Angiotensin-converting enzyme inhibitor-induced renal failure

Abstract

Angiotensin-converting enzyme inhibitor-induced renal failure is now a well-recognized phenomenon that appears to occur almost exclusively in patients with a preexisting reduction in renal perfusion pressure, especially those with renovascular disease. In the latter group of patients, renal failure probably results from some combination of reduced poststenotic renal perfusion pressure and a unique disturbance in the autoregulation of glomerular filtration rate. Although traditionally regarded as functional and reversible, recent animal studies suggest that angiotensin-converting enzyme inhibitor-induced reductions of glomerular filtration rate may lead to progressive renal atrophy, an observation that raises concerns about the long-term safety of these agents in patients with renovascular disease. On the other hand, the deleterious consequences of angiotensin-converting enzyme inhibition in renovascular disease have been exploited as aids in the diagnosis of this disorder. Whether the adjunctive use of angiotensin-converting enzyme inhibitors will prove to be useful in screening large populations of hypertensive patients for renovascular hypertension remains to be determined. However, such adjunctive tests appear to be useful in judging the functional significance of angiographically documented renal artery stenosis.

Management of atherosclerotic renovascular disease after Cardiovascular Outcomes in Renal Atherosclerotic Lesions (CORAL)

“…We anticipate that more patients will surface to subspecialty attention as they develop evident progressive disease associated with advancing clinical manifestations including worsening CKD and/or pulmonary edema out of proportion to cardiac disease. In some cases, renal function may improve and/or stabilize after withdrawal of renin-angiotensin system blockade, which some argue should be an essential step in identifying critical ARVD [58]. The role of the nephrologist will be to identify this subgroup of patients at risk of developing ischemic nephropathy and other high-risk manifestations of ARVD at a time when they still may benefit…”

Unilateral atrophic kidney in a 45-year-old woman

“…Starting an ACE inhibitor or an ARB blunts this normal autoregulatory response and causes a hemodynamically mediated decline in the GFR. 33 However, despite the initial reduction in fi ltration in the stenotic kidney, the total GFR is usually maintained due to an approximately equivalent increase in fi ltration in the contralateral kidney. This is because blocking the vasoconstrictive effect of angiotensin II eventually decreases renal vascular resistance and ultimately preserves renal blood fl ow.…”