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    "textoCompleto" => "<p class="elsevierStylePara">The epidemiological picture of chronic kidney disease &#40;CKD&#41; has seen a dramatic change in the past two decades&#46; Initially restricted to low-incidence diseases such as classical nephropathies &#40;glomerulopathies&#44; cystic diseases&#44; interstitial nephropathies&#41; and to a specialised field of medical care &#40;nephrology&#41;&#44; the currently predominant CKD affects a significant percentage of the population due to aging and three highly prevalent disorders including essential hypertension &#40;HT&#41;&#44; diabetes&#44; and vascular disease&#46; Many patients who are seen by multiple specialties&#44; particulary Primary Care&#44; have CKD&#46; Patients with end-stage renal disease &#40;ESRD&#41; who are on renal-replacement therapies by means of dialysis and transplantation are considered the tip of the iceberg of the public-health problem&#44; which is CKD in the population&#46;</p><p class="elsevierStylePara">The terms nephrosclerosis or hypertensive nephropathy are usually applied to CKD associated to HT&#46; In practice&#44; nephrosclerosis is an entity with a non-specific clinical picture&#44; which groups together hypertensive patients with CKD with those in whom no other recognisable causes of the pathology can be appreciated&#46;<span class="elsevierStyleSup">1-3</span></p><p class="elsevierStylePara">In nephrosclerosis&#44; the most characteristic microscopic lesion is hyalinosis of afferent arterioles&#46; The vascular changes produce vasoconstriction&#44; glomerular ischaemia &#40;retraction of the glomerular tuft with focal or global sclerosis&#41;&#44; and in some areas&#44; interstitial fibrosis and tubular atrophy&#46; Other authors point out that the hyalinisation of afferent arterioles initially causes vasodilatation&#44; glomerular hypertrophy and&#44; in the long term&#44; glomerulosclerosis lesions that would favour the development of proteinuria and disease progression&#46; These abnormalities are more frequent in black patients&#46;<span class="elsevierStyleSup">4-7</span></p><p class="elsevierStylePara">Its causal relationship to HT is still under debate&#46; It is not at all clear that treated HT can lead to ESRD&#46;<span class="elsevierStyleSup">8-10</span> Therefore&#44; some authors have postulated that renal structural abnormalities may precede hypertension and that nephrosclerosis is an intrinsic process of the preglomerular renal microvasculature with loss of self-regulatory capacity&#46; This anomaly would result in excessive preglomerular vasoconstriction<span class="elsevierStyleSup">3&#44;7 </span>or persistent vasodilation of the afferent arteriole&#46;<span class="elsevierStyleSup">5&#44;6</span> Chronically impaired renal plasma flow in the long run would lead to hypertension and renal failure&#46;</p><p class="elsevierStylePara">Vascular nephropathy in the United States&#44; as well as in Europe and Spain&#44; is the second most common cause of ESRD&#46; However&#44; this observation has been histologically confirmed in very few cases&#46; The diagnosis of nephrosclerosis is usually made by exclusion in the absence of signs suggesting another type of nephropathy or another possible clinical situation &#40;advanced age&#44; long-standing hypertension&#44; left ventricular hypertrophy&#44; originally-mild renal insufficiency and proteinuria less than 0&#46;5-1g&#47;day&#41;&#46; As with diabetic nephropathy&#44; one almost never resorts to renal biopsy to confirm the diagnosis&#46; This attitude may be reasonable in many cases but is undoubtedly a source of misdiagnosis&#46;<span class="elsevierStyleSup">11&#44;12</span> Compared with primary glomerular nephropathies or diabetic nephropathy&#44; progression of renal failure is slow in most cases&#44; especially in Caucasians&#46; Kidney function can remain stable over long periods of time if HT is adequately controlled&#46; However&#44; in a poorly determined&#44; but probably small proportion of cases&#44; the disease progresses until it reaches ESRD&#46;<span class="elsevierStyleSup">12&#44;13</span> In patients with renal failure&#44; vascular nephropathy is the most common indication for hospital consultations to nephrology services in our country&#46; Up to 39&#37; of cases of CKD have this aetiology&#44; surpassing diabetic nephropathy &#40;20&#37;&#41; and glomerular nephropathy &#40;14&#37;&#41;&#46;<span class="elsevierStyleSup">14</span> Despite the small percentage of patients with disease progression&#44; its high prevalence justifies its place as the second leading cause of ESRD&#46;</p><p class="elsevierStylePara">There are no well-recognised factors for progression of the disease&#44; which hampers the implementation of preventive measures&#46; Some commonly cited risk factors are African race&#44; the degree of renal failure at diagnosis&#44; systolic blood pressure &#40;SBP&#41; and the degree of proteinuria&#46;<span class="elsevierStyleSup">15-17</span> In the AASK study&#44; patients with proteinuria below 0&#46;3g&#47;day and who had received an angiotensin converting enzyme inhibitor &#40;ACE-I&#41;&#44; ramipril&#44; showed slower disease progression&#46; In this study&#44; age over 70 years was a factor that was inversely correlated with progression of renal failure&#46;<span class="elsevierStyleSup">18&#44;19</span></p><p class="elsevierStylePara">Among whites&#44; there are only a few cases&#44; perhaps in those who are genetically predisposed&#44; of patients with an unfavourable clinical course&#46; Disease progression can be aided by the concomitant presence of atherosclerotic lesions in the aorta and main renal arteries and processes such as type-2 diabetes&#44; hyperuricaemia and dyslipidaemia&#46; The age of onset for ESRD is between 45 and 64 years for African Americans&#44; whereas it is over 65 years for Caucasian Americans&#46;<span class="elsevierStyleSup">2&#44;3</span></p><p class="elsevierStylePara">In the last decade&#44; the disease is being diagnosed in patients older than 65-70 years of age with vascular disease in other locations&#46; In these cases&#44; nephrosclerosis could be the manifestation of diffuse atherosclerosis in renal arterioles&#46;<span class="elsevierStyleSup">20</span> It has also been noted that the presence of concomitant cardiovascular disease is a risk factor for progression of renal failure&#46; Elsayed et al&#46;&#44; in a study of 13&#44;826 subjects included in the Atherosclerosis Risk in Communities Study and the Cardiovascular Health Study&#44; found that cardiovascular disease at baseline predicted the development of CKD &#40;HR &#61; 1&#46;75&#44; p &#60; 0&#46;001&#41;&#46;<span class="elsevierStyleSup">21</span></p><p class="elsevierStylePara">The publication of an original study concerning nephrosclerosis in this issue of NEFROLOGIA should be welcomed&#44; given the small number of publications on the subject&#8212;which is the Cinderella of renal diseases despite its high prevalence&#46;<span class="elsevierStyleSup">22</span> Robles et al&#46;<span class="elsevierStyleSup">23</span> conducted a retrospective analysis of 479 hypertensive patients with renal disease treated in an outpatient nephrology clinic for 17 consecutive years &#40;1991-2007&#41;&#46; This clinic cared for an area with approximately 650&#44;000 inhabitants and&#44; in that period&#44; 5&#44;071 patients were treated for unspecified conditions&#44; so it is not possible to determine the overall prevalence of the disease&#46; The diagnosis was made based on clinical criteria&#44; except in 60 patients &#40;12&#46;5&#37;&#41; who&#44; having proteinuria exceeding 1g&#47;day&#44; were subjected to biopsy&#46; The average age of patients was 66 years&#44; and 57&#37; of them were men&#46; According to the article&#44; 34&#37; had diabetes mellitus&#46; The basic aim of the study was to examine the evolving implications of the disease over three consecutive 5- year periods&#46; The authors verify that the average incidence of nephrosclerosis was 44 cases per million population &#40;PMP&#41; and that there was a progressive increase of it&#44; from 31&#46;8 PMP in 1991-1995 to 32&#46;1 PMP in 1996-2000 and 54&#46;4 PMP in 2001- 2006&#46; The average age of the patients showed a &#8220;J&#8221; curve &#40;69&#44; 65&#44; and 67 years&#44; respectively&#41;&#46; Atotal of 53 patients &#40;11&#46;1&#37;&#41; started renal replacement therapy&#46; The mortality rate before the arrival of such treatment was 4&#44; 16 and 19&#37;&#44; respectively&#46; The authors concluded that the incidence of the disease has grown in recent years even though the preventive therapeutic measures in the most recent period were theoretically better&#46;</p><p class="elsevierStylePara">In the last two decades&#44; the continuous increase in life expectancy and the growing permissiveness for the entry of patients with stage 5 CKD into dialysis programs has enabled patients over the age of 65 to become the largest group in these programs&#46; Vascular nephropathy&#44; diabetes and CKD of unknown aetiology&#44; which is predominant in patients over 65 years of age&#44; are the main causes of ESRD&#46;<span class="elsevierStyleSup">24</span> It is likely that a significant percentage of cases of unknown cause correspond to hypertensive nephropathy&#46; Therefore&#44; the true prevalence of this process is not known&#46; As with the aforementioned study&#44; the inclusion of patients is usually done exclusively by clinical criteria that&#44; moreover&#44; are not uniform across studies&#46; The clinical-pathologic correlation is less obvious than that described in patients with diabetic nephropathy&#46;</p><p class="elsevierStylePara">In nephrosclerosis&#44; clinical markers are less consistent than those described in diabetics with established nephropathy &#40;diabetic retinopathy&#44; proteinuria exceeding 1g&#47;day&#44; and renal failure&#41; &#40;Table 1&#41;&#46;<span class="elsevierStyleSup">25</span> However&#44; it is possible that a large proportion of patients with stages 3-4 CKD and over 70-75 years of age who are treated in outpatient nephrology clinics correspond to cases of nephrosclerosis&#46;<span class="elsevierStyleSup">14 </span></p><p class="elsevierStylePara">The percentage of patients who progress to ESRD is also unknown&#46; Since the disease rarely progresses&#44; in many cases those patients who are in better clinical condition are discharged and therefore lost to follow-up&#46; This may explain the difference in progression between the study by Robles et al&#46; &#40;11&#46;6&#37;&#41; and a multicentre prospective study carried out in our country that excluded baseline cases of &#8220;historical&#8221; nephrosclerosis and included only incident cases &#40;n &#61; 430&#41; over the course of one year&#46; Preliminary results after two years of monitoring show that progression has been observed in only 3&#46;9&#37; of patients&#44; with notable markers of progression being the presence of higher baseline SBP and a higher rate of associated cardiovascular events&#46;<span class="elsevierStyleSup">26 </span></p><p class="elsevierStylePara">Two recent studies have provided a new approach to the pathogenesis of the disease&#44; at least in the African-American race&#46; The study by Kao et al&#46;&#44; which included 1&#44;372 patients&#44; revealed a close relationship between the presence of ESRD secondary to hypertensive nephrosclerosis in patients without diabetes&#44; as well as some polymorphisms of the <span class="elsevierStyleItalic">MYH9 </span>gene<span class="elsevierStyleItalic">&#44; </span>located on chromosome 22&#44; that encodes the heavy chain of the non-muscle protein myosin IIA&#46;<span class="elsevierStyleSup">27</span> The study by Kopp et al&#46; reported the exact same association between these polymorphisms of this gene and the presence of idiopathic focal segmental glomerulosclerosis &#40;FSGS&#41; or secondary to HIV infection&#46;<span class="elsevierStyleSup">28</span> In another study&#44; Freedman et al&#46; confirmed the presence of <span class="elsevierStyleItalic">MYH9 </span>gene polymorphisms in 696 African-American subjects with hypertensive nephropathy and ESRD compared with 948 control individuals without CKD&#46;<span class="elsevierStyleSup">29</span> The above mentioned <span class="elsevierStyleItalic">MYH9 </span>gene polymorphisms are less common in Caucasians&#44; but they have been studied and it is not possible to determine whether they could also be markers of the disease&#46; It appears that&#44; in early stages&#44; myosin IIA is present mainly in podocytes and causes structural abnormalities&#46; Recently&#44; the role of podocyte loss and dysfunction has been described in the pathogenesis of the disease&#46;<span class="elsevierStyleSup">29-31</span></p><p class="elsevierStylePara">Based on these studies&#44; some editorials have stated that nephrosclerosis should no longer be considered a disease secondary to HT&#46; At least among patients of African descent&#44; it appears to be a genetically based disease&#46; Polymorphisms of this gene may be markers of various renal diseases that may be grouped in the same histologic group&#44; the one that includes FSGS&#46; This entity could include&#44; in addition to the idiopathic form and the collapsing form as observed in HIV infection&#44; hypertensive nephropathy&#44; which would be a primitive renal disease&#46; One may speculate that treatment could be approached with new perspectives and include more than blocking the renin-angiotensin system and strict control of blood pressure&#46;<span class="elsevierStyleSup">32-35</span></p><p class="elsevierStylePara">However&#44; there are still many unknowns about these findings&#46; The studies referred to were performed in patients with nephrosclerosis that was not confirmed with renal biopsies&#46; Clinical diagnosis of nephrosclerosis may hide cases of malignant hypertension&#44; ischaemic nephropathy&#44; atheroembolic nephropathy and some types of primary glomerular nephropathy&#46; This marks the opportunity to reassess the cases in the AASK study&#44; which is the only study with a high number of patients who underwent renal biopsy&#44;<span class="elsevierStyleSup">15&#44;17</span> and also the need to design prospective studies to further evaluate the relationship of this genetic polymorphism with disease progression&#46;</p><p class="elsevierStylePara">In Caucasians almost everything still needs to be done&#46; There are no studies to support that these or other <span class="elsevierStyleItalic">MYH9 </span>gene polymorphisms might be involved in disease&#46; We do not know if the nephrosclerosis that is described in the African-American race with histological support of FSGS&#44; high levels of proteinuria&#44; and an abnormality in the <span class="elsevierStyleItalic">MYH9 </span>gene<span class="elsevierStyleItalic">&#44; </span>is the same type of process which is seen more commonly in Caucasians&#58; in elderly patients&#44; those with significant vascular comorbidity&#44; minimal proteinuria&#44; and in whom progression of CKD is uncommon&#46; It is possible that this process is merely a magnification of renal aging&#46;</p><p class="elsevierStylePara">Finally&#44; it should be noted that some studies carried out over a decade ago verified a direct relationship between nephrosclerosis and the DD genotype of the ACE gene in Caucasians&#46; The D allele appeared to be predominant in hypertensive patients with nephrosclerosis and could be a marker of progression&#46; Although the number of patients was small&#44; the studies included histological support and control groups of hypertensive patients without renal impairment&#46;<span class="elsevierStyleSup">36&#44;37</span></p><p class="elsevierStylePara">In summary&#44; it seems that prospective studies need to be designed in the future with prolonged follow-up intervals that allow us to know the true nature of the disease and limit the proportion of cases progressing to stage 5 CKD&#46; Analysis of markers of progression must include both classical clinical markers and genetic markers described above&#44; and it may be reasonable&#44; at least in a subset of the population chosen at random&#44; to obtain histological confirmation of the disease&#46; This would be the basis for recognising whether renoprotective and cardioprotective treatments prescribed so far &#40;in the form of renin-angiotensin system blockers&#44; lipid lowering agents&#44; antiplatelet agents&#44; etc&#46;&#41; have had a real preventive role&#46; In addition&#44; it would be useful to clarify whether the objective of reducing blood pressure to below 130&#47;80mmHg is effective in this disease and to investigate other potential therapeutic goals&#46;</p><p class="elsevierStylePara">KEY CONCEPTS</p><p class="elsevierStylePara">1&#46; Nephrosclerosis is seen in patients with chronic kidney disease and essential hype rtension with no other cause of kidney disease&#46;</p><p class="elsevierStylePara">2&#46; Nephrosclerosis is the second most frequent cause of terminal chronic kidney disease and the first cause of nephrology hospital consultations in our country&#46; 3&#46; The causal relationship with hypertension is still a subject for debate&#46;</p><p class="elsevierStylePara">4&#46; In Caucasians&#44; progression of kidney failure is infrequent in most cases&#46;</p><p class="elsevierStylePara">5&#46; The factors that cause progression are not well recognised&#46; Factors that are usually mentioned are&#58; black race&#44; degree of kidney failure on diagnosis&#44; systolic blood pressure&#44; degree of proteinuria and degree of associated cardiovascular comorbidity&#46;</p><p class="elsevierStylePara">6&#46; There is no evidence that a target blood pressure of &#60;130&#47;80 mmHg is more effective than a target blood pressure of &#60;140&#47;90 mmHg at preventing disease progression&#46; Renin-angiotensin system blockers are used in the first step of treatment&#44; although it has been shown to be effective only in cases with proteinuria &#40;albumin&#47;creatinine ratio &#62;300 mg&#47;g&#41;&#46; The renoprotective effect of lipidlowering and antiaggregant agents requires greater research&#46;</p><p class="elsevierStylePara">7&#46; A relationship with disease has been found in Afro-Americans due to polymorphisms in the MYH9 gene&#46; There have been no studies performed in Caucasians&#46;</p><p class="elsevierStylePara">8&#46; Prospective studies with histological support are necessary to recognise the clinical and genetic markers that condition progression in not Afro-American patients&#46;&#160;&#160; &#160;</p><p class="elsevierStylePara"><a href="grande&#47;10329&#95;18030&#95;5466&#95;en&#95;table1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10329_18030_5466_en_table1.gif" alt="Diagnosis of nephrosclerosis&#46; Suspected clinical data"></img></a></p><p class="elsevierStylePara">Table 1&#46; Diagnosis of nephrosclerosis&#46; Suspected clinical data</p>"
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Nephrosclerosis. The Cinderella of chronic kidney disease
Nefroangioesclerosis. La cenicienta de la enfermedad renal crónica.
Rafael Marína, Manuel Gorostidib, Beatriz Diez Ojeac
a Unidad de Nefrología e Hipertensión, Centro Médico de Asturias, Oviedo, Asturias, España,
b Servicio de Nefrología, Hospital Universitario Central de Asturias, Oviedo, Asturias, España,
c Servicio de Nefrología, Hospital Valle del Nalón, Langreo, Asturias, España,
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    "textoCompleto" => "<p class="elsevierStylePara">The epidemiological picture of chronic kidney disease &#40;CKD&#41; has seen a dramatic change in the past two decades&#46; Initially restricted to low-incidence diseases such as classical nephropathies &#40;glomerulopathies&#44; cystic diseases&#44; interstitial nephropathies&#41; and to a specialised field of medical care &#40;nephrology&#41;&#44; the currently predominant CKD affects a significant percentage of the population due to aging and three highly prevalent disorders including essential hypertension &#40;HT&#41;&#44; diabetes&#44; and vascular disease&#46; Many patients who are seen by multiple specialties&#44; particulary Primary Care&#44; have CKD&#46; Patients with end-stage renal disease &#40;ESRD&#41; who are on renal-replacement therapies by means of dialysis and transplantation are considered the tip of the iceberg of the public-health problem&#44; which is CKD in the population&#46;</p><p class="elsevierStylePara">The terms nephrosclerosis or hypertensive nephropathy are usually applied to CKD associated to HT&#46; In practice&#44; nephrosclerosis is an entity with a non-specific clinical picture&#44; which groups together hypertensive patients with CKD with those in whom no other recognisable causes of the pathology can be appreciated&#46;<span class="elsevierStyleSup">1-3</span></p><p class="elsevierStylePara">In nephrosclerosis&#44; the most characteristic microscopic lesion is hyalinosis of afferent arterioles&#46; The vascular changes produce vasoconstriction&#44; glomerular ischaemia &#40;retraction of the glomerular tuft with focal or global sclerosis&#41;&#44; and in some areas&#44; interstitial fibrosis and tubular atrophy&#46; Other authors point out that the hyalinisation of afferent arterioles initially causes vasodilatation&#44; glomerular hypertrophy and&#44; in the long term&#44; glomerulosclerosis lesions that would favour the development of proteinuria and disease progression&#46; These abnormalities are more frequent in black patients&#46;<span class="elsevierStyleSup">4-7</span></p><p class="elsevierStylePara">Its causal relationship to HT is still under debate&#46; It is not at all clear that treated HT can lead to ESRD&#46;<span class="elsevierStyleSup">8-10</span> Therefore&#44; some authors have postulated that renal structural abnormalities may precede hypertension and that nephrosclerosis is an intrinsic process of the preglomerular renal microvasculature with loss of self-regulatory capacity&#46; This anomaly would result in excessive preglomerular vasoconstriction<span class="elsevierStyleSup">3&#44;7 </span>or persistent vasodilation of the afferent arteriole&#46;<span class="elsevierStyleSup">5&#44;6</span> Chronically impaired renal plasma flow in the long run would lead to hypertension and renal failure&#46;</p><p class="elsevierStylePara">Vascular nephropathy in the United States&#44; as well as in Europe and Spain&#44; is the second most common cause of ESRD&#46; However&#44; this observation has been histologically confirmed in very few cases&#46; The diagnosis of nephrosclerosis is usually made by exclusion in the absence of signs suggesting another type of nephropathy or another possible clinical situation &#40;advanced age&#44; long-standing hypertension&#44; left ventricular hypertrophy&#44; originally-mild renal insufficiency and proteinuria less than 0&#46;5-1g&#47;day&#41;&#46; As with diabetic nephropathy&#44; one almost never resorts to renal biopsy to confirm the diagnosis&#46; This attitude may be reasonable in many cases but is undoubtedly a source of misdiagnosis&#46;<span class="elsevierStyleSup">11&#44;12</span> Compared with primary glomerular nephropathies or diabetic nephropathy&#44; progression of renal failure is slow in most cases&#44; especially in Caucasians&#46; Kidney function can remain stable over long periods of time if HT is adequately controlled&#46; However&#44; in a poorly determined&#44; but probably small proportion of cases&#44; the disease progresses until it reaches ESRD&#46;<span class="elsevierStyleSup">12&#44;13</span> In patients with renal failure&#44; vascular nephropathy is the most common indication for hospital consultations to nephrology services in our country&#46; Up to 39&#37; of cases of CKD have this aetiology&#44; surpassing diabetic nephropathy &#40;20&#37;&#41; and glomerular nephropathy &#40;14&#37;&#41;&#46;<span class="elsevierStyleSup">14</span> Despite the small percentage of patients with disease progression&#44; its high prevalence justifies its place as the second leading cause of ESRD&#46;</p><p class="elsevierStylePara">There are no well-recognised factors for progression of the disease&#44; which hampers the implementation of preventive measures&#46; Some commonly cited risk factors are African race&#44; the degree of renal failure at diagnosis&#44; systolic blood pressure &#40;SBP&#41; and the degree of proteinuria&#46;<span class="elsevierStyleSup">15-17</span> In the AASK study&#44; patients with proteinuria below 0&#46;3g&#47;day and who had received an angiotensin converting enzyme inhibitor &#40;ACE-I&#41;&#44; ramipril&#44; showed slower disease progression&#46; In this study&#44; age over 70 years was a factor that was inversely correlated with progression of renal failure&#46;<span class="elsevierStyleSup">18&#44;19</span></p><p class="elsevierStylePara">Among whites&#44; there are only a few cases&#44; perhaps in those who are genetically predisposed&#44; of patients with an unfavourable clinical course&#46; Disease progression can be aided by the concomitant presence of atherosclerotic lesions in the aorta and main renal arteries and processes such as type-2 diabetes&#44; hyperuricaemia and dyslipidaemia&#46; The age of onset for ESRD is between 45 and 64 years for African Americans&#44; whereas it is over 65 years for Caucasian Americans&#46;<span class="elsevierStyleSup">2&#44;3</span></p><p class="elsevierStylePara">In the last decade&#44; the disease is being diagnosed in patients older than 65-70 years of age with vascular disease in other locations&#46; In these cases&#44; nephrosclerosis could be the manifestation of diffuse atherosclerosis in renal arterioles&#46;<span class="elsevierStyleSup">20</span> It has also been noted that the presence of concomitant cardiovascular disease is a risk factor for progression of renal failure&#46; Elsayed et al&#46;&#44; in a study of 13&#44;826 subjects included in the Atherosclerosis Risk in Communities Study and the Cardiovascular Health Study&#44; found that cardiovascular disease at baseline predicted the development of CKD &#40;HR &#61; 1&#46;75&#44; p &#60; 0&#46;001&#41;&#46;<span class="elsevierStyleSup">21</span></p><p class="elsevierStylePara">The publication of an original study concerning nephrosclerosis in this issue of NEFROLOGIA should be welcomed&#44; given the small number of publications on the subject&#8212;which is the Cinderella of renal diseases despite its high prevalence&#46;<span class="elsevierStyleSup">22</span> Robles et al&#46;<span class="elsevierStyleSup">23</span> conducted a retrospective analysis of 479 hypertensive patients with renal disease treated in an outpatient nephrology clinic for 17 consecutive years &#40;1991-2007&#41;&#46; This clinic cared for an area with approximately 650&#44;000 inhabitants and&#44; in that period&#44; 5&#44;071 patients were treated for unspecified conditions&#44; so it is not possible to determine the overall prevalence of the disease&#46; The diagnosis was made based on clinical criteria&#44; except in 60 patients &#40;12&#46;5&#37;&#41; who&#44; having proteinuria exceeding 1g&#47;day&#44; were subjected to biopsy&#46; The average age of patients was 66 years&#44; and 57&#37; of them were men&#46; According to the article&#44; 34&#37; had diabetes mellitus&#46; The basic aim of the study was to examine the evolving implications of the disease over three consecutive 5- year periods&#46; The authors verify that the average incidence of nephrosclerosis was 44 cases per million population &#40;PMP&#41; and that there was a progressive increase of it&#44; from 31&#46;8 PMP in 1991-1995 to 32&#46;1 PMP in 1996-2000 and 54&#46;4 PMP in 2001- 2006&#46; The average age of the patients showed a &#8220;J&#8221; curve &#40;69&#44; 65&#44; and 67 years&#44; respectively&#41;&#46; Atotal of 53 patients &#40;11&#46;1&#37;&#41; started renal replacement therapy&#46; The mortality rate before the arrival of such treatment was 4&#44; 16 and 19&#37;&#44; respectively&#46; The authors concluded that the incidence of the disease has grown in recent years even though the preventive therapeutic measures in the most recent period were theoretically better&#46;</p><p class="elsevierStylePara">In the last two decades&#44; the continuous increase in life expectancy and the growing permissiveness for the entry of patients with stage 5 CKD into dialysis programs has enabled patients over the age of 65 to become the largest group in these programs&#46; Vascular nephropathy&#44; diabetes and CKD of unknown aetiology&#44; which is predominant in patients over 65 years of age&#44; are the main causes of ESRD&#46;<span class="elsevierStyleSup">24</span> It is likely that a significant percentage of cases of unknown cause correspond to hypertensive nephropathy&#46; Therefore&#44; the true prevalence of this process is not known&#46; As with the aforementioned study&#44; the inclusion of patients is usually done exclusively by clinical criteria that&#44; moreover&#44; are not uniform across studies&#46; The clinical-pathologic correlation is less obvious than that described in patients with diabetic nephropathy&#46;</p><p class="elsevierStylePara">In nephrosclerosis&#44; clinical markers are less consistent than those described in diabetics with established nephropathy &#40;diabetic retinopathy&#44; proteinuria exceeding 1g&#47;day&#44; and renal failure&#41; &#40;Table 1&#41;&#46;<span class="elsevierStyleSup">25</span> However&#44; it is possible that a large proportion of patients with stages 3-4 CKD and over 70-75 years of age who are treated in outpatient nephrology clinics correspond to cases of nephrosclerosis&#46;<span class="elsevierStyleSup">14 </span></p><p class="elsevierStylePara">The percentage of patients who progress to ESRD is also unknown&#46; Since the disease rarely progresses&#44; in many cases those patients who are in better clinical condition are discharged and therefore lost to follow-up&#46; This may explain the difference in progression between the study by Robles et al&#46; &#40;11&#46;6&#37;&#41; and a multicentre prospective study carried out in our country that excluded baseline cases of &#8220;historical&#8221; nephrosclerosis and included only incident cases &#40;n &#61; 430&#41; over the course of one year&#46; Preliminary results after two years of monitoring show that progression has been observed in only 3&#46;9&#37; of patients&#44; with notable markers of progression being the presence of higher baseline SBP and a higher rate of associated cardiovascular events&#46;<span class="elsevierStyleSup">26 </span></p><p class="elsevierStylePara">Two recent studies have provided a new approach to the pathogenesis of the disease&#44; at least in the African-American race&#46; The study by Kao et al&#46;&#44; which included 1&#44;372 patients&#44; revealed a close relationship between the presence of ESRD secondary to hypertensive nephrosclerosis in patients without diabetes&#44; as well as some polymorphisms of the <span class="elsevierStyleItalic">MYH9 </span>gene<span class="elsevierStyleItalic">&#44; </span>located on chromosome 22&#44; that encodes the heavy chain of the non-muscle protein myosin IIA&#46;<span class="elsevierStyleSup">27</span> The study by Kopp et al&#46; reported the exact same association between these polymorphisms of this gene and the presence of idiopathic focal segmental glomerulosclerosis &#40;FSGS&#41; or secondary to HIV infection&#46;<span class="elsevierStyleSup">28</span> In another study&#44; Freedman et al&#46; confirmed the presence of <span class="elsevierStyleItalic">MYH9 </span>gene polymorphisms in 696 African-American subjects with hypertensive nephropathy and ESRD compared with 948 control individuals without CKD&#46;<span class="elsevierStyleSup">29</span> The above mentioned <span class="elsevierStyleItalic">MYH9 </span>gene polymorphisms are less common in Caucasians&#44; but they have been studied and it is not possible to determine whether they could also be markers of the disease&#46; It appears that&#44; in early stages&#44; myosin IIA is present mainly in podocytes and causes structural abnormalities&#46; Recently&#44; the role of podocyte loss and dysfunction has been described in the pathogenesis of the disease&#46;<span class="elsevierStyleSup">29-31</span></p><p class="elsevierStylePara">Based on these studies&#44; some editorials have stated that nephrosclerosis should no longer be considered a disease secondary to HT&#46; At least among patients of African descent&#44; it appears to be a genetically based disease&#46; Polymorphisms of this gene may be markers of various renal diseases that may be grouped in the same histologic group&#44; the one that includes FSGS&#46; This entity could include&#44; in addition to the idiopathic form and the collapsing form as observed in HIV infection&#44; hypertensive nephropathy&#44; which would be a primitive renal disease&#46; One may speculate that treatment could be approached with new perspectives and include more than blocking the renin-angiotensin system and strict control of blood pressure&#46;<span class="elsevierStyleSup">32-35</span></p><p class="elsevierStylePara">However&#44; there are still many unknowns about these findings&#46; The studies referred to were performed in patients with nephrosclerosis that was not confirmed with renal biopsies&#46; Clinical diagnosis of nephrosclerosis may hide cases of malignant hypertension&#44; ischaemic nephropathy&#44; atheroembolic nephropathy and some types of primary glomerular nephropathy&#46; This marks the opportunity to reassess the cases in the AASK study&#44; which is the only study with a high number of patients who underwent renal biopsy&#44;<span class="elsevierStyleSup">15&#44;17</span> and also the need to design prospective studies to further evaluate the relationship of this genetic polymorphism with disease progression&#46;</p><p class="elsevierStylePara">In Caucasians almost everything still needs to be done&#46; There are no studies to support that these or other <span class="elsevierStyleItalic">MYH9 </span>gene polymorphisms might be involved in disease&#46; We do not know if the nephrosclerosis that is described in the African-American race with histological support of FSGS&#44; high levels of proteinuria&#44; and an abnormality in the <span class="elsevierStyleItalic">MYH9 </span>gene<span class="elsevierStyleItalic">&#44; </span>is the same type of process which is seen more commonly in Caucasians&#58; in elderly patients&#44; those with significant vascular comorbidity&#44; minimal proteinuria&#44; and in whom progression of CKD is uncommon&#46; It is possible that this process is merely a magnification of renal aging&#46;</p><p class="elsevierStylePara">Finally&#44; it should be noted that some studies carried out over a decade ago verified a direct relationship between nephrosclerosis and the DD genotype of the ACE gene in Caucasians&#46; The D allele appeared to be predominant in hypertensive patients with nephrosclerosis and could be a marker of progression&#46; Although the number of patients was small&#44; the studies included histological support and control groups of hypertensive patients without renal impairment&#46;<span class="elsevierStyleSup">36&#44;37</span></p><p class="elsevierStylePara">In summary&#44; it seems that prospective studies need to be designed in the future with prolonged follow-up intervals that allow us to know the true nature of the disease and limit the proportion of cases progressing to stage 5 CKD&#46; Analysis of markers of progression must include both classical clinical markers and genetic markers described above&#44; and it may be reasonable&#44; at least in a subset of the population chosen at random&#44; to obtain histological confirmation of the disease&#46; This would be the basis for recognising whether renoprotective and cardioprotective treatments prescribed so far &#40;in the form of renin-angiotensin system blockers&#44; lipid lowering agents&#44; antiplatelet agents&#44; etc&#46;&#41; have had a real preventive role&#46; In addition&#44; it would be useful to clarify whether the objective of reducing blood pressure to below 130&#47;80mmHg is effective in this disease and to investigate other potential therapeutic goals&#46;</p><p class="elsevierStylePara">KEY CONCEPTS</p><p class="elsevierStylePara">1&#46; Nephrosclerosis is seen in patients with chronic kidney disease and essential hype rtension with no other cause of kidney disease&#46;</p><p class="elsevierStylePara">2&#46; Nephrosclerosis is the second most frequent cause of terminal chronic kidney disease and the first cause of nephrology hospital consultations in our country&#46; 3&#46; The causal relationship with hypertension is still a subject for debate&#46;</p><p class="elsevierStylePara">4&#46; In Caucasians&#44; progression of kidney failure is infrequent in most cases&#46;</p><p class="elsevierStylePara">5&#46; The factors that cause progression are not well recognised&#46; Factors that are usually mentioned are&#58; black race&#44; degree of kidney failure on diagnosis&#44; systolic blood pressure&#44; degree of proteinuria and degree of associated cardiovascular comorbidity&#46;</p><p class="elsevierStylePara">6&#46; There is no evidence that a target blood pressure of &#60;130&#47;80 mmHg is more effective than a target blood pressure of &#60;140&#47;90 mmHg at preventing disease progression&#46; Renin-angiotensin system blockers are used in the first step of treatment&#44; although it has been shown to be effective only in cases with proteinuria &#40;albumin&#47;creatinine ratio &#62;300 mg&#47;g&#41;&#46; The renoprotective effect of lipidlowering and antiaggregant agents requires greater research&#46;</p><p class="elsevierStylePara">7&#46; A relationship with disease has been found in Afro-Americans due to polymorphisms in the MYH9 gene&#46; There have been no studies performed in Caucasians&#46;</p><p class="elsevierStylePara">8&#46; Prospective studies with histological support are necessary to recognise the clinical and genetic markers that condition progression in not Afro-American patients&#46;&#160;&#160; &#160;</p><p class="elsevierStylePara"><a href="grande&#47;10329&#95;18030&#95;5466&#95;en&#95;table1&#46;jpg" class="elsevierStyleCrossRefs"><img src="10329_18030_5466_en_table1.gif" alt="Diagnosis of nephrosclerosis&#46; Suspected clinical data"></img></a></p><p class="elsevierStylePara">Table 1&#46; Diagnosis of nephrosclerosis&#46; Suspected clinical data</p>"
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Nefrología (English Edition)