Ischemic nephropathy ' pathogenesis and treatment

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Four years survival in patients with RAS <75% of diameter was 89%, whereas in those with ≥75% narrowing survival was only 57%.6 Johansson et al. observed 164 patients with RAS >50% over 7 years.7 During this period 33 patients died and only in 2 patients the progression to stage 5 of chronic kidney disease (CKD) was observed. Risk of death in patients with RAS >50% was over 3 times higher than in general population.7 Therefore, it is important to stress that patients with ischemic nephropathy are more likely to die due to cardiovascular complications than to progress to CKD stage 5.Atherosclerotic RAS can lead to the ischemic nephropathy (ischemic renal disease). Ischemic nephropathy is defined by the gradual reduction of the glomerular filtration rate (GFR) or a loss of renal parenchyma caused by vascular occlusion, not attributable to the other causes. Therefore, the ischemic nephropathy is characterized by a reduction of blood flow to the renal parenchyma beyond the level of renal autoregulation.In patients with CKD stage 5 caused by ischemic nephropathy, survival during renal replacement therapy is also poor. Mailloux et al. observed a 25-months median survival and 18% 5 years survival rate in hemodialysis patients suffered from ischemic nephropathy which was significantly lower than 133 months median and 77% 5 years survival in hemodialysis patients with polycystic kidney disease.8  EPIDEMIOLOGY The exact prevalence of ischemic nephropathy is difficult to estimate. The disease is often asymptomatic and few patients are screened unless they have clinical symptoms. Moreover, there are no precise, clinically useful and widely accepted diagnostic criteria of ischemic nephropathy.Therefore, the percentage of patients who develop CKD stage 5 due to ischemic nephropathy is difficult to assess. Scoble et al. performed renal arteriography in all patients entering the hemodialysis programme.9 Ischemic nephropathy as a cause of terminal CKD was found in 6% of the entire group of patients.8 However, among patients older than 50 years ischemic nephropathy as a cause CKD stage 5 was observed in 14%.9 In the other studies ischemic nephropathy was diagnosed as a cause of CKD stage 5 in 11% and in 27% of patients respectively.10,11 Mailloux et al. in one centre study identified ischemic nephropathy as a cause of CKD stage 5 in 12.2% of patients entering the hemodialysis programme.12 In this study, ischemic nephropathy was the third greatest cause of CKD stage 5 after diabetes mellitus and chronic glomerulonephritis. Using the data from the United States Renal Data System, Fatica et al. reviewed the primary causes of CKD stage 5 and found that the incidence of ischemic nephropathy causing CKD stage 5 increased from 1.4% in 1991 to 2.1% per year in 1997.13 The risk of CKD stage 5 from ischemic nephropathy versus CKD stage 5 from other causes was positively correlated with the age of these patients and was higher in males. Result of this analysis may suggest that the prevalence of ischemic nephropathy is increasing during the recent years, especially among older, male individuals. PATHOLOGY The main macroscopic feature of ischemic nephropathy is the reduction of kidney size. In a study by Dean et al. a decreased kidney size over 10% was noted on serial intravenous pyelograms in 37% of RAS patients.14 Schreiber et al. examined in the retrospective study kidney length changes that were associated with arteriographic progression of RAS.15 Decrease in kidney size was defined as a >1.5cm difference in pole-to-pole measurements on serial x-ray pictures. Forty four percent of patients with atherosclerotic RAS have demonstrated the disease progression and 70% of these patients showed significant decrease of kidney size.15 Caps et al. showed the reduction of kidney size during two years observation period in 20.8% kidneys with ≥60% RAS.16It is not completely clear whether reduced kidney size always indicates irreversible parenchymal changes. In the histology of ischemic nephropathy both reversible tubular atrophy and glomerular collapse and irreversible glomerulosclerosis and interstitial fibrosis are present. Therefore, only result of renal biopsy is able to distinguish between the above mentioned causes of kidney atrophy, but it is rarely done in these settings because of the procedural risk of complications and no clear therapeutic implications. The earliest and the most pronounced histopathologic feature of the ischemic nephropathy are tubulointerstitial lesions.17,18 In 62 patients with RAS who underwent nephrectomy of a small kidney for uncontrolled hypertension, the predominant pattern of injury was significant tubulointerstitial atrophy with relative glomerular sparing.19 Tubuloinsterstitial lesions may mediate the CKD progression towards irreversible damage. At the early phase of this process, cellular activation takes place, as mononuclear cells migrate into the interstitium and myofibroblasts release inflammatory mediators that lead to inflammation.20 Apoptosis induces tubular atrophy which also occurred in patients with ischemic nephropathy.21 This phase of disease may still be partly reversible until fibrosis begins.22 Subsequent fibrosis leads to the kidney permanent damage.Glomerulosclerosis is a late event in patients with ischemic nephropathy. Glomerular lesions are initially minimal in experimental animals with chronic ischemic nephropathy and observed only when severe stenosis is present.17,19,23,24 In some patients glomerular collapse with loss of tuft volume due to hypoperfusion is observed. Moreover fibrosis in the interstitial tissue in the vicinity of Bowman capsule of glomerulus can obstruct the origin of proximal tubuli and may lead to development of atubular, nonfunctioning glomeruli.In addition to tubulointerstitial injury, in patients with ischemic nephropathy atheroembolic intrarenal disease or severe small vessel disease are frequently observed. Keddis et al. in histopathological examination found that intrarenal atheroembolism were present in 39% of small kidneys nephrectomized due to uncontrolled hypertension.19 Renal microvascular disease in patients with ischemic nephropathy may lead to vascular rarefaction within interstitium (reduced number or length of peritubular capillaries) and to increase in vascular wall/lumen ratio.25,26 The cause of these lesions is prolonged periods of vasoconstriction which leads to permanent structural changes in the microcirculation.27 Since microvascular remodeling correlates with the renal scarring, it may have an important implication on CKD progression in atherosclerotic renovascular disease.28The severity of histopathological damage in renal parenchyma is an important determinant of renal outcome in patients with ischemic nephropathy. Wright et al. investigated the impact of histological lesions on renal functional outcome in a small group of patients whose renal biopsies suggested ischemic nephropathy, irrespective of whether significant RAS has been demonstrated in angiography.29 The authors found a tight relationship between decreases in estimated GFR (eGFR) over time and renal damage score.29 PATHOGENESIS The pathogenesis of ischemic nephropathy is more complex than just narrowing of the renal artery from atherosclerosis. In contrast to the results from the animal experiments (for example Goldblatt hypertension in dogs induced by clamp to the renal artery) in which RAS is accompanied by the intact renal vascular tree, in humans with atherosclerotic RAS the renal vasculature is often damaged. Therefore in animal model GFR decrease due to RAS is the reversible phenomenon. In contrast, in the majority of patients with atherosclerotic RAS, due to irreversibility of vascular and interstitial lesions, GFR decrease is irreversible. Although ischemic nephropathy is caused by RAS, the relationship between RAS intensity and presence of ischemic nephropathy or the severity of renal dysfunction is weak. In a study of 71 patients with atherosclerotic RAS, Suresh et al. found that renal function was equally decreased in patients with mild proximal renovascular disease as in those with severe RAS.30 Similarly, Cheung et al. assessed time of progression to CKD stage 5 in patients with unilateral atherosclerotic renal artery occlusion and contralateral <50% or >50% RAS.31 Irrespective of whether the nonocluded artery was normal or had stenosis of varying significance, time to starting renal replacement therapy or death did not correlate with renovascular anatomy.31 The most likely explanation of these observations is that decrease of GFR in patients with RAS is mainly not determined by severity of RAS, but to the extend kidney lesions downstream of the RAS. It seems that reduction of the kidney length may be a better indicator of progression of ischemic nephropathy than the degree of RAS. As much as renal atrophy can be attributed to lack of blood flow, changes in kidney size seems to be more reasonable outcome measure of the effect of reduction of blood flow.The kidneys physiologically receive relative blood supply three to five fold higher than heart or liver. It seems that in kidneys perfusion pressure below 70-80mmHg (correlates with >70% of RAS) overcome adaptive mechanisms and lead to hypoxia. However pathological changes do not appear to be directly related to the parenchymal tissue hypoxia. Patients with ischemic nephropathy are heterogeneous with respect to the degree of hypoxia in kidney tissue. In the early stages of ischemic nephropathy renal hypoxia in viable tissues seems to be present. Experimental study in pigs, showed during acute RAS, a decrease of regional intrarenal tissue oxygenation (measured directly with oxygen electrodes). Result of this experimental study confirmed the existence of hypoxia in kidney tissues.32In contrast to this experimental observations, some recently performed clinical studies in the later stages of the disease, did not confirm the presence of hypoxia in the kidney tissue of patients with ischemic nephropathy. Renal tissue oxygenation was analyzed in patients with RAS by blood oxygen level-dependent magnetic resonance imaging (BOLD-MRI) technique. This technique uses the paramagnetic properties of desoxygenated hemoglobin. During oxygen extraction from the blood, increasing tissue concentrations of desoxygenated hemoglobin led to a decrease of transverse relaxation time (T2*) and an increase in the rate of spin dephasing (R2*).33,34 Based on the estimation of these parameters, tissue oxygenation can be visualized. With this technique Gloviczki et al. studied patients with RAS accompanied by reduction volume of kidney downstream to RAS.35 In this study, they demonstrated preserved medullary and cortical tissue oxygenation. It may be caused by the decrease of oxygen consumption by failed kidney. In the other study, measurement of oxygen tension in the renal veins of patients with RAS, also did not demonstrate desaturation.36 The preserved tissue oxygenation in kidney with RAS is manifested by normal plasma erythropoietin concentration in its renal vein.37 Based on the above mentioned data, it may be proposed that in the early stages, renal hypoxia plays a crucial role in the pathogenesis of ischemic nephropathy. However, in the later stages, tubulointerstitial fibrosis dominates.38Renal hypoperfusion, leads to increased secretion of renin and generation of angiotensin II (Ang II).39 Recent studies confirmed that stenosis must be advanced in order to determine the hemodynamic effect. Careful studies using expanded balloons in humans indicate that an aortic–renal gradient exceeding 25 mmHg is necessary to increase renin secretion.39 This coincides with cross-sectional vascular occlusion approaching 70–80%. Ang II increases the expression of the transforming growth factor β (TGF-β) and platelet-derived growth factor-B (PDGF-B), resulting in the accumulation of extracellular matrix and collagen type IV in the perivascular tissue, interstitium and finally in the glomeruli (Figure 1).22,40The progressive kidney fibrosis may occur also through the other mechanisms of tissue and vascular injury - aldosterone–mediated damage, sympathetic overactivity and increased release of reactive oxygen species (ROS).Ang II stimulates the production of ROS. Lerman et al. demonstrated increased oxidative stress in pig model of RAS and Higashi et al. and Minuz et al. in patients with RAS.41-43 ROS increases renal vascular tone, sensitivity to vasoconstrictors and leads to endothelial dysfunction.44 The interaction of ROS with nitric oxide (NO) decreases bioavailability of the latter and results in formation of the prooxidant peroxynitrite. Reduction of NO activity allows vasopressors like angiotensin II and endothelin-1 (ET-1) to dominate and to lead to vasoconstriction and as a consequence to GFR decrease.Ischemic nephropathy is characterized by the endothelial disfunction. The importance of the endothelial damage in ischemic nephropathy was demonstrated in an experimental porcine model. A single intrarenal infusion of autologous endothelial progenitor cells (EPC) preserves microvascular architecture and function and decreases microvascular remodeling.45 CLINICAL PICTURE AND DIAGNOSIS The clinical presentation of patients likely to develop ischemic nephropathy consist of: older age (over 50 years), hypertension (usually severe or difficult to treat), history of smoking, hypercholesterolemia, coronary heart disease or the other clinical manifestation of atherosclerosis. Such a patient has gradually decreasing GFR, mild to moderate proteinuria and bland urinary sediment. Loss of GFR, as in the other nephropathies, may be an useful parameter for progression of ischemic nephropathy.Proteinuria may also be recognized as a marker of severity of ischemic nephropathy. Makanjuola et al. surveyed 94 patients with atherosclerotic RAS. Fifty two percent of the patients had proteinuria. In patients with GFR ≥50ml/min mean urinary protein excretion was 400mg/24h, and in patients with GFR <50ml/min proteinuria ranged from 500mg/24h to 2.4g/24h.46It is important to stress that precise, clinically useful diagnostic criteria of ischemic nephropathy have not been established, yet. The diagnostic evaluation of patients with suspected ischemic nephropathy is similar to the evaluation of patients with presumed RAS. TREATMENT At the present time concerted medical management (includes lifestyle modifications – among others smoking cessation, antihypertensive drugs, statins and antiplatelet treatment) remains the main treatment option for all patients with ischemic nephropathy. The optimal blood pressure in patients with ischemic nephropathy is unknown. Recent experimental studies suggested that novel approaches to treat the renal parenchyma directly, such as antioxidants, statins, VEGF and EPC may improve renal injury even without correcting the RAS.45,47-50There is also a great need to identify accurately those individuals with ischemic nephropathy who will derive clinical benefit from renal revascularization. It is thought that only in the selected patients revascularisation is indicated.51 Exclusively patients with ischemic nephropathy with potentially reversible both interstitial and glomerular lesion may benefit from revascularisation. These patients should be characterized by only limited interstitial fibrosis and mainly no sclerotic glomeruli. Currently there are no good and clinically useful markers which allow to identify such patients i.e. there are no reliable tools to predict the reversibility of ischemic lesions in the kidney. In order to do it with contemprorary available methods the following strategies were proposed (Table 1).511/ Measurement of the kidney length by the ultrasound examination. Small cirrhotic kidney (longitudinal diameter less than 8.0cm) suggests advanced kidney fibrosis. However patients with concomitant kidney disease as diabetic kidney disease or amyloidosis may present normal kidney size despite advanced fibrosis. Moreover it is not completely clear whether reduced renal size always indicates irreversible parenchymal changes. There are series of patients with good renal functional outcome after revascularisation besides found before this procedure renal atrophy.52 2/ Assessment of the intrarenal resistance by Doppler sonography. Resistance index (RI) higher than 0.8 suggests advanced kidney fibrosis.53 However, the predictive value of increased RI is not unanimously accepted.543/ Measurement of the pressure gradient across a stenosis of the main artery invasively during arteriography. The gradient is directly proportional to the resistance in the renal vasculature downstream. The peak pressure gradient ≥70%, may predict that stenosis itself is hemodynamically important and influences the blood kidney supply and give a hope for reversibility of the interstitial and glomerular lesions.It should be stressed that none of the above mentioned methods was validated in the properly controlled clinical studies. All of this tests are to some extend inadequate in predicting which patient with ischemic nephropathy will benefit from revascularization. Because of clinical applicability and non invasive character both length kidney measurement, by the ultrasound examination and assessment of the intrarenal resistance, by Doppler sonography were currently broadly used.In future BOLD-MRI may also be useful for prediction the reversibility of ischemic lesions in the kidney. Presence of local ischemia hypothetically may predict reversibility of the changes. BOLD-MRI allows to analyze the patterns of regional tissue oxygenation in ischemic kidneys. This technique uses the paramagnetic properties of desoxygenated hemoglobin. During oxygen extraction from the blood, increasing tissue concentrations of desoxygenated hemoglobin led to a decrease of transverse relaxation time (T2*) and an increase in the rate of spin dephasing (R2*).33,34 Two diagnostic approach with the use of BOLD-MRI techniques were studied in patients with RAS: BOLD-MRI measurements combined with isotopic single kidney glomerular filtration rate (isoSK-GFR) and BOLD-MRI before and after furosemide treatment.55,56Chrysochou et al. in preliminary, prospective pilot study showed that BOLD-MRI measurements combined with isoSK-GFR may be prognostic markers of renal functional recovery after revascularization. They showed that high R2*:isoSK-GFR ratio predicts a renal recovery after revascularization.55 The ratio of R2*:isoSK-GFR reflects metabolically active, hypoxic renal tissue, that is, the presence of potentially salvageable renal tissue. Such kidney parenchyma has not yet been subject to the deleterious cascade of ischemic events that results in irreversible structural changes.Textor et al. have shown that furosemide (which inhibits medullary tubular sodium transport and oxygen consumption) decreases medullary deoxyhaemoglobin concentration (measured by R2*) in patients with normal-sized kidneys downstream to a high-grade RAS.56 In the atrophic kidneys distal to total occlusion, furosemide did not decrease deoxyhaemoglobin concentration. It suggest low kidney tissues viability. Therefore R2* mapping may distinguish between severely compromised but viable parenchyma (high basal values of R2* which would fall after the administration of furosemide) present in those kidneys likely to improve after revascularization and non-functional scarred tissue (low basal values of R2*, unaffected by furosemide).56Currently, in daily clinical practice it is thought that revascularisation in patients with ischemic nephropathy is not indicated in several clinical situation like: a) in patients with normotension or when normal blood pressure is obtained with antihypertensive therapy, b) when stenosed renal artery is supplying small cirrhotic kidney (longitudinal diameter less than 8.0cm in adult patient) c) in patients with high intrarenal resistance assessed by Doppler sonography (RI higher than 0.8) corresponding to the advanced kidney fibrosis due to chronic ischemic nephropathy.Key concept: The prevalence of ischemic nephropathy seems to increase, especially among older individuals. It’s pathogenesis is more complex than just narrowing of the renal artery from atherosclerosis. Precise, clinically useful diagnostic criteria of ischemic nephropathy have not been established, yet. Concerted medical management remains now the main therapeutic option for majority of patients with this disease and only in the selected patients revascularisation is nowadays indicated. Conflict of interest The authors declare that there is no conflict of interest associated with this manuscript.<a href="grande/11472_108_29486_en_11472_t1.jpg" class="elsevierStyleCrossRefs"><img src="11472_108_29486_en_11472_t1.jpg" alt="Predictors of salvageability of ischemic nephropathy after revascularisation"></img></a>Table 1. Predictors of salvageability of ischemic nephropathy after revascularisation<a href="grande/11472_108_29487_en_11472_f1.jpg" class="elsevierStyleCrossRefs"><img src="11472_108_29487_en_11472_f1.jpg" alt="Pathogenesis of ischemic nephropathy"></img></a>Figure 1. Pathogenesis of ischemic nephropathy" "pdfFichero" => "P1-E541-S3622-A11472-EN.pdf" "tienePdf" => true "PalabrasClave" => array:2 [ "es" => array:5 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437885" "palabras" => array:1 [ 0 => "Angioplastia renal" ] ] 1 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437887" "palabras" => array:1 [ 0 => "Tratamiento médico" ] ] 2 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437889" "palabras" => array:1 [ 0 => "Estenosis de la arteria renal" ] ] 3 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437891" "palabras" => array:1 [ 0 => "Enfermedad renal crónica" ] ] 4 => array:4 [ "clase" => "keyword" "titulo" => "Palabras clave" "identificador" => "xpalclavsec437893" "palabras" => array:1 [ 0 => "Nefropatía isquémica" ] ] ] "en" => array:5 [ 0 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437886" "palabras" => array:1 [ 0 => "Renal angioplasty" ] ] 1 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437888" "palabras" => array:1 [ 0 => "Medical therapy" ] ] 2 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437890" "palabras" => array:1 [ 0 => "Renal artery stenosis" ] ] 3 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437892" "palabras" => array:1 [ 0 => "Chronic kidne disease" ] ] 4 => array:4 [ "clase" => "keyword" "titulo" => "Keywords" "identificador" => "xpalclavsec437894" "palabras" => array:1 [ 0 => "Ischemic nephropathy" ] ] ] ] "tieneResumen" => true "resumen" => array:2 [ "es" => array:1 [ "resumen" => "En esta revisión nos gustaría realizar un resumen del conocimiento actual sobre la patogénesis y el tratamiento de la nefropatía isquémica. Los datos epidemiológicos sugieren que la prevalencia de la nefropatía isquémica aumenta, especialmente en los individuos de mayor edad. La patogénesis de esta enfermedad es más compleja que el mero estrechamiento de la arteria renal a causa de la ateroesclerosis. El sistema renina angiotensina, los factores de crecimiento, las diferentes citoquinas y las quimiocinas pueden estar implicados en la patogénesis de la nefropatía isquémica. Específicamente, los criterios diagnósticos de utilidad clínica de la nefropatía isquémica aún están por determinar. La gestión médica acordada de forma conjunta sigue siendo por el momento la principal opción terapéutica para la mayoría de los pacientes con esta patología y hoy en día, la revascularización está indicada únicamente en pacientes seleccionados." ] "en" => array:1 [ "resumen" => "In this review paper we would like to summarized the current knowledge concerning the  pathogenesis and treatment of ischemic nephropathy. Epidemiological data suggest that the prevalence of ischemic nephropathy increases, especially among older individuals. The pathogenesis of this disease is more complex than just narrowing of the renal artery due to atherosclerosis. Renin-angiotension system, growth factors, different cytokines and chemokines may participate in the pathogenesis of ischemic nephropathy. Precise, clinically useful diagnostic criteria of the ischemic nephropathy have not been established, yet. Concerted medical management remains now the main therapeutic option for majority of patients with this disease and only in the selected patients revascularisation is nowadays indicated." ] ] "multimedia" => array:2 [ 0 => array:8 [ "identificador" => "fig1" "etiqueta" => "Tab. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11472_108_29486_en_11472_t1.jpg" "Alto" => 308 "Ancho" => 600 "Tamanyo" => 172793 ] ] "descripcion" => array:1 [ "en" => "Predictors of salvageability of ischemic nephropathy after revascularisation" ] ] 1 => array:8 [ "identificador" => "fig2" "etiqueta" => "Fig. 1" "tipo" => "MULTIMEDIAFIGURA" "mostrarFloat" => true "mostrarDisplay" => false "copyright" => "Elsevier España" "figura" => array:1 [ 0 => array:4 [ "imagen" => "11472_108_29487_en_11472_f1.jpg" "Alto" => 765 "Ancho" => 600 "Tamanyo" => 231355 ] ] "descripcion" => array:1 [ "en" => "Pathogenesis of ischemic nephropathy" ] ] ] "bibliografia" => array:2 [ "titulo" => "Bibliography" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:56 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:3 [ "referenciaCompleta" => "Kuroda S, Nishida N, Uzu T, Takeji M, Nishimura M, Fujii T, et al. 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Nefropatía isquémica: patogénesis y tratamiento

Marcin Adamczaka, Andrzej Wieceka

a Department of Nephrology, Endocrinology and Metabolic Diseases, Medical University of Silesia, Katowice, Poland,

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    "textoCompleto" => "<p class="elsevierStylePara"><span class="elsevierStyleBold">INTRODUCTION</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">Atherosclerotic renal artery stenosis &#40;RAS&#41; is often one of the sign of generalized atherosclerotic disease&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">1-3</span></span>&#160;Patients with atherosclerotic RAS are at a high risk of cardiovascular death&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">4</span></span>&#160;Conlon et al&#46; found in patients who underwent cardiac catheterization&#44; that 4 years survival was 86&#37; in those subjects without RAS and only 65&#37; in those with RAS&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">5</span></span>&#160;The degree of RAS does also significantly influence the survival&#46; Four years survival in patients with RAS &#60;75&#37; of diameter was 89&#37;&#44; whereas in those with &#8805;75&#37; narrowing survival was only 57&#37;&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">6</span></span>&#160;Johansson et al&#46; observed 164 patients with RAS &#62;50&#37; over 7 years&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">7</span></span>&#160;During this period 33 patients died and only in 2 patients the progression to stage 5 of chronic kidney disease &#40;CKD&#41; was observed&#46; Risk of death in patients with RAS &#62;50&#37; was over 3 times higher than in general population&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">7</span></span>&#160;Therefore&#44; it is important to stress that patients with ischemic nephropathy are more likely to die due to cardiovascular complications than to progress to CKD stage 5&#46;</p><p class="elsevierStylePara">Atherosclerotic RAS can lead to the ischemic nephropathy &#40;ischemic renal disease&#41;&#46; Ischemic nephropathy is defined by the gradual reduction of the glomerular filtration rate &#40;GFR&#41; or a loss of renal parenchyma caused by vascular occlusion&#44; not attributable to the other causes&#46; Therefore&#44; the ischemic nephropathy is characterized by a reduction of blood flow to the renal parenchyma beyond the level of renal autoregulation&#46;</p><p class="elsevierStylePara">In patients with CKD stage 5 caused by ischemic nephropathy&#44; survival during renal replacement therapy is also poor&#46; Mailloux et al&#46; observed a 25-months median survival and 18&#37; 5 years survival rate in hemodialysis patients suffered from ischemic nephropathy which was significantly lower than 133 months median and 77&#37; 5 years survival in hemodialysis patients with polycystic kidney disease&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">8</span></span><span class="elsevierStyleBold"><span class="elsevierStyleBold">&#160;</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">&#160;</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">EPIDEMIOLOGY</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">&#160;</span></span></p><p class="elsevierStylePara">The exact prevalence of ischemic nephropathy is difficult to estimate&#46; The disease is often asymptomatic and few patients are screened unless they have clinical symptoms&#46; Moreover&#44; there are no precise&#44; clinically useful and widely accepted diagnostic criteria of ischemic nephropathy&#46;</p><p class="elsevierStylePara">Therefore&#44; the percentage of patients who develop CKD stage 5 due to ischemic nephropathy is difficult to assess&#46; Scoble et al&#46; performed renal arteriography in all patients entering the hemodialysis programme&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">9</span></span>&#160;Ischemic nephropathy as a cause of terminal CKD was found in 6&#37; of the entire group of patients&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">8</span></span>&#160;However&#44; among patients older than 50 years ischemic nephropathy as a cause CKD stage 5 was observed in 14&#37;&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">9</span></span>&#160;In the other studies ischemic nephropathy was diagnosed as a cause of CKD stage 5 in 11&#37; and in 27&#37; of patients respectively&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">10&#44;11</span></span>&#160;Mailloux et al&#46; in one centre study identified ischemic nephropathy as a cause of CKD stage 5 in 12&#46;2&#37; of patients entering the hemodialysis programme&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">12</span></span>&#160;In this study&#44; ischemic nephropathy was the third greatest cause of CKD stage 5 after diabetes mellitus and chronic glomerulonephritis&#46; Using the data from the&#160;<span class="elsevierStyleItalic"><span class="elsevierStyleItalic">United States Renal Data System</span></span>&#44; Fatica et al&#46; reviewed the primary causes of CKD stage 5 and found that the incidence of ischemic nephropathy causing CKD stage 5 increased from 1&#46;4&#37; in 1991 to 2&#46;1&#37; per year in 1997&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">13</span></span>&#160;The risk of CKD stage 5 from ischemic nephropathy versus CKD stage 5 from other causes was positively correlated with the age of these patients and was higher in males&#46; Result of this analysis may suggest that the prevalence of ischemic nephropathy is increasing during the recent years&#44; especially among older&#44; male individuals&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">&#160;</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">PATHOLOGY</span></span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The main macroscopic feature of ischemic nephropathy is the reduction of kidney size&#46; In a study by Dean et al&#46; a decreased kidney size over 10&#37; was noted on serial intravenous pyelograms in 37&#37; of RAS patients&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">14</span></span><span class="elsevierStyleSup">&#160;</span>Schreiber et al&#46; examined in the retrospective study kidney length changes that were associated with arteriographic progression of RAS&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">15</span></span>&#160;Decrease in kidney size was defined as a &#62;1&#46;5cm difference in pole-to-pole measurements on serial x-ray pictures&#46; Forty four percent of patients with atherosclerotic RAS have demonstrated the disease progression and 70&#37; of these patients showed significant decrease of kidney size&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">15</span></span>&#160;Caps et al&#46; showed the reduction of kidney size during two years observation period in 20&#46;8&#37; kidneys with &#8805;60&#37; RAS&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">16</span></span></p><p class="elsevierStylePara">It is not completely clear whether reduced kidney size always indicates irreversible parenchymal changes&#46; In the histology of ischemic nephropathy both reversible tubular atrophy and glomerular collapse and irreversible glomerulosclerosis and interstitial fibrosis are present&#46; Therefore&#44; only result of renal biopsy is able to distinguish between the above mentioned causes of kidney atrophy&#44; but it is rarely done in these settings because of the procedural risk of complications and no clear therapeutic implications&#46; </p><p class="elsevierStylePara">The earliest and the most pronounced histopathologic feature of the ischemic nephropathy are tubulointerstitial lesions&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">17&#44;18</span></span>&#160;In 62 patients with RAS who underwent nephrectomy of a small kidney for uncontrolled hypertension&#44; the predominant pattern of injury was significant tubulointerstitial atrophy with relative glomerular sparing&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">19</span></span><span class="elsevierStyleSup">&#160;</span>Tubuloinsterstitial lesions may mediate the CKD progression towards irreversible damage&#46; At the early phase of this process&#44; cellular activation takes place&#44; as mononuclear cells migrate into the interstitium and myofibroblasts release inflammatory mediators that lead to inflammation&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">20</span></span>&#160;Apoptosis induces tubular atrophy which also occurred in patients with ischemic nephropathy&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">21</span></span>&#160;This phase of disease may still be partly reversible until fibrosis begins&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">22</span></span>&#160;Subsequent fibrosis leads to the kidney permanent damage&#46;</p><p class="elsevierStylePara">Glomerulosclerosis is a late event in patients with ischemic nephropathy&#46; Glomerular lesions are initially minimal in experimental animals with chronic ischemic nephropathy and observed only when severe stenosis is present&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">17&#44;19&#44;23&#44;24</span></span>&#160;In some patients glomerular collapse with loss of tuft volume due to hypoperfusion is observed&#46; Moreover fibrosis in the interstitial tissue in the vicinity of Bowman capsule of glomerulus can obstruct the origin of proximal tubuli and may lead to development of atubular&#44; nonfunctioning glomeruli&#46;</p><p class="elsevierStylePara">In addition to tubulointerstitial injury&#44; in patients with ischemic nephropathy atheroembolic intrarenal disease or severe small vessel disease are frequently observed&#46; Keddis et al&#46; in histopathological examination found that intrarenal atheroembolism were present in 39&#37; of small kidneys nephrectomized due to uncontrolled hypertension&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">19</span></span>&#160;Renal microvascular disease in patients with ischemic nephropathy may lead to vascular rarefaction within interstitium &#40;reduced number or length of peritubular capillaries&#41; and to increase in vascular wall&#47;lumen ratio&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">25&#44;26</span></span>&#160;The cause of these lesions is prolonged periods of vasoconstriction which leads to permanent structural changes in the microcirculation&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">27</span></span><span class="elsevierStyleSup">&#160;</span>Since microvascular remodeling correlates with the renal scarring&#44; it may have an important implication on CKD progression in atherosclerotic renovascular disease&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">28</span></span></p><p class="elsevierStylePara">The severity of histopathological damage in renal parenchyma is an important determinant of renal outcome in patients with ischemic nephropathy&#46; Wright et al&#46; investigated the impact of histological lesions on renal functional outcome in a small group of patients whose renal biopsies suggested ischemic nephropathy&#44; irrespective of whether significant RAS has been demonstrated in angiography&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">29</span></span>&#160;The authors found a tight relationship between decreases in estimated GFR &#40;eGFR&#41; over time and renal damage score&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">29</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">&#160;</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">PATHOGENESIS</span></span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The pathogenesis of ischemic nephropathy is more complex than just narrowing of the renal artery from atherosclerosis&#46; In contrast to the results from the animal experiments &#40;for example Goldblatt hypertension in dogs induced by clamp to the renal artery&#41; in which RAS is accompanied by the intact renal vascular tree&#44; in humans with atherosclerotic RAS the renal vasculature is often damaged&#46; Therefore in animal model GFR decrease due to RAS is the reversible phenomenon&#46; In contrast&#44; in the majority of patients with atherosclerotic RAS&#44; due to irreversibility of vascular and interstitial lesions&#44; GFR decrease is irreversible&#46;&#160;</p><p class="elsevierStylePara">Although ischemic nephropathy is caused by RAS&#44; the relationship between RAS intensity and presence of ischemic nephropathy or the severity of renal dysfunction is weak&#46; In a study of 71 patients with atherosclerotic RAS&#44; Suresh et al&#46; found that renal function was equally decreased in patients with mild proximal renovascular disease as in those with severe RAS&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">30</span></span>&#160;Similarly&#44; Cheung et al&#46; assessed time of progression to CKD stage 5 in patients with unilateral atherosclerotic renal artery occlusion and contralateral &#60;50&#37; or &#62;50&#37; RAS&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">31</span></span>&#160;Irrespective of whether the nonocluded artery was normal or had stenosis of varying significance&#44; time to starting renal replacement therapy or death did not correlate with renovascular anatomy&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">31</span></span>&#160;The most likely explanation of these observations is that decrease of GFR in patients with RAS is mainly not determined by severity of RAS&#44; but to the extend kidney lesions downstream of the RAS&#46; It seems that reduction of the kidney length may be a better indicator of progression of ischemic nephropathy than the degree of RAS&#46; As much as renal atrophy can be attributed to lack of blood flow&#44; changes in kidney size seems to be more reasonable outcome measure of the effect of reduction of blood flow&#46;</p><p class="elsevierStylePara">The kidneys physiologically receive relative blood supply three to five fold higher than heart or liver&#46; It seems that in kidneys perfusion pressure below 70-80mmHg &#40;correlates with &#62;70&#37; of RAS&#41; overcome adaptive mechanisms and lead to hypoxia&#46; However pathological changes do not appear to be directly related to the parenchymal tissue hypoxia&#46; Patients with ischemic nephropathy are heterogeneous with respect to the degree of hypoxia in kidney tissue&#46; In the early stages of ischemic nephropathy renal hypoxia in viable tissues seems to be present&#46; Experimental study in pigs&#44; showed during acute RAS&#44; a decrease of regional intrarenal tissue oxygenation &#40;measured directly with oxygen electrodes&#41;&#46; Result of this experimental study confirmed the existence of hypoxia in kidney tissues&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">32</span></span></p><p class="elsevierStylePara">In contrast to this experimental observations&#44; some recently performed clinical studies in the later stages of the disease&#44; did not confirm the presence of hypoxia in the kidney tissue of patients with ischemic nephropathy&#46; Renal tissue oxygenation was analyzed in patients with RAS by blood oxygen level-dependent magnetic resonance imaging &#40;BOLD-MRI&#41; technique&#46; This technique uses the paramagnetic properties of desoxygenated hemoglobin&#46; During oxygen extraction from the blood&#44; increasing tissue concentrations of desoxygenated hemoglobin led to a decrease of transverse relaxation time &#40;T2&#42;&#41; and an increase in the rate of spin dephasing &#40;R2&#42;&#41;&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">33&#44;34</span></span>&#160;Based on the estimation of these parameters&#44; tissue oxygenation can be visualized&#46; With this technique Gloviczki et al&#46; studied patients with RAS accompanied by reduction volume of kidney downstream to RAS&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">35</span></span><span class="elsevierStyleSup"> </span>In this study&#44; they demonstrated preserved medullary and cortical tissue oxygenation&#46; It may be caused by the decrease of oxygen consumption by failed kidney&#46; In the other study&#44; measurement of oxygen tension in the renal veins of patients with RAS&#44; also did not demonstrate desaturation&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">36 </span></span></p><p class="elsevierStylePara">The preserved tissue oxygenation in kidney with RAS is manifested by normal plasma erythropoietin concentration in its renal vein&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">37</span></span>&#160;Based on the above mentioned data&#44; it may be proposed that in the early stages&#44; renal hypoxia plays a crucial role in the pathogenesis of ischemic nephropathy&#46; However&#44; in the later stages&#44; tubulointerstitial fibrosis dominates&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">38</span></span></p><p class="elsevierStylePara">Renal hypoperfusion&#44; leads to increased secretion of renin and generation of angiotensin II &#40;Ang II&#41;&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">39</span></span>&#160;Recent studies confirmed that stenosis must be advanced in order to determine the hemodynamic effect&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">&#160;</span></span>Careful studies using expanded balloons in humans indicate that an aortic&#8211;renal gradient exceeding 25 mmHg is necessary to increase renin secretion&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">39</span></span>&#160;This coincides with cross-sectional vascular occlusion approaching 70&#8211;80&#37;&#46; Ang II increases the expression of the transforming growth factor &#946; &#40;TGF-&#946;&#41; and platelet-derived growth factor-B &#40;PDGF-B&#41;&#44; resulting in the accumulation of extracellular matrix and collagen type IV in the perivascular tissue&#44; interstitium and finally in the glomeruli &#40;Figure 1&#41;&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">22&#44;40</span></span></p><p class="elsevierStylePara">The progressive kidney fibrosis may occur also through the other mechanisms of tissue and vascular injury - aldosterone&#8211;mediated damage&#44; sympathetic overactivity and increased release of reactive oxygen species &#40;ROS&#41;&#46;</p><p class="elsevierStylePara">Ang II stimulates the production of ROS&#46; Lerman et al&#46; demonstrated increased oxidative stress in pig model of RAS and Higashi et al&#46; and Minuz et al&#46; in patients with RAS&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">41-43</span></span>&#160;ROS increases renal vascular tone&#44; sensitivity to vasoconstrictors and leads to endothelial dysfunction&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">44</span></span><span class="elsevierStyleSup">&#160;</span>The interaction of ROS with nitric oxide &#40;NO&#41; decreases bioavailability of the latter and results in formation of the prooxidant peroxynitrite&#46; Reduction of NO activity allows vasopressors like angiotensin II and endothelin-1 &#40;ET-1&#41; to dominate and to lead to vasoconstriction and as a consequence to GFR decrease&#46;</p><p class="elsevierStylePara">Ischemic nephropathy is characterized by the endothelial disfunction&#46; The importance of the endothelial damage in ischemic nephropathy was demonstrated in an experimental porcine model&#46; A single intrarenal infusion of autologous endothelial progenitor cells &#40;EPC&#41; preserves microvascular architecture and function and decreases microvascular remodeling&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">45</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">&#160;</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">CLINICAL PICTURE AND DIAGNOSIS</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">&#160;</span></p><p class="elsevierStylePara">The clinical presentation of patients likely to develop ischemic nephropathy consist of&#58; older age &#40;over 50 years&#41;&#44; hypertension &#40;usually severe or difficult to treat&#41;&#44; history of smoking&#44; hypercholesterolemia&#44; coronary heart disease or the other clinical manifestation of atherosclerosis&#46; Such a patient has gradually decreasing GFR&#44; mild to moderate proteinuria and bland urinary sediment&#46; Loss of GFR&#44; as in the other nephropathies&#44; may be an useful parameter for progression of ischemic nephropathy&#46;</p><p class="elsevierStylePara">Proteinuria may also be recognized as a marker of severity of ischemic nephropathy&#46; Makanjuola et al&#46; surveyed 94 patients with atherosclerotic RAS&#46; Fifty two percent of the patients had proteinuria&#46; In patients with GFR &#8805;50ml&#47;min mean urinary protein excretion was 400mg&#47;24h&#44; and in patients with GFR &#60;50ml&#47;min proteinuria ranged from 500mg&#47;24h to 2&#46;4g&#47;24h&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">46</span></span></p><p class="elsevierStylePara">It is important to stress that precise&#44; clinically useful diagnostic criteria of ischemic nephropathy have not been established&#44; yet&#46; The diagnostic evaluation of patients with suspected ischemic nephropathy is similar to the evaluation of patients with presumed RAS&#46;</p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">TREATMENT</span></span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">At the present time concerted medical management &#40;includes lifestyle modifications &#8211; among others smoking cessation&#44; antihypertensive drugs&#44; statins and antiplatelet treatment&#41; remains the main treatment option for all patients with ischemic nephropathy&#46; The optimal blood pressure in patients with ischemic nephropathy is unknown&#46; Recent experimental studies suggested that novel approaches to treat the renal parenchyma directly&#44; such as antioxidants&#44; statins&#44; VEGF and EPC may improve renal injury even without correcting the RAS&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">45&#44;47-50</span></span></p><p class="elsevierStylePara">There is also a great need to identify accurately those individuals with ischemic nephropathy who will derive clinical benefit from renal revascularization&#46; It is thought that only in the selected patients revascularisation is indicated&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">51</span></span>&#160;Exclusively patients with ischemic nephropathy with potentially reversible both interstitial and glomerular lesion may benefit from revascularisation&#46; These patients should be characterized by only limited interstitial fibrosis and mainly no sclerotic glomeruli&#46; Currently there are no good and clinically useful markers which allow to identify such patients i&#46;e&#46; there are no reliable tools to predict the reversibility of ischemic lesions in the kidney&#46; In order to do it with contemprorary available methods the following strategies were proposed &#40;Table 1&#41;&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">51</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">1&#47;&#160;Measurement of the kidney length by the ultrasound examination&#46;</span>&#160;Small cirrhotic kidney &#40;longitudinal diameter less than 8&#46;0cm&#41; suggests advanced kidney fibrosis&#46; However patients with concomitant kidney disease as diabetic kidney disease or amyloidosis may present normal kidney size despite advanced fibrosis&#46; Moreover it is not completely clear whether reduced renal size always indicates irreversible parenchymal changes&#46; There are series of patients with good renal functional outcome after revascularisation besides found before this procedure renal atrophy&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">52&#160;</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">2&#47;&#160;Assessment of the intrarenal resistance by Doppler sonography&#46;</span>&#160;Resistance index &#40;RI&#41; higher than 0&#46;8 suggests advanced kidney fibrosis&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">53</span></span> However&#44; the predictive value of increased RI is not unanimously accepted&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">54</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">3&#47;&#160;Measurement of the pressure gradient across a stenosis of the main artery invasively during arteriography&#46;</span>&#160;The gradient is directly proportional to the resistance in the renal vasculature downstream&#46; The peak pressure gradient &#8805;70&#37;&#44; may predict that stenosis itself is hemodynamically important and influences the blood kidney supply and give a hope for reversibility of the interstitial and glomerular lesions&#46;</p><p class="elsevierStylePara">It should be stressed that none of the above mentioned methods was validated in the properly controlled clinical studies&#46; All of this tests are to some extend inadequate in predicting which patient with ischemic nephropathy will benefit from revascularization&#46; Because of clinical applicability and non invasive character both length kidney measurement&#44; by the ultrasound examination and assessment of the intrarenal resistance&#44; by Doppler sonography were currently broadly used&#46;</p><p class="elsevierStylePara">In future BOLD-MRI may also be useful for prediction the reversibility of ischemic lesions in the kidney&#46; Presence of local ischemia hypothetically may predict reversibility of the changes&#46; BOLD-MRI allows to analyze the patterns of regional tissue oxygenation in ischemic kidneys&#46; This technique uses the paramagnetic properties of desoxygenated hemoglobin&#46; During oxygen extraction from the blood&#44; increasing tissue concentrations of desoxygenated hemoglobin led to a decrease of transverse relaxation time &#40;T2&#42;&#41; and an increase in the rate of spin dephasing &#40;R2&#42;&#41;&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">33&#44;34</span></span>&#160;Two diagnostic approach with the use of BOLD-MRI techniques were studied in patients with RAS&#58; BOLD-MRI measurements combined with isotopic single kidney glomerular filtration rate &#40;isoSK-GFR&#41; and BOLD-MRI before and after furosemide treatment&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">55&#44;56</span></span></p><p class="elsevierStylePara">Chrysochou et al&#46; in preliminary&#44; prospective pilot study showed that BOLD-MRI measurements combined with isoSK-GFR may be prognostic markers of renal functional recovery after revascularization&#46; They showed that high R2&#42;&#58;isoSK-GFR ratio predicts a renal recovery after revascularization&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">55</span></span>&#160;The ratio of R2&#42;&#58;isoSK-GFR reflects metabolically active&#44; hypoxic renal tissue&#44; that is&#44; the presence of potentially salvageable renal tissue&#46; Such kidney parenchyma has not yet been subject to the deleterious cascade of ischemic events that results in irreversible structural changes&#46;</p><p class="elsevierStylePara">Textor et al&#46; have shown that furosemide &#40;which inhibits medullary tubular sodium transport and oxygen consumption&#41; decreases medullary deoxyhaemoglobin concentration &#40;measured by R2&#42;&#41; in patients with normal-sized kidneys downstream to a high-grade RAS&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">56</span></span><span class="elsevierStyleSup"> </span>In the atrophic kidneys distal to total occlusion&#44; furosemide did not decrease deoxyhaemoglobin concentration&#46; It suggest low kidney tissues viability&#46; Therefore R2&#42; mapping may distinguish between severely compromised but viable parenchyma &#40;high basal values of R2&#42; which would fall after the administration of furosemide&#41; present in those kidneys likely to improve after revascularization and non-functional scarred tissue &#40;low basal values of R2&#42;&#44; unaffected by furosemide&#41;&#46;<span class="elsevierStyleSup"><span class="elsevierStyleSup">56</span></span></p><p class="elsevierStylePara">Currently&#44; in daily clinical practice it is thought that revascularisation in patients with ischemic nephropathy is not indicated in several clinical situation like&#58; a&#41; in patients with normotension or when normal blood pressure is obtained with antihypertensive therapy&#44; b&#41; when stenosed renal artery is supplying small cirrhotic kidney &#40;longitudinal diameter less than 8&#46;0cm in adult patient&#41; c&#41; in patients with high intrarenal resistance assessed by Doppler sonography &#40;RI higher than 0&#46;8&#41; corresponding to the advanced kidney fibrosis due to chronic ischemic nephropathy&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">Key concept&#58;</span></span>&#160;The prevalence of ischemic nephropathy seems to increase&#44; especially among older individuals&#46; It&#8217;s pathogenesis is more complex than just narrowing of the renal artery from atherosclerosis&#46; Precise&#44; clinically useful diagnostic criteria of ischemic nephropathy have not been established&#44; yet&#46; Concerted medical management remains now the main therapeutic option for majority of patients with this disease and only in the selected patients revascularisation is nowadays indicated&#46;</p><p class="elsevierStylePara"><span class="elsevierStyleBold"><span class="elsevierStyleBold">&#160;</span></span></p><p class="elsevierStylePara"><span class="elsevierStyleBold">Conflict of interest</span></p><p class="elsevierStylePara">&#160;</p><p class="elsevierStylePara">The authors declare that there is no conflict of interest associated with this manuscript&#46;</p><p class="elsevierStylePara"><a href="grande&#47;11472&#95;108&#95;29486&#95;en&#95;11472&#95;t1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11472_108_29486_en_11472_t1.jpg" alt="Predictors of salvageability of ischemic nephropathy after revascularisation"></img></a></p><p class="elsevierStylePara">Table 1&#46; Predictors of salvageability of ischemic nephropathy after revascularisation</p><p class="elsevierStylePara"><a href="grande&#47;11472&#95;108&#95;29487&#95;en&#95;11472&#95;f1&#46;jpg" class="elsevierStyleCrossRefs"><img src="11472_108_29487_en_11472_f1.jpg" alt="Pathogenesis of ischemic nephropathy"></img></a></p><p class="elsevierStylePara">Figure 1&#46; Pathogenesis of ischemic nephropathy</p>"
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        "resumen" => "<p class="elsevierStylePara">En esta revisi&#243;n nos gustar&#237;a realizar un resumen del conocimiento actual sobre la patog&#233;nesis y el tratamiento de la nefropat&#237;a isqu&#233;mica&#46; Los datos epidemiol&#243;gicos sugieren que la prevalencia de la nefropat&#237;a isqu&#233;mica aumenta&#44; especialmente en los individuos de mayor edad&#46; La patog&#233;nesis de esta enfermedad es m&#225;s compleja que el mero estrechamiento de la arteria renal a causa de la ateroesclerosis&#46; El sistema renina angiotensina&#44; los factores de crecimiento&#44; las diferentes citoquinas y las quimiocinas pueden estar implicados en la patog&#233;nesis de la nefropat&#237;a isqu&#233;mica&#46; Espec&#237;ficamente&#44; los criterios diagn&#243;sticos de utilidad cl&#237;nica de la nefropat&#237;a isqu&#233;mica a&#250;n est&#225;n por determinar&#46; La gesti&#243;n m&#233;dica acordada de forma conjunta sigue siendo por el momento la principal opci&#243;n terap&#233;utica para la mayor&#237;a de los pacientes con esta patolog&#237;a y hoy en d&#237;a&#44; la revascularizaci&#243;n est&#225; indicada &#250;nicamente en pacientes seleccionados&#46;</p>"
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        "resumen" => "<p class="elsevierStylePara">In this review paper we would like to summarized the current knowledge concerning the&#160; pathogenesis and treatment of ischemic nephropathy&#46; Epidemiological data suggest that the prevalence of ischemic nephropathy increases&#44; especially among older individuals&#46; The pathogenesis of this disease is more complex than just narrowing of the renal artery due to atherosclerosis&#46; Renin-angiotension system&#44; growth factors&#44; different cytokines and chemokines may participate in the pathogenesis of ischemic nephropathy&#46; Precise&#44; clinically useful diagnostic criteria of the ischemic nephropathy have not been established&#44; yet&#46; Concerted medical management remains now the main therapeutic option for majority of patients with this disease and only in the selected patients revascularisation is nowadays indicated&#46;</p>"
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Article information

ISSN: 20132514
Original language: English

DOI:10.3265/Nefrologia.pre2012.Apr.11472

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Year/Month	Html	Pdf	Total

2024 November	18	4	22
2024 October	172	33	205
2024 September	156	31	187
2024 August	178	60	238
2024 July	173	33	206
2024 June	165	52	217
2024 May	145	38	183
2024 April	94	35	129
2024 March	71	24	95
2024 February	52	31	83
2024 January	56	27	83
2023 December	76	30	106
2023 November	94	34	128
2023 October	97	29	126
2023 September	95	35	130
2023 August	58	27	85
2023 July	91	26	117
2023 June	122	20	142
2023 May	105	31	136
2023 April	90	23	113
2023 March	71	20	91
2023 February	52	14	66
2023 January	59	34	93
2022 December	57	27	84
2022 November	57	40	97
2022 October	65	30	95
2022 September	50	45	95
2022 August	54	45	99
2022 July	61	47	108
2022 June	62	53	115
2022 May	45	30	75
2022 April	70	52	122
2022 March	89	58	147
2022 February	93	48	141
2022 January	116	37	153
2021 December	80	44	124
2021 November	97	43	140
2021 October	156	56	212
2021 September	101	44	145
2021 August	123	41	164
2021 July	79	30	109
2021 June	82	33	115
2021 May	179	30	209
2021 April	169	41	210
2021 March	135	57	192
2021 February	119	13	132
2021 January	74	18	92
2020 December	61	13	74
2020 November	75	23	98
2020 October	59	25	84
2020 September	71	14	85
2020 August	63	16	79
2020 July	75	19	94
2020 June	74	21	95
2020 May	96	10	106
2020 April	88	25	113
2020 March	96	13	109
2020 February	103	31	134
2020 January	67	20	87
2019 December	82	15	97
2019 November	77	26	103
2019 October	89	18	107
2019 September	81	31	112
2019 August	56	18	74
2019 July	78	37	115
2019 June	89	32	121
2019 May	131	22	153
2019 April	201	58	259
2019 March	135	36	171
2019 February	119	27	146
2019 January	102	33	135
2018 December	182	47	229
2018 November	145	17	162
2018 October	141	16	157
2018 September	163	20	183
2018 August	120	18	138
2018 July	75	13	88
2018 June	80	11	91
2018 May	99	15	114
2018 April	89	9	98
2018 March	78	11	89
2018 February	65	6	71
2018 January	62	11	73
2017 December	86	9	95
2017 November	79	14	93
2017 October	68	13	81
2017 September	65	9	74
2017 August	72	6	78
2017 July	73	13	86
2017 June	61	6	67
2017 May	68	10	78
2017 April	84	20	104
2017 March	67	16	83
2017 February	76	5	81
2017 January	39	17	56
2016 December	129	4	133
2016 November	142	16	158
2016 October	199	11	210
2016 September	258	12	270
2016 August	313	11	324
2016 July	235	15	250
2016 June	146	0	146
2016 May	135	0	135
2016 April	150	0	150
2016 March	107	0	107
2016 February	120	0	120
2016 January	176	0	176
2015 December	144	0	144
2015 November	124	0	124
2015 October	101	0	101
2015 September	108	0	108
2015 August	93	0	93
2015 July	86	0	86
2015 June	59	0	59
2015 May	56	0	56
2015 April	8	0	8

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