Atherosclerotic renal vascular disease can impair kidney perfusion and lead to deterioration of kidney function. The mechanisms by which reversible tissue injury becomes irreversible are not yet certain, although multiple pathways for activation of inflammatory cytokines and tissue fibrosis have been identified. The clinical hallmark of this disorder is loss of glomerular filtration beyond renal artery stenosis affecting the entire renal mass, usually associated with progressive hypertension and fluid retention. Some investigators believe that 12% to 18% of patients reaching end-stage renal disease in western countries may have lost kidney function because of azotemic renovascular disease. This is an important disorder to identify, because reduction of arterial pressure from antihypertensive therapy may further reduce kidney perfusion. Although administration of angiotensin-converting enzyme (ACE) inhibitors and angiotensin II antagonists lead to functional loss of glomerular filtration rate (GFR) beyond a stenotic lesion because of the removal of efferent actions of angiotensin II, other antihypertensive agents reduce renal perfusion also. Restoration of renal blood flow by surgical or endovascular methods can prevent progressive disease and sometimes improves renal function. However, clinical series commonly indicate that some patients lose further kidney function after revascularization. This may be explained partly by undetected renal atheremboli or other toxicity related to vascular repair. Hence, selection of patients for renal revascularization requires careful consideration of comorbid disease risk and the balance of risks and benefits regarding progressive renal disease. Searching for better methods of identifying those individuals at risk for irreversible loss of renal function and who might benefit from vascular repair is a high research priority. Copyright (C) 2000 by W.B. Saunders Company.
|Original language||English (US)|
|Number of pages||14|
|Journal||Seminars in nephrology|
|State||Published - Sep 26 2000|
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