{"title":"Néphroangiosclérose","authors":"M. Beaufils","doi":"10.1016/j.emcnep.2005.07.001","DOIUrl":null,"url":null,"abstract":"<div><p>Nephrosclerosis is the renal disease which appears as a consequence of long-standing (and generally poorly treated) hypertension. It is manifested as a slowly progressive renal failure that may eventually lead to end-stage renal failure. It is considered responsible for more than 20% of patients entering dialysis in the United States. In fact, nephrosclerosis is relatively frequent in the Afro-American population, but it seems very rare in other groups. Hypertension results in vascular, glomerular, then interstitial lesions of the kidney. Hypertensive renal damage is more pronounced when systemic blood pressure is transmitted to the glomerular circulation, due to altered self-regulation. The frequency of nephrosclerosis is obviously overestimated, due to the lack of renal biopsy; moreover the precession of hypertension on renal disease is rarely established. Doubt has been cast on this concept. The alternative hypothesis is that the primary abnormality is renal, mostly congenital, and responsible for the elevation of blood pressure. Blood pressure and renal injury are then engaged in a vicious circle, aggravating each other. Anyway, lowering blood pressure is the only therapeutic measure able to stop the self-aggravation loop. Some antihypertensive drugs, especially those inhibiting the renin angiotensin system, have a direct action on renal haemodynamics, and seem to be nephroprotective beyond the lowering of blood pressure.</p></div>","PeriodicalId":100433,"journal":{"name":"EMC - Néphrologie","volume":"2 3","pages":"Pages 103-124"},"PeriodicalIF":0.0000,"publicationDate":"2005-08-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.emcnep.2005.07.001","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"EMC - Néphrologie","FirstCategoryId":"1085","ListUrlMain":"https://www.sciencedirect.com/science/article/pii/S1638624805000083","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Nephrosclerosis is the renal disease which appears as a consequence of long-standing (and generally poorly treated) hypertension. It is manifested as a slowly progressive renal failure that may eventually lead to end-stage renal failure. It is considered responsible for more than 20% of patients entering dialysis in the United States. In fact, nephrosclerosis is relatively frequent in the Afro-American population, but it seems very rare in other groups. Hypertension results in vascular, glomerular, then interstitial lesions of the kidney. Hypertensive renal damage is more pronounced when systemic blood pressure is transmitted to the glomerular circulation, due to altered self-regulation. The frequency of nephrosclerosis is obviously overestimated, due to the lack of renal biopsy; moreover the precession of hypertension on renal disease is rarely established. Doubt has been cast on this concept. The alternative hypothesis is that the primary abnormality is renal, mostly congenital, and responsible for the elevation of blood pressure. Blood pressure and renal injury are then engaged in a vicious circle, aggravating each other. Anyway, lowering blood pressure is the only therapeutic measure able to stop the self-aggravation loop. Some antihypertensive drugs, especially those inhibiting the renin angiotensin system, have a direct action on renal haemodynamics, and seem to be nephroprotective beyond the lowering of blood pressure.