">&#8226;&#160;In CKD patients&#44; the objective of anti-hypertensive treatment is threefold&#58; to reduce BP&#44; to reduce the risk of cardiovascular complications and to slow down CKD progression&#46;</p><p class="elsevierStylePara">&#8226;&#160;In patients with CKD and an ACR &#60;30mg&#47;g&#44; the recommended BP control target is &#8804;140&#47;90mmHg&#46; If the ACR is &#8805;30mg&#47;g&#44; a stricter target is suggested&#44; with BP &#8804;130&#47;80mmHg&#44; both in patients with and those without DM&#46;</p><p class="elsevierStylePara">&#8226;&#160;The drugs of first choice are those that block the renin-angiotensin system actions&#44; either ACEI or ARBs&#46;</p><p class="elsevierStylePara">&#8226;&#160;The use of anti-hypertensive drug combinations is recommended to achieve the control objectives&#46; This combination must include a thiazide or loop diuretic depending on the severity of CKD&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Hyperglycaemia management in chronic kidney disease</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Management objectives</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">How is metabolic control assessed&#63;&#160;</p><p class="elsevierStylePara">Glycated haemoglobin A<span class="elsevierStyleInf">1C</span> &#40;HbA<span class="elsevierStyleInf">1C</span>&#41; is the reference parameter for assessing metabolic control in patients with chronic renal failure &#40;CRF&#41; and we must bear in mind factors that limit its usefulness as a glycaemic control marker&#44; such as transfusions and treatment with erythropoietin&#46;<span class="elsevierStyleSup">38-43</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Objectives of glycaemic control</p><p class="elsevierStylePara">The guidelines recommend that in patients with short-term DM and without a decrease in life expectancy&#44; the target must be HbA<span class="elsevierStyleInf">1C</span> &#60;7 &#40;&#60;53mmol&#47;mol&#41;&#46;<span class="elsevierStyleSup">44</span></p><p class="elsevierStylePara">By contrast&#44; for patients with long-term DM with a previous history of poor glycaemic control or with a condition that decreases life expectancy&#44; the control target must be individualised&#44; avoiding therapeutic strategies that involve an unacceptable increase in the risk of hypoglycaemia&#46;</p><p class="elsevierStylePara">There is no evidence that indicate what the optimal HbA<span class="elsevierStyleInf">1C </span>level is for dialysis patients&#46;</p><p class="elsevierStylePara">It is necessary to bear in mind that the risk of severe hypoglycaemia in patients with renal failure on intensive treatment is very high and is increased by a decreased intake&#44; a change in meal times and the presence of autonomic neuropathy&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Oral anti-diabetic drugs<span class="elsevierStyleSup">44</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Secretagogues&#160;</p><p class="elsevierStylePara">Sulfonylureas &#40;SU&#41; are not the first choice drug in renal failure&#46;</p><p class="elsevierStylePara">Glibenclamide and glimepiride are metabolised in the liver to weaker metabolites&#44; but are eliminated in urine&#44; and as such&#44; even in low doses&#44; their use is not recommended in patients with CRF&#46;</p><p class="elsevierStylePara">Glipizide is metabolised to inactive metabolites and&#44; consequently&#44; it would be the only SU that could be administered in CRF&#44; but its use is not permitted with a low GFR &#40;CCr &#60;30ml&#47;m&#41;&#46;</p><p class="elsevierStylePara">Repaglinide is metabolised in the liver and less than 10&#37; is eliminated via the kidneys&#46; Nevertheless&#44; a low dose of treatment &#40;0&#46;5mg&#41; should initially be administered&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Metformin&#160;</p><p class="elsevierStylePara">Metformin is mainly eliminated in urine without being metabolised&#46; In its data sheet&#44; its use is not recommended with an eGFR &#60;60ml&#47;min&#44; but this recommendation is not usually followed in normal clinical practice&#46; With an eGFR &#60;45ml&#47;min&#44; it is recommended to monitor glycaemia and renal function frequently and not administer it with an eGFR &#60;30ml&#47;min&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Alpha-glucosidase inhibitors</p><p class="elsevierStylePara">Both acarbose and miglitol and their metabolites accumulate in renal failure and their use is therefore not recommended&#46;<span class="elsevierStyleSup">45</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Glitazones&#160;</p><p class="elsevierStylePara">Glitazones are metabolised in the liver and less than 2&#37; is eliminated in urine&#46; There is therefore no accumulation of active metabolites in renal failure&#46; However&#44; given that their use increases the risk of oedema&#44; heart failure and osteoporosis&#44; it is limited in these patients and contraindicated in those on dialysis&#46;&#160;</p><p class="elsevierStylePara">Dipeptidyl peptidase-4 inhibitors&#160;</p><p class="elsevierStylePara">When there is an eGFR greater than 50ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span><span class="elsevierStyleInf">&#44;</span> no gliptine requires adjustment&#46; Sitagliptin&#44; vildagliptin and saxagliptin require a dose adjustment whenever the GFR is less than 50ml&#47;minute&#46;</p><p class="elsevierStylePara">Sitagliptin must be used at doses of 50mg and 25mg whenever the GFR is between 50 and 30ml&#47;minute and less than 30ml&#47;minute&#44; respectively&#46;</p><p class="elsevierStylePara">Vildagliptin must be used at doses of 50mg whenever the GFR is less than 50ml&#47;minute&#44; including in ESRD requiring dialysis&#46;</p><p class="elsevierStylePara">Saxagliptin must be used at doses of 2&#46;5mg in patients with a GFR of less than 50ml&#47;minute&#46; Saxagliptin is not indicated in patients with ESRD or those on dialysis&#46;</p><p class="elsevierStylePara">Linagliptin does not require dose adjustment in any stage of CKD&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Glucagon-like peptide-1 analogues&#160;</p><p class="elsevierStylePara">Liraglutide is only indicated in patients with an eGFR &#62;60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#46; Experience with liraglutide and exenatide in this field is very limited&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Insulin&#160;</p><p class="elsevierStylePara">Insulin requirements are very variable and as such&#44; individualisation of treatment is essential&#46; We can indicate the following initial rules that must be adapted to each patient through glucose control&#58;</p><p class="elsevierStylePara">&#8226;&#160;CCr &#62;50&#58; does not require a dose adjustment&#46;</p><p class="elsevierStylePara">&#8226;&#160;CCr 50-10&#58; will require a 75&#37; reduction of the previous insulin dose&#46;</p><p class="elsevierStylePara">&#8226;&#160;CCr &#60;10&#58; will require a 50&#37; reduction of the previous insulin dose&#46;</p><p class="elsevierStylePara">The insulin regimen will be adapted to the control target and may be a conventional therapy or an intensive treatment&#44; although we should remember that the basal-bolus regimen has a lower rate of hypoglycaemia&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Objectives and management of dyslipidaemia&#160;</span></p><p class="elsevierStylePara">One of the factors that increase renal damage and accelerate renal function deterioration is dyslipidaemia&#44; independently of its arteriosclerosis-promoting effect&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Risk stratification</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">In accordance with the latest European guidelines&#44; CKD individuals must be considered to be patients with high or very high cardiovascular risk&#44; without the need to apply risk scales&#46; As such&#44; CKD patients with a GFR &#60;60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2 </span>are classified as having a very high cardiovascular risk&#46;<span class="elsevierStyleSup">46</span></p><p class="elsevierStylePara">Dyslipidaemia screening must be performed systematically&#46; Although LDL &#40;low-density lipoprotein&#41; cholesterol is the main risk predictor&#44; non-HDL &#40;high-density lipoprotein&#41; cholesterol may be better&#44; as is the case in diabetics or metabolic syndrome patients&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Evidence on the benefit of treating dyslipidaemia on chronic kidney disease</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Data obtained by <span class="elsevierStyleItalic">post hoc</span> analysis support the ability of statins to reduce cardiovascular complications in patients with stages 2 and 3 CKD&#46;<span class="elsevierStyleSup">47&#44;48</span></p><p class="elsevierStylePara">The results in stages 4 and 5 or in HD are not as clear&#46;<span class="elsevierStyleSup">49&#44;50</span> However&#44; in the SHARP &#40;Study of Heart and Renal Protection&#41; study&#44; a 17&#37; reduction in cardiovascular events was observed in patients with stages 3&#44; 4 and 5 CKD treated with simvastatin-ezetimibe compared with placebo&#46;<span class="elsevierStyleSup">51</span> This reduction was not observed in patients treated with dialysis&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Lifestyle recommendations</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Diet is the main determinant of cholesterol levels&#46; The basic advice is therefore dietary&#46; It is recommended that 30&#37; or less of the total calories come from fatty foods and that less than 10&#37; be saturated fats&#46; It is advised that no more than 300mg&#47;day of cholesterol be consumed&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Lipid-lowering drugs and chronic kidney disease</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Statins</p><p class="elsevierStylePara">It is not necessary to adjust statin dose&#44; except in very advanced stages of CKD<span class="elsevierStyleSup">3-5</span> and only for those that are eliminated via the kidney&#46; They are the treatment of choice&#46; CKD&#44; as well as old age&#44; female sex&#44; a low BMI&#44; liver dysfunction&#44; alcohol consumption&#44; systemic diseases and hypothyroidism&#44; increase the risk of side effects&#44; however&#44; these are not common&#46;</p><p class="elsevierStylePara">Drugs that are eliminated via the liver are the drugs of choice &#40;fluvastatin&#44; atorvastatin&#44; pitavastatin and ezetimibe&#41;&#46; Statins metabolised via CYP3A4 &#40;atorvastatin&#44; lovastatin&#44; simvastatin&#41; may increase side effects by enhancing pharmacological interactions when they are administered with certain inducing drugs &#40;phenytoin&#44; phenobarbital&#44; barbiturates&#44; rifampicin&#44; dexamethasone&#44; cyclophosphamide&#44; carbamazepine&#44; omeprazole&#41; or inhibitors&#46;</p><p class="elsevierStylePara">For kidney transplant patients&#44; certain interactions must be borne in mind&#44; particularly with cyclosporine and statins&#44; such as atorvastatin&#44; lovastatin and simvastatin&#44; since they may increase their levels and the risk of myopathy&#46; Fluvastatin&#44; pravastatin&#44; pitavastatin and rosuvastatin are less likely to interact&#46; Although tacrolimus is also metabolised by CYP3A4&#44; it seems that there is less risk of it interacting with statins&#46; In these patients&#44; statins must be introduced at low doses&#44; titrated with caution and the interactions must be monitored&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Fibrates&#160;</p><p class="elsevierStylePara">Most guidelines recommend gemfibrozil as the fibrate of choice and they recommend avoiding the others&#46; The risk of myopathy increases more than five times when it is combined with a statin and this is greater in CKD&#46; The association with statins may cause acute renal failure due to rhabdomyolysis&#46; If this combination is necessary&#44; fenofibrate must be used and strict monitoring must be carried out&#46; The normal dose of gemfibrozil is 600mg&#47;day and it can be used in patients with a GFR of between 15 and 59ml&#47;min&#46; Its use is not advised if the GFR is &#60;15ml&#47;min&#46; However&#44; given the lack of evidence on the cardiovascular benefit of hypertriglyceridaemia treatment with fibrates and their potential side effects&#44; treatment with fibrates is not recommended in CKD&#44; particularly in combination with statins&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Ezetimibe&#160;</p><p class="elsevierStylePara">Its efficacy along with simvastatin has been demonstrated in CKD patients in the SHARP study&#46;<span class="elsevierStyleSup">51</span> A dose adjustment is not necessary for renal failure&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Control objectives</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">CKD is a coronary heart disease risk equivalent&#59; therefore&#44; the objectives are the same as in patients with ischaemic heart disease&#46;</p><p class="elsevierStylePara">The therapeutic objective in CKD patients &#40;GFR &#60;60ml&#47;m&#41; is LDL cholesterol &#60;70mg&#47;dl or a 50&#37; reduction if the previous objective is not achievable&#46;<span class="elsevierStyleSup">16 </span>However&#44; recently the KDIGO guidelines for treating dyslipidaemia in CKD recommend therapy with statins for all adults &#62;50 years of age&#44; independently of LDL cholesterol levels&#46; Based on the SHARP study and in the <span class="elsevierStyleItalic">post hoc </span>analysis of clinical trials with statins compared with a placebo that studied CKD patients&#44; a strategy for &#8220;treating cardiovascular risk&#8221; has been established&#46; Likewise&#44; initiating treatment with statins in stage 5 CKD patients not on dialysis is not recommended&#46;<span class="elsevierStyleSup">52</span></p><p class="elsevierStylePara">After the creation of this document&#44; the new international guidelines on dyslipidaemia management in CKD &#40;Kidney Int Suppl 2013&#59; 3&#40;3&#41;&#58; 259-305&#41; were published&#44; which suggest not pursuing objectives&#44; but rather a strategy of &#8220;action&#8221;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Smoking</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Smoking is one of the factors directly involved in kidney disease progression and data have been published that link this habit to renal function deterioration in the general population &#40;the MRFIT study&#44;<span class="elsevierStyleSup">53 </span>the study by Briganti et al&#46;<span class="elsevierStyleSup">56</span>&#41; and in diabetics&#46;<span class="elsevierStyleSup">57-60</span></p><p class="elsevierStylePara">Therefore&#44; in all patients with CKD &#40;as with the general population&#41;&#44; we must ask patients about their tobacco consumption in all consultations that we perform &#40;both in primary and in specialised care&#41;&#46; Empathetic but firm and motivated advice should be given to smokers to encourage them to quit smoking&#44; and emphasis must be put on the individual benefits and the help available to achieve it &#40;systematic minimal intervention&#44; cognitive-behavioural techniques&#44; pharmacological treatment&#44; etc&#46;&#41;&#46;</p><p class="elsevierStylePara">In kidney disease patients&#44; nicotine replacement therapy &#40;patches&#44; chewing gum&#44; sweets&#41; seems to be safe&#44; as well as their combination with lower doses than normal of bupropion &#40;150mg&#47;24h&#41; in advanced stages of the disease&#46; Varenicline use at normal doses seems safe and&#44; as with bupropion&#44; it can be used at half the dose &#40;1mg&#47;24h&#41; of that of patients with moderately decreased renal function and in the general population&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Obesity</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">There are few specially designed clinical trials in this regard&#44; but there are data that support that the reduction of weight and intake of fat may decrease the risk of CKD&#46;<span class="elsevierStyleSup">61 </span></p><p class="elsevierStylePara">Treatment of obesity in CKD patients must be non-pharmacological and consist of physical exercise and a low-calorie diet&#44; in accordance with the recommendations of the corresponding section of these guidelines&#46;</p><p class="elsevierStylePara">The only drug authorised in Spain for treating obesity&#44; orlistat&#44; is indicated in individuals with a BMI higher than 30kg&#47;m<span class="elsevierStyleSup">2</span>&#46; It has interactions with many drugs and has not been studied in CKD patients&#44; and as such&#44; its use does not appear to be advisable in them&#46; The use of drugs to reduce appetite is not indicated in CKD patients&#46;<span class="elsevierStyleSup"> </span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Hyperuricaemia</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Hyperuricaemia is defined as the increase of uric acid levels above their solubility level in plasma&#46; This occurs in males with uric acid values greater than 7mg&#47;dl and in females&#44; due to the oestrogenic effect&#44; with values greater than 6mg&#47;dl&#46; Hyperuricaemia may be asymptomatic or cause diseases such as uric nephrolithiasis&#44; nephropathy due to uric acid&#44; tophaceous gout&#44; acute gouty arthritis and asymptomatic hyperuricaemia&#46; An increased cardiovascular risk has been reported with uric acid values in the high normal limit&#44; above 5&#46;2mg&#47;dl&#46;<span class="elsevierStyleSup">62&#44;63</span></p><p class="elsevierStylePara">It has been demonstrated that allopurinol and other xanthine oxidase inhibitors have effects on the circulatory system that are independent of uric acid concentration&#46;<span class="elsevierStyleSup">64-66</span></p><p class="elsevierStylePara">The clinical guidelines do not recommend treating asymptomatic hyperuricaemia&#44; since this would only be supported by two randomised clinical trials&#46;<span class="elsevierStyleSup">67&#44;68 </span>Another drug&#44; febuxostat&#44; has recently become available for treating hyperuricaemia in patients with a history of gout or uric arthritis&#46; In those with symptomatic hyperuricaemia and mild to moderate renal failure&#44; febuxostat administration has demonstrated greater efficacy and a similar safety to allopurinol&#44; without the need to adjust the dose&#46;<span class="elsevierStyleSup">69</span></p><p class="elsevierStylePara">Colchicine is indicated for treating acute gout attacks&#46; In patients with a GFR between 30 and 50ml&#47;min&#44; the dose must be reduced&#46; If the GFR is less than 30ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; colchicine use is contraindicated&#46; In the event of an acute gout crisis in these patients with a reduced eGFR&#44; intramuscular tetracosactrin &#40;Nuvacthen depot<span class="elsevierStyleSup">&#174;</span>&#41; may be administered for three days or corticosteroids in doses of 2-30mg&#47;day with a rapid reduction until they are discontinued after 5-7 days&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Anaemia</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The main cause of anaemia in CKD patients is the inadequate production of endogenous erythropoietin&#44; a hormone that acts on the differentiation and maturation of red blood cell precursors&#46; In CKD patients&#44; anaemia is defined as a situation in which Hb concentration in blood is two standard deviations below the mean Hb concentration of the general population&#44; corrected for age and sex&#46;<span class="elsevierStyleSup">70 </span>The lower limit of Hb levels from which anaemia is considered to exist in females is 11&#46;5g&#47;l&#44;<span class="elsevierStyleSup">71 </span>according to the S&#46;E&#46;N&#46; and 12g&#47;l according to the World Health Organization &#40;WHO&#41;&#44; the Kidney Disease Outcomes Quality Initiative &#40;KDOQI&#41; and the European Renal Best Practice &#40;ERBP&#41;&#46;<span class="elsevierStyleSup">72 </span>The lower limit of Hb values in males younger than 70 according to the S&#46;E&#46;N&#46;&#44; KDOQI and ERBP is 13&#46;5g&#47;l and 13g&#47;l according to the WHO&#46; For males older than 70 years of age&#44; the S&#46;E&#46;N&#46; and the WHO set the lower Hb limits at 12g&#47;l and the KDOQI and ERBP set it at 13&#46;5g&#47;l&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Diagnosis of anaemia and iron and erythropoiesis-stimulating agent administration assessment and criteria</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Characteristics of anaemia in chronic kidney disease</p><p class="elsevierStylePara">Anaemia associated with CKD is usually normocytic and normochromic in origin and is related to a decrease in erythropoietin production by peritubular cells&#44; low bone marrow response&#44; an increased production of hepcidin and a decrease in the availability of iron for erythropoiesis&#46;<span class="elsevierStyleSup">73</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">When to start the study of anaemia in chronic kidney disease</p><p class="elsevierStylePara">&#8226;&#160;When Hb is &#60;11g&#47;dl in premenopausal females and prepubertal patients&#46;</p><p class="elsevierStylePara">&#8226;&#160;When Hb is &#60;12g&#47;dl in adult males and postmenopausal females&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">How to study anaemia in chronic kidney disease&#44; laboratory requests</p><p class="elsevierStylePara">&#8226;&#160;Haematocrit &#40;Ht&#41;-Hb&#46;</p><p class="elsevierStylePara">&#8226;&#160;Haemocytometer readings&#58; mean corpuscular volume &#40;MCV&#41;&#44; mean corpuscular Hb &#40;MCH&#41;&#44; mean corpuscular Hb concentration &#40;MCHC&#41;&#46;</p><p class="elsevierStylePara">Reticulocytes&#46;</p><p class="elsevierStylePara">&#8226;&#160;Iron parameters&#58; serum iron&#44; ferritin&#44; transferrin&#44; TSI&#46;</p><p class="elsevierStylePara">&#8226;&#160;Rule out intestinal blood losses &#40;if microcytic hypochromic anaemia or suspicion of digestive bleeding&#41;&#46;</p><p class="elsevierStylePara">&#8226;&#160;In patients with stage 5 CKD on HD&#44; samples are taken immediately before dialysis&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Haemoglobin targets</p><p class="elsevierStylePara">In adult CKD patients&#44; Hb control targets between 10 and 12g&#47;dl must be aimed for and symptoms and comorbidity must be assessed&#46; If in patients with stages 3B to 5 CKD Hb &#60;10&#46;5g&#47;dl is found&#44; they should be referred to Nephrology if they were not being followed-up or they should be reviewed at an early stage&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Iron metabolism required before the start of treatment with erythropoiesis-stimulating agents</p><p class="elsevierStylePara">Sufficient caution should be taken to achieve and maintain target Ht&#47;Hb&#58;</p><p class="elsevierStylePara">&#8226;&#160;TSI &#8805;20&#37; and &#60;50&#37;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">During treatment with erythropoiesis-stimulating agents &#40;ESA&#41;&#44; iron metabolism should be studied every three months&#44; if the patient receives intravenous Fe&#46;</p><p class="elsevierStylePara">In patients with ESA without intravenous Fe&#44; the monitoring should be monthly until Hb has stabilised between 10 and 12g&#47;dl&#46;</p><p class="elsevierStylePara">In diabetic patients&#44; it is recommended to not start treatment with ESA until Hb &#60;10g&#47;dl has been achieved&#44; if the patient has a history of stroke&#46;</p><p class="elsevierStylePara">In patients not treated with EPO&#44; the target must be TSI &#8805;20&#37; and Ferritin &#8805;100ng&#47;ml&#46; Patients must be monitored every 3-6 months&#46;</p><p class="elsevierStylePara">The test must be carried out 15 days after the last dose of intravenous Fe is administered&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Intravenous iron administration regimen</p><p class="elsevierStylePara">It is administered with the purpose of preventing deficiency and maintaining iron reserves in order that the target Ht&#47;Hb is achieved and maintained&#46; The administration must be carried out in the hospital&#46; With certain joint protocols&#44; some intravenous Fe may be administered in the health centre under medical supervision&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Oral iron administration regimen</p><p class="elsevierStylePara">&#8226;&#160;Adults&#58; 200mg&#47;day&#46;</p><p class="elsevierStylePara">&#8226;&#160;Children&#58; 2-3mg&#47;kg&#47;day&#46;</p><p class="elsevierStylePara">In pre-dialysis&#44; home dialysis and PD adults who do not achieve adequate iron reserves with Fe by the oral route&#44; a 100mg infusion of Fe dextran or 500-1000mg of intravenous Fe carboxymaltose should be administered and this process should be repeated as necessary in accordance with the iron parameters&#46; Another option is intravenous iron sucrose &#40;maximum 200mg&#47;dose&#41;&#46;</p><p class="elsevierStylePara">It is considered unlikely for HD patients to achieve the target with oral Fe&#44; and as such&#44; intravenous iron will be required&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Route of erythropoiesis-stimulating agent administration&#160;</p><p class="elsevierStylePara">Subcutaneous administration is indicated in HD&#44; PD and home dialysis patients&#44; with the injection location being rotated&#46;</p><p class="elsevierStylePara">The intraperitoneal route would be possible when doses are administered to the empty abdomen or with a low amount of peritoneal fluid&#46; Higher doses may be required using this route&#46;</p><p class="elsevierStylePara">The intravenous route would be indicated in the case of high doses &#40;volume&#41; or recurrent ecchymosis at the site of injection&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">EPO dose and adjustment&#160;</p><p class="elsevierStylePara">It is prescribed by Nephrology services&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Transfusions in chronic kidney disease patients</p><p class="elsevierStylePara">&#8226;&#160;In patients with functional anaemia&#46;</p><p class="elsevierStylePara">&#8226;&#160;In patients who are resistant to EPO with chronic blood loss&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Potential adverse side effects of treatment with erythropoiesis-stimulating agents</p><p class="elsevierStylePara">HBP&#44; seizures&#44; arteriovenous fistula thrombosis&#44; increase in blood viscosity&#46; Treatment with ESA when there is Hb &#62;13g&#47;dl has been associated with high levels of cardiovascular disease&#44; although without an increase in mortality&#46;<span class="elsevierStyleSup">74</span></p><p class="elsevierStylePara">Anaemia control in CKD patients must incorporate educational programmes for patients that include information about the health issue&#44; professional support and lifestyle guidance&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Detection of mineral and bone metabolism disorders</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Calcium and phosphorus metabolism disorders in CKD are associated with various complications that are beyond simple bone involvement and include other systems&#44; particularly the cardiovascular system &#40;for example&#44; calcifications&#41;&#46; The earliest clinical manifestation is an increase in the parathyroid hormone &#40;PTH&#41;&#44; caused by active vitamin D deficiency &#40;calcitriol&#41;&#44; phosphate retention &#40;with or without hyperphosphataemia&#41; and&#47;or marked hyperphosphataemia&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Detection and treatment objectives</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">&#8226;&#160;Avoid hyperphosphataemia&#46;</p><p class="elsevierStylePara">&#8226;&#160;Maintain normal levels of calcium and phosphorus&#46;</p><p class="elsevierStylePara">&#8226;&#160;Avoid the onset and progression of secondary hyperparathyroidism&#46;</p><p class="elsevierStylePara">According to the 2003 K-DOQI&#44; 2007 S&#46;E&#46;N&#46; and 2011 S&#46;E&#46;N&#46; guidelines&#44;<span class="elsevierStyleSup">75-77 </span>the therapeutic objective is variable in different stages of CKD&#44; but it may be summarised by saying that we should aim to maintain calcium&#44; phosphate and PTH within the normal limits&#46; In stage 4&#44; it is even advised to maintain PTH values slightly higher than normal values&#46; The guidelines also recommend measuring calcidiol &#40;25-OH-vitamin D&#41; in order to diagnose the deficiency or insufficiency of vitamin D&#46; These levels should ideally be greater than 20-30ng&#47;m &#40;50-75nmol&#47;l&#41;&#46;</p><p class="elsevierStylePara">A small degree of stable hyperparathyroidism is not a concern&#44; but progressive hyperparathyroidism&#44; with PTH values that are two or three times higher than the reference value&#44; require consultation with Nephrology specialists&#46; Nephrologists should also be consulted for patients with high levels of phosphate that are greater than 5mg&#47;dl &#40;1&#46;40mmol&#47;l&#41;&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Treatment</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Treatment will be carried out through diet&#44; phosphate binders&#44; native or active vitamin D&#44; and&#47;or selective activation of vitamin D receptors&#46; Calcimimetics may be used in dialysis patients&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Drugs for adequate maintenance of mineral metabolism</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Phosphate binders</p><p class="elsevierStylePara">These are administered with meals&#46; Binders with calcium include calcium carbonate&#44; calcium acetate or its combination with magnesium&#46; Binders without calcium or aluminium include sevelamer and lanthanum carbonate&#46; Aluminium compounds are excellent binders&#44; but are not recommended over long periods&#44; given that they may induce aluminium intoxication in CKD patients&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Treatment of vitamin D deficiency</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Cholecalciferol &#40;D3&#41;&#58; Belenguer<span class="elsevierStyleSup">&#174;</span> or Kern<span class="elsevierStyleSup">&#174;</span></span><span class="elsevierStyleBold">vitamin D3 </span>&#40;cholecalciferol&#44; 800IU &#61; 12 drops&#44; 50&#160;000IU &#61; 25ml&#41;&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Calcifediol &#40;25-OH-vitamin D&#41;&#58; Hidroferol<span class="elsevierStyleSup">&#174;</span></span> 0&#46;266mg &#40;calcifediol 16&#160;000&#160;IU&#41;&#46;</p><p class="elsevierStylePara">The purpose of fortnightly or monthly calcifediol administration in vials is to normalise calcidiol levels &#40;25-OH &#62;20-30ng&#47;ml&#41; independently or not of a decrease in PTH&#46; It should be managed with the utmost care and it is necessary to measure calcium and phosphorus in its control&#44; since in patients with advanced CKD&#44; it may increase them&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Treatment of secondary hyperparathyroidism</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Calcitriol and vitamin D analogues&#58;</span> renal hydroxylation is not required to obtain the active form&#46; These include <span class="elsevierStyleBold">Rocaltrol<span class="elsevierStyleItalic"><span class="elsevierStyleSup">&#174;</span></span></span> &#40;calcitriol&#59; 1&#44;25-&#40;OH&#41;<span class="elsevierStyleInf">2</span>-D<span class="elsevierStyleInf">3</span>&#41; and&#160;<span class="elsevierStyleBold">Etalpha<span class="elsevierStyleItalic"><span class="elsevierStyleSup">&#174;</span></span></span> &#40;alfacalcidol&#59; 1&#945;-&#40;OH&#41;-D<span class="elsevierStyleInf">3</span>&#41;&#46; Alfacalcidol requires activation in the liver&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Selective vitamin D receptor activators&#58;</span><span class="elsevierStyleBold">Zemplar<span class="elsevierStyleItalic"><span class="elsevierStyleSup">&#174;</span></span></span> &#40;paricalcitol&#41;&#58; there is a lower likelihood of hypercalcaemia and hyperphosphataemia&#44; and it seems to induce fewer vascular calcifications&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#8226;&#160;Calcimimetics&#58;</span><span class="elsevierStyleBold">Mimpara<span class="elsevierStyleItalic"><span class="elsevierStyleSup">&#174;</span></span></span> &#40;cinacalcet&#41;&#58; indicated in the treatment of hyperparathyroidism in dialysis and in primary hyperparathyroidism&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Detection and treatment of acidosis</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">A situation of metabolic acidosis not compensated with venous bicarbonate &#60;15mmol&#47;l will require intravenous treatment in the hospital&#46; Mild metabolic acidosis &#40;bicarbonate between 15 and 20mmol&#47;l&#41; may require the administration of oral bicarbonate&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Other attitudes</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Preparation for renal replacement therapy and start time</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The optimal initiation of renal replacement therapy &#40;RRT&#41; is that which is planned&#46; The lack of planning unnecessarily increases the use of catheters in HD&#44; causing higher morbidity&#44; infections and increased hospitalisation&#46;</p><p class="elsevierStylePara">A referral of the patient to the nephrologist at the appropriate time means that the patient will receive the best information on the possible RRT techniques&#58; PD&#44; HD and home HD&#44; as well as the possibility of an early or living donor renal transplantation&#44; if this were available&#46; This adequate referral decreases complications&#44; particularly infectious and cardiovascular complications and has a significant impact on survival&#46;</p><p class="elsevierStylePara">RRT is considered when the GFR is &#60;15ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span> or earlier if there are signs or symptoms of uraemia or a difficulty in controlling hydration &#40;carried out frequently in diabetic patients&#41;&#44; HBP that is difficult to control or a deterioration of nutritional status&#46;</p><p class="elsevierStylePara">In general&#44; dialysis is introduced whenever the GFR is between 8 and 10ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span> and it is essential with a GFR &#60;6ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#44; even in the absence of symptoms of uraemia&#46; In high-risk patients&#44; we insist that the early introduction of dialysis should be considered and it should be personalised&#46;</p><p class="elsevierStylePara">It is necessary to bear in mind that the patient may be suitably studied and prepared for a potential living donor renal transplantation &#40;if this is possible&#41; before dialysis is initiated&#46; Likewise&#44; they can be studied and placed on the waiting list for a deceased donor renal transplantation&#44; where possible&#44; before starting dialysis&#46; This is what we call early renal transplantation&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Follow-up</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">Patients with stages 4-5 CKD should be monitored preferably by the nephrologist&#44; in close collaboration with the Primary Care doctor and the nursing staff&#46;</p><p class="elsevierStylePara">The frequency of visits must be established every three months in stage 4 CKD and every month in pre-dialysis stage 5 CKD&#46; This frequency may be modified according to the doctor&#8217;s opinion&#46;</p><p class="elsevierStylePara">In each visit&#44; it is advisable to provide detailed information about the laboratory test&#44; changes to treatment&#44; its justification and&#44; where appropriate&#44; a prognostic assessment&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Roles of the Primary Care doctor in addressing and following up chronic kidney disease determined by the stage of disease</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">&#8226;&#160;Follow-up of elderly patients&#44; with a stable GFR&#44; who due to age&#44; quality of life or other reasons&#44; do not receive RRT&#44; ESA and&#47;or medication for secondary hyperparathyroidism&#46;</p><p class="elsevierStylePara">&#8226;&#160;Control of cardiovascular risk factors&#46;</p><p class="elsevierStylePara">&#8226;&#160;Monitoring of CKD progression factors&#46;</p><p class="elsevierStylePara">&#8226;&#160;Monitoring of nephrotoxicity in order to avoid iatrogeny in any process&#46;</p><p class="elsevierStylePara">&#8226;&#160;Special attention must be paid to&#58;</p><p class="elsevierStylePara">&#160; &#160;-&#160;Avoiding NSAID use&#44; whenever possible&#46;</p><p class="elsevierStylePara">&#160; &#160;-&#160;Avoiding hyperkalaemia associated with the use of drugs&#46;</p><p class="elsevierStylePara">&#160; &#160;-&#160;Avoiding&#47;adjusting the use of oral anti-diabetics in accordance with the eGFR&#46;</p><p class="elsevierStylePara">&#160; &#160; -&#160;Avoiding&#44; insofar as possible&#44; use of iodine contrasts and adjusting all drugs to the patient&#8217;s eGFR&#46;</p><p class="elsevierStylePara">&#8226;&#160;Participation in therapeutic compliance and referral to Nephrology in the case of acute deterioration of renal function or complications&#46;</p><p class="elsevierStylePara">&#8226;&#160;Vaccination&#58; hepatitis B virus&#44; pneumococcus&#44; flu&#44; etc&#46;</p><p class="elsevierStylePara">&#8226;&#160;Collaboration in palliative activities&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Keys for managing haemodialysis&#47;peritoneal dialysis patients in Primary Care</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">&#8226;&#160;Facilitation of the disease adaptation process in accordance with age&#44; the family situation&#44; educational and work conditions&#44; the form of occurrence and development of the disease&#44; trust in the healthcare system&#44; etc&#46;</p><p class="elsevierStylePara">&#8226;&#160;Knowledge by the GP of the different options and implementation of the latter &#40;frequency&#44; location where it is performed&#44; potential complications according to the alternative chosen&#41;&#46;</p><p class="elsevierStylePara">&#8226;&#160;Good relationship and communication channel with the reference Nephrology Service&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Keys for managing kidney transplant patients</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The same applies as in the previous case but with a very intense interaction with the nephrologist&#44; for special requirements related to immunosuppression&#44; pharmacological interactions and vaccinations&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Keys for follow-up of terminal uraemia at home&#46; Palliative treatment</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The objective of home management of terminal uraemia is to facilitate the wellbeing of uraemic patients who cannot undergo dialysis&#44; minimising the physical&#44; family and healthcare impact of their condition and optimising the resources of our National Health System&#46; This requires close coordination between Nephrology and Primary Care&#46; In health areas where there are home support teams&#44; whether they are dependent on Primary Care or Specialist Care&#44; their inclusion in the therapeutic team could be very useful&#46;</p><p class="elsevierStylePara">The individualisation of the decision with the agreement of the patient&#44; family and professionals is recommended&#46; It is useful for the decision to be made at an early stage&#44; since it allows follow-up to be organised before a very significant deterioration has occurred in the patient&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Acknowledgements</span></p><p class="elsevierStylePara">We would like to thank Esteve and Abbvie laboratories for their logistical support in the project&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The authors declare that they have no conflicts of interest related to the contents of this article&#46;</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56728&#95;en&#95;t1&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56728_en_t1.jpg" alt="Chronic kidney disease risk factors"></img></a></p><p class="elsevierStylePara">Table 1&#46; Chronic kidney disease risk factors</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56729&#95;en&#95;t2&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56729_en_t2.jpg" alt="Equations to use in methods for measuring creatinine without traceability to IDMS &#40;non-standardised&#41;"></img></a></p><p class="elsevierStylePara">Table 2&#46; Equations to use in methods for measuring creatinine without traceability to IDMS &#40;non-standardised&#41;</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56730&#95;en&#95;t3&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56730_en_t3.jpg" alt="Equations to use in methods for measuring creatinine with traceability to IDMS &#40;standardised&#41;"></img></a></p><p class="elsevierStylePara">Table 3&#46; Equations to use in methods for measuring creatinine with traceability to IDMS &#40;standardised&#41;</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56731&#95;en&#95;t4&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56731_en_t4.jpg" alt="Prognosis of chronic kidney disease by estimated glomerular filtration rate and albuminuria &#40;6&#41;"></img></a></p><p class="elsevierStylePara">Table 4&#46; Prognosis of chronic kidney disease by estimated glomerular filtration rate and albuminuria &#40;6&#41;</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56732&#95;en&#95;t5&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56732_en_t5.jpg" alt="Predictors of chronic kidney disease progression"></img></a></p><p class="elsevierStylePara">Table 5&#46; Predictors of chronic kidney disease progression</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56737&#95;en&#95;t6&#95;copy1&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56737_en_t6_copy1.jpg" alt="Frequency of monitoring visits &#40;number of annual visits&#41;"></img></a></p><p class="elsevierStylePara">Table 6&#46; Frequency of monitoring visits &#40;number of annual visits&#41;</p><p class="elsevierStylePara"><a href="grande&#47;12455&#95;16025&#95;56738&#95;en&#95;t7&#46;jpg" class="elsevierStyleCrossRefs"><img src="12455_16025_56738_en_t7.jpg" alt="Objectives by specialty in chronic kidney disease patient follow-up "></img></a></p><p class="elsevierStylePara">Table 7&#46; 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        "resumen" => "<p class="elsevierStylePara">La enfermedad renal cr&#243;nica &#40;ERC&#41; es un importante problema de salud p&#250;blica que puede afectar en sus diferentes estadios a cerca del 10&#160;&#37; de la poblaci&#243;n espa&#241;ola y que supone una elevada morbilidad y mortalidad&#44; as&#237; como un importante consumo de recursos al Sistema Nacional de Salud&#46; Diez sociedades cient&#237;ficas involucradas en el manejo del paciente renal nos hemos puesto de acuerdo para hacer una puesta al d&#237;a del anterior documento de consenso sobre ERC de 2007&#46; El presente es la edici&#243;n abreviada del documento general extenso&#44; que puede ser consultado en las p&#225;ginas web de cada una de las sociedades firmantes&#46; Contiene los siguientes aspectos&#58; definici&#243;n&#44; epidemiolog&#237;a y factores de riesgo de la ERC&#46; Criterios de diagn&#243;stico&#44; evaluaci&#243;n y estadiaje&#160; de la ERC&#44; albuminuria y estimaci&#243;n del filtrado glomerular&#46; Concepto y factores de progresi&#243;n&#46; Criterios de derivaci&#243;n a Nefrolog&#237;a&#46; Seguimiento del paciente&#44; actitudes y objetivos por especialidad&#46; Prevenci&#243;n de la nefrotoxicidad&#46; Detecci&#243;n del da&#241;o cardiovascular&#46; Actitudes&#44; estilo de vida y tratamiento&#58; manejo de la hipertensi&#243;n arterial&#44; dislipemia&#44; hiperglucemia&#44; tabaquismo&#44; obesidad&#44; hiperuricemia&#44; anemia&#44; alteraciones del metabolismo mineral y &#243;seo&#46; Seguimiento coordinado por Atenci&#243;n Primaria-otras especialidades-Nefrolog&#237;a&#46; Manejo del paciente en tratamiento renal sustitutivo&#44; hemodi&#225;lisis&#44; di&#225;lisis peritoneal y trasplante renal&#46; Tratamiento paliativo de la uremia terminal&#46; Esperamos que sirva de gran ayuda en el manejo multidisciplinar del paciente con ERC&#44; a la vista de las recomendaciones m&#225;s actualizadas&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">Chronic kidney disease &#40;CKD&#41; is a major public health problem that&#44; in its different stages&#44; may affect up to 10&#37; of the Spanish population and results in high morbidity and mortality&#44; as well as high consumption of National Health System resources&#46; Ten scientific societies involved in the management of kidney patients agreed to update the 2007 CKD consensus document&#46; The current version is an abridged edition of the detailed general document&#44; which can be consulted on the webpages of each signatory society&#46; It includes the following aspects&#58; CKD definition&#44; epidemiology and risk factors and criteria on diagnosis&#44; assessment and staging of CKD&#44; albuminuria and glomerular filtration estimation&#46; Progression factors and concept&#46; Criteria for referral to Nephrology&#46; Patient follow-up&#44; attitudes and objectives by specialty&#46; Prevention of nephrotoxicity&#46; Detection of cardiovascular damage&#46; Attitudes&#44; lifestyle and treatment&#58; management of high blood pressure&#44; dyslipidaemia&#44; hyperglycaemia&#44; smoking&#44; obesity&#44; hyperuricaemia&#44; anaemia and mineral and bone metabolism disorders&#46; Coordinated follow-up by Primary Care &#8211; other specialties &#8211; Nephrology&#46; Management of renal replacement therapy&#44; haemodialysis&#44; peritoneal dialysis and renal transplantation patients&#46; Palliative treatment of terminal uraemia&#46; We hope that this document will be very useful in the multidisciplinary management of CKD patients&#44; in view of the updated recommendations&#46;</p>"
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