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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">To the Editor&#44;</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CASE REPORT</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">44-year-old patient&#44; nurse&#44; with no history of interest except hypertension &#40;AHT&#41; of 10 years progression&#44; being treated with enalapril 30&#160;mg&#44; nicardipine 10&#160;mg and hydrochlorothiazide 25&#160;mg&#44; without regular monitoring of blood pressure &#40;BP&#41;&#46; The patient sought consultation due to raised levels of BP &#40;160-180&#47;95-100mmHg&#41; for 4-5 months with frequent hypertensive crisis that caused admission to the Emergency Department&#46; The patient did not show signs of taking non-steriodal anti-inflammatory drugs&#44; nor history of lithiasis or urinary infection&#44; although chronic inguinal pain on the left side contributed to dysmenorrhoea and no study was carried out&#46; Examination revealed&#58; body mass index 29&#160;kg&#47;m<span class="elsevierStyleSup">2</span>&#44; BP 167&#47;94&#160;mmHg&#44; 87&#160;bpm&#44; normal cardiopulmonary auscultation&#44; enlarged abdomen and minimal bilateral malleolar oedema&#46;</p><p class="elsevierStylePara">Complementary examinations were also performed&#44; with the following results&#58;</p><ul><li>Ambulatory BP monitoring &#40;ABPM&#41;&#58; diurnal average 151&#47;80mmHg&#44; 61bpm&#44; pulse pressure 70&#46;6mmHg&#59; nocturnal average 137&#47;70mmHg&#44; 57bpm&#44; pulse pressure 66&#46;8mmHg&#46; Maximum diurnal BP 183&#47;99mmHg&#44; maximum nocturnal BP 171&#47;95mmHg&#46; Non-dipper BP pattern&#46;</li><li>Electrocardiogram&#58; sinus rhythm 72bpm&#59; Sokolow-Lyon index &#60;35mm&#59; asymmetric reversal of T-wave&#46;</li><li>Echocardiogram&#58; interventricular septum 12mm&#46;</li><li>Normal thoracic radiographs&#46;</li><li>Normal funduscopy&#46;</li><li>Abdominal ultrasound&#58; right kidney &#40;RK&#41; 13cm&#44; normal differentiation&#59; left kidney &#40;LK&#41; 25cm&#44; hydronephrotic&#44; without corticomedullary differentiation&#46;</li><li>Biochemical tests showed&#58; normal haemogram&#44; hepatic lipid profile&#44; uric acid&#44; ions and glycemia&#46; Urea&#58; 31mg&#47;dl&#44; creatinine 0&#46;79mg&#47;dl&#44; glomerular filtration rate &#40;MDRD-4&#41; &#62;60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#46;</li><li>Plasma renin activity &#40;PRA&#41; 1&#46;35ng&#47;ml&#47;h &#40;normal radioimmunoassay range 0&#46;2-3&#46;3ng&#47;ml&#47;h&#41;&#46;</li><li>Urine&#58; proteinuria 0&#46;11g&#47;24hr&#44; creatinine 161mg&#47;d&#44; Na 241mEq&#47;l&#44; fractional excretion of Na 0&#46;78&#37;&#46; Sediment&#58; 5 red blood cells&#47;field&#44; 30 leukocytes&#47;field&#44; negative nitrites&#59; creatinine clearance 113ml&#47;min&#46;</li><li>CT Angiogram &#40;axial computed tomography&#41;&#58; lithiasis and maximum ureterohydronephrosis on the left-side that caused traction of the ipsilateral renal artery &#40;Figure 1&#41;&#46;</li><li>Technetium Tc 99m Dimercaptosuccinic Acid Scintigraphy&#58; DR 100&#160;&#37;&#44; IR 0&#160;&#37;&#46;</li></ul><p class="elsevierStylePara">The patient was diagnosed with moderate risk stage 2 HBP&#44; initially of renovascular aetiology and failure of the RK&#44; and it was decided to carry out laparoscopic nephrectomy on the left side which went smoothly&#46; The anatomical pathology of the specimen reported a hydronephrotic kidney with lithiasis&#44; chronic pyelonephritis in the stage of exacerbation&#44; acute fibrino-hemorrhagic pyelonephritis&#44; uriniferous cysts and chronic erosive urethritis &#40;Figure 2&#41;&#46;</p><p class="elsevierStylePara">Progress from a clinical point of view was favourable&#46; Renal clearance and creatinine slightly and temporarily deteriorated following nephrectomy&#44; returning to their baseline levels in less than 15 days&#46; BP dropped signficantly&#46; Postoperative renogram revealed a RK with good vascularisation and radiotracer uptake capacity&#44; as well as adequate response to the diuretic&#46; Sequential images and the renographic curve showed adequate elimination&#44; without ectasia or obstructive behaviour&#46; At present&#44; three years after surgery&#44; BP remains well controlled &#40;self-measurement and ABPM&#41; with lecarnidipine 20mg&#47;day &#40;10mg in the summer&#41;&#44; and presents 1&#46;1mg&#47;dl of creatinine&#44; clearance of 71ml&#47;min and proteinuria 0&#46;09g&#47;day&#46; The patient has not re-experienced inguinal pain&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Nephrolithiasis&#44; in spite of techniques such as ureteroscopy&#44; lithotomy or lithotripsy&#44; is one of the causes that lead to the development of chronic renal failure&#46;<span class="elsevierStyleSup">1</span> The asymptomatic form is more frequent than expected&#44; reaching 11&#160;&#37; prevalence in a study carried out in potential donors&#46;<span class="elsevierStyleSup">2</span> The evolution of these &#8220;healthy carriers&#8221; of nephrolithiasis has not been studied&#44; the risk of chronic kidney disease being controversial&#44; which seems to relate to the size&#44; the composition and the location of the calculus&#44; among other factors&#46;<span class="elsevierStyleSup">3-7</span> The same occurred with the asymptomatic bacteriuria&#44; whose need for antiobiotic and&#47;or surgical treatment is dependant on&#44; in addition to microbiology and the age of the patient&#44; the existence or not of morphological changes in the urinary tract&#44; since it seems that these are one of the main factors that directly influence the perpetuation of renal failure&#46;<span class="elsevierStyleSup">8</span> In our case&#44; there was no possibility of this approach&#44; since the diagnosis of both disorders was carried out simultaneously and the renal failure of the suffering kidney was already established&#46; The microbiology and the composition of the calculus was unknown in our case &#40;histological examination of the lithiasis was not carried out because urine calcium oxalate was normal&#41;&#46; In addition&#44; there was no family history of lithiasis and no prevous imaging of the reno-ureteral system&#46; Thus&#44; we did not know whether the liathisis was the cause of the infections or viceversa&#46;<span class="elsevierStyleSup">9</span></p><p class="elsevierStylePara">In terms of imaging diagnosis&#44; in the ultrasound there was no clear image of the nephrolithiasis&#44; likely due to the location of the calculus obstruction&#44; clearly showing up in the CT scan and in the surgical specimen&#46; The CT has&#44; likewise&#44; greater sensitivity than the ultrasound to detect nephrolithiasis &#60;5mm&#44; as well as other renal anomolies&#46;<span class="elsevierStyleSup">10</span> A Doppler ultrasound was not carried out because of the anthropometric characteristics of the patient &#40;obesity&#41;&#44; directly indicating CT-angiogram under protocol of nephroprotection&#44; given the presumption of unilateral functional nullity&#46;</p><p class="elsevierStylePara">We understand the pathophysiology as to why this patient developed HBP at 34 as multifactorial&#58; a&#41; the stretching of the renal artery due to traction of the hydronephrotic kidney caused its stenosis&#44; and subsequent activation of the renin-angiotensin-aldosterone system &#40;RAAS&#41;&#44; similar to what happens in some cases of renal ptosis&#46;<span class="elsevierStyleSup">11</span> Although we do not have previous images to establish a differential diagnosis of hypoplastic renal artery&#44; the patient presented ultrasound pregnancy check-ups without changes&#59; b&#41; nephrolithiasis determined a state of obstructive uropathy and with that the formation of uriniferous cysts that compressed the renal parenchyma&#44; also activating RAAS&#59;<span class="elsevierStyleSup">12</span> c&#41; interstitial inflammation as an immune response to the urinary infection reduced the area of the peritubular capillaries&#44; hindering the mechanism of natriuresis because of pressure&#46;<span class="elsevierStyleSup">13</span> The PARA of the patient was within the normal range because of its suppression in the contralateral kidney&#44; as well as&#44; in the majority of individuals&#44; this figure being normal once HBP was established&#46;<span class="elsevierStyleSup">14</span> The elevated excretion of sodium in the urine indicated increased ingestion&#44; and its fractional excretion &#60;&#160;1&#160;&#37;&#44; an increase in its tubular reabsorption &#40;obstructive uropathy that can also present itself in the non-functioning kidney with 0&#160;&#37; of participation in the scintography&#41;&#44; despite presenting low doses of thiazide diuretic&#46;</p><p class="elsevierStylePara">The laparoscopic nephrectomy was carried out routinely in patients with complicated lithiasis and also in renal artery stenosis&#44; both separately&#46;<span class="elsevierStyleSup">15&#44;16</span> What is unique about our case is the conjunction of both illness and the mechanical aetiological component of arterial stenosis&#44; not giving an option for endovascular treatment&#46;</p><p class="elsevierStylePara">Having revised the histology of the specimen&#44; although the extensive fibrosis did not allow the aetiology of the chronicity to be well seen&#44; it seems that the predominant factor of nephropathy could be the tubulo-intersitial&#44; caused by primary infection and&#47;or obstruction&#46; Ischaemic nephrosclerosis&#44; reflected as areas of haemorrhage and intimal thickening&#44; seems to remain&#44; at least&#44; in the background in this case&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CONCLUSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Different factors can cause HBP&#46; Giant hydronephrosis can cause stenosis by stretching the renal artery&#44; causing renovascular hypertension&#46; Nephrectomy is the main therapeutic option in cases of functional nullity&#46; Urinary infections and nephrolithiasis can also contribute to the development of HBP&#44; but the necessary approach when faced with bacteriuria and&#47;or nephrolithiasis remains in controversy&#44; unless morphological changes develop which are perpetuated by the factors that predispose the development of chronic renal disease&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</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;11883&#95;19157&#95;56753&#95;en&#95;ref&#46;1188328128&#95;11883&#95;19115&#95;53504&#95;es&#95;11883&#95;figura1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11883_19157_56753_en_ref.1188328128_11883_19115_53504_es_11883_figura1.jpg" alt="CT Angiogram&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; CT Angiogram&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11883&#95;19157&#95;56755&#95;en&#95;ref&#46;1188328128&#95;11883&#95;19115&#95;53506&#95;es&#95;11883&#95;figura2&#46;jpg" class="elsevierStyleCrossRefs"><img src="11883_19157_56755_en_ref.1188328128_11883_19115_53506_es_11883_figura2.jpg" alt="Surgical anatomical pathology&#46;"></img></a></p><p class="elsevierStylePara">Figure 2&#46; 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Multifactorial hypertension of nephro-urological aetiology. A case study.
Hipertensión multifactorial de etiología nefrourológica. A propósito de un caso
Adoración Martín-Gómeza, Francisco J. González-Martínezb, Francisco Pulido-Fernándezc, Emilia Medina-Estévezc, M. Eugenia Palacios-Gómezd, J. Miguel García-Díeze, Antonio Hernández-Laof, J. Ramón Gómez-Fuentesg
a Unidad de Nefrología, Hospital de Poniente, El Ejido, Almería
b Unidad de Nefrología, Complejo Hospitalario Torrecárdenas, Almería,
c Servicio de Anatomía Patológica, Complejo Hospitalario Torrecárdenas, Almería,
d Unidad de Nefrología, Hospital de Poniente, El Ejido, Almería,
e Servicio de Radiología, Complejo Hospitalario Torrecárdenas, Almería,
f Servicio de Urología, Complejo Hospitalario Torrecárdenas, Almería,
g Servicio de Medicina Nuclear, Complejo Hospitalario Torrecárdenas, Almería,
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Examination revealed&#58; body mass index 29&#160;kg&#47;m<span class="elsevierStyleSup">2</span>&#44; BP 167&#47;94&#160;mmHg&#44; 87&#160;bpm&#44; normal cardiopulmonary auscultation&#44; enlarged abdomen and minimal bilateral malleolar oedema&#46;</p><p class="elsevierStylePara">Complementary examinations were also performed&#44; with the following results&#58;</p><ul><li>Ambulatory BP monitoring &#40;ABPM&#41;&#58; diurnal average 151&#47;80mmHg&#44; 61bpm&#44; pulse pressure 70&#46;6mmHg&#59; nocturnal average 137&#47;70mmHg&#44; 57bpm&#44; pulse pressure 66&#46;8mmHg&#46; Maximum diurnal BP 183&#47;99mmHg&#44; maximum nocturnal BP 171&#47;95mmHg&#46; Non-dipper BP pattern&#46;</li><li>Electrocardiogram&#58; sinus rhythm 72bpm&#59; Sokolow-Lyon index &#60;35mm&#59; asymmetric reversal of T-wave&#46;</li><li>Echocardiogram&#58; interventricular septum 12mm&#46;</li><li>Normal thoracic radiographs&#46;</li><li>Normal funduscopy&#46;</li><li>Abdominal ultrasound&#58; right kidney &#40;RK&#41; 13cm&#44; normal differentiation&#59; left kidney &#40;LK&#41; 25cm&#44; hydronephrotic&#44; without corticomedullary differentiation&#46;</li><li>Biochemical tests showed&#58; normal haemogram&#44; hepatic lipid profile&#44; uric acid&#44; ions and glycemia&#46; Urea&#58; 31mg&#47;dl&#44; creatinine 0&#46;79mg&#47;dl&#44; glomerular filtration rate &#40;MDRD-4&#41; &#62;60ml&#47;min&#47;1&#46;73m<span class="elsevierStyleSup">2</span>&#46;</li><li>Plasma renin activity &#40;PRA&#41; 1&#46;35ng&#47;ml&#47;h &#40;normal radioimmunoassay range 0&#46;2-3&#46;3ng&#47;ml&#47;h&#41;&#46;</li><li>Urine&#58; proteinuria 0&#46;11g&#47;24hr&#44; creatinine 161mg&#47;d&#44; Na 241mEq&#47;l&#44; fractional excretion of Na 0&#46;78&#37;&#46; Sediment&#58; 5 red blood cells&#47;field&#44; 30 leukocytes&#47;field&#44; negative nitrites&#59; creatinine clearance 113ml&#47;min&#46;</li><li>CT Angiogram &#40;axial computed tomography&#41;&#58; lithiasis and maximum ureterohydronephrosis on the left-side that caused traction of the ipsilateral renal artery &#40;Figure 1&#41;&#46;</li><li>Technetium Tc 99m Dimercaptosuccinic Acid Scintigraphy&#58; DR 100&#160;&#37;&#44; IR 0&#160;&#37;&#46;</li></ul><p class="elsevierStylePara">The patient was diagnosed with moderate risk stage 2 HBP&#44; initially of renovascular aetiology and failure of the RK&#44; and it was decided to carry out laparoscopic nephrectomy on the left side which went smoothly&#46; The anatomical pathology of the specimen reported a hydronephrotic kidney with lithiasis&#44; chronic pyelonephritis in the stage of exacerbation&#44; acute fibrino-hemorrhagic pyelonephritis&#44; uriniferous cysts and chronic erosive urethritis &#40;Figure 2&#41;&#46;</p><p class="elsevierStylePara">Progress from a clinical point of view was favourable&#46; Renal clearance and creatinine slightly and temporarily deteriorated following nephrectomy&#44; returning to their baseline levels in less than 15 days&#46; BP dropped signficantly&#46; Postoperative renogram revealed a RK with good vascularisation and radiotracer uptake capacity&#44; as well as adequate response to the diuretic&#46; Sequential images and the renographic curve showed adequate elimination&#44; without ectasia or obstructive behaviour&#46; At present&#44; three years after surgery&#44; BP remains well controlled &#40;self-measurement and ABPM&#41; with lecarnidipine 20mg&#47;day &#40;10mg in the summer&#41;&#44; and presents 1&#46;1mg&#47;dl of creatinine&#44; clearance of 71ml&#47;min and proteinuria 0&#46;09g&#47;day&#46; The patient has not re-experienced inguinal pain&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">DISCUSSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Nephrolithiasis&#44; in spite of techniques such as ureteroscopy&#44; lithotomy or lithotripsy&#44; is one of the causes that lead to the development of chronic renal failure&#46;<span class="elsevierStyleSup">1</span> The asymptomatic form is more frequent than expected&#44; reaching 11&#160;&#37; prevalence in a study carried out in potential donors&#46;<span class="elsevierStyleSup">2</span> The evolution of these &#8220;healthy carriers&#8221; of nephrolithiasis has not been studied&#44; the risk of chronic kidney disease being controversial&#44; which seems to relate to the size&#44; the composition and the location of the calculus&#44; among other factors&#46;<span class="elsevierStyleSup">3-7</span> The same occurred with the asymptomatic bacteriuria&#44; whose need for antiobiotic and&#47;or surgical treatment is dependant on&#44; in addition to microbiology and the age of the patient&#44; the existence or not of morphological changes in the urinary tract&#44; since it seems that these are one of the main factors that directly influence the perpetuation of renal failure&#46;<span class="elsevierStyleSup">8</span> In our case&#44; there was no possibility of this approach&#44; since the diagnosis of both disorders was carried out simultaneously and the renal failure of the suffering kidney was already established&#46; The microbiology and the composition of the calculus was unknown in our case &#40;histological examination of the lithiasis was not carried out because urine calcium oxalate was normal&#41;&#46; In addition&#44; there was no family history of lithiasis and no prevous imaging of the reno-ureteral system&#46; Thus&#44; we did not know whether the liathisis was the cause of the infections or viceversa&#46;<span class="elsevierStyleSup">9</span></p><p class="elsevierStylePara">In terms of imaging diagnosis&#44; in the ultrasound there was no clear image of the nephrolithiasis&#44; likely due to the location of the calculus obstruction&#44; clearly showing up in the CT scan and in the surgical specimen&#46; The CT has&#44; likewise&#44; greater sensitivity than the ultrasound to detect nephrolithiasis &#60;5mm&#44; as well as other renal anomolies&#46;<span class="elsevierStyleSup">10</span> A Doppler ultrasound was not carried out because of the anthropometric characteristics of the patient &#40;obesity&#41;&#44; directly indicating CT-angiogram under protocol of nephroprotection&#44; given the presumption of unilateral functional nullity&#46;</p><p class="elsevierStylePara">We understand the pathophysiology as to why this patient developed HBP at 34 as multifactorial&#58; a&#41; the stretching of the renal artery due to traction of the hydronephrotic kidney caused its stenosis&#44; and subsequent activation of the renin-angiotensin-aldosterone system &#40;RAAS&#41;&#44; similar to what happens in some cases of renal ptosis&#46;<span class="elsevierStyleSup">11</span> Although we do not have previous images to establish a differential diagnosis of hypoplastic renal artery&#44; the patient presented ultrasound pregnancy check-ups without changes&#59; b&#41; nephrolithiasis determined a state of obstructive uropathy and with that the formation of uriniferous cysts that compressed the renal parenchyma&#44; also activating RAAS&#59;<span class="elsevierStyleSup">12</span> c&#41; interstitial inflammation as an immune response to the urinary infection reduced the area of the peritubular capillaries&#44; hindering the mechanism of natriuresis because of pressure&#46;<span class="elsevierStyleSup">13</span> The PARA of the patient was within the normal range because of its suppression in the contralateral kidney&#44; as well as&#44; in the majority of individuals&#44; this figure being normal once HBP was established&#46;<span class="elsevierStyleSup">14</span> The elevated excretion of sodium in the urine indicated increased ingestion&#44; and its fractional excretion &#60;&#160;1&#160;&#37;&#44; an increase in its tubular reabsorption &#40;obstructive uropathy that can also present itself in the non-functioning kidney with 0&#160;&#37; of participation in the scintography&#41;&#44; despite presenting low doses of thiazide diuretic&#46;</p><p class="elsevierStylePara">The laparoscopic nephrectomy was carried out routinely in patients with complicated lithiasis and also in renal artery stenosis&#44; both separately&#46;<span class="elsevierStyleSup">15&#44;16</span> What is unique about our case is the conjunction of both illness and the mechanical aetiological component of arterial stenosis&#44; not giving an option for endovascular treatment&#46;</p><p class="elsevierStylePara">Having revised the histology of the specimen&#44; although the extensive fibrosis did not allow the aetiology of the chronicity to be well seen&#44; it seems that the predominant factor of nephropathy could be the tubulo-intersitial&#44; caused by primary infection and&#47;or obstruction&#46; Ischaemic nephrosclerosis&#44; reflected as areas of haemorrhage and intimal thickening&#44; seems to remain&#44; at least&#44; in the background in this case&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">CONCLUSION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Different factors can cause HBP&#46; Giant hydronephrosis can cause stenosis by stretching the renal artery&#44; causing renovascular hypertension&#46; Nephrectomy is the main therapeutic option in cases of functional nullity&#46; Urinary infections and nephrolithiasis can also contribute to the development of HBP&#44; but the necessary approach when faced with bacteriuria and&#47;or nephrolithiasis remains in controversy&#44; unless morphological changes develop which are perpetuated by the factors that predispose the development of chronic renal disease&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflicts of interest</span></p><p class="elsevierStylePara">&#160;</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;11883&#95;19157&#95;56753&#95;en&#95;ref&#46;1188328128&#95;11883&#95;19115&#95;53504&#95;es&#95;11883&#95;figura1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11883_19157_56753_en_ref.1188328128_11883_19115_53504_es_11883_figura1.jpg" alt="CT Angiogram&#46;"></img></a></p><p class="elsevierStylePara">Figure 1&#46; CT Angiogram&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11883&#95;19157&#95;56755&#95;en&#95;ref&#46;1188328128&#95;11883&#95;19115&#95;53506&#95;es&#95;11883&#95;figura2&#46;jpg" class="elsevierStyleCrossRefs"><img src="11883_19157_56755_en_ref.1188328128_11883_19115_53506_es_11883_figura2.jpg" alt="Surgical anatomical pathology&#46;"></img></a></p><p class="elsevierStylePara">Figure 2&#46; 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Article information
ISSN: 20132514
Original language: English
DOI:10.3265/Nefrologia.pre2014.Jan.11883
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