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Captopril-Induced Renal Insufficiency and the Role of Sodium Balance

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▸Requests for reprints should be addressed to Donald E. Hricik, M.D.; Department of Medicine, University Hospitals of Cleveland, 2065 Adelbert Road; Cleveland, OH 44106.

Case Western Reserve University School of Medicine; Cleveland, Ohio

Ann Intern Med. 1985;103(2):222-223. doi:10.7326/0003-4819-103-2-222
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Acute reversible renal failure may complicate therapy with Captopril in patients with bilateral renal-artery stenoses or renal-artery stenosis in a solitary kidney (1-6). The concomitant use of diuretic agents in many of the reported cases of captopril-induced renal insufficiency has led to speculation that diuretic therapy or sodium depletion may contribute to the decrement in glomerular filtration rate mediated by angiotensin-converting enzyme inhibitors in the presence of a fixed reduction in renal perfusion pressure (1, 6). To determine the influence of sodium balance on captopril-induced renal insufficiency, the renal hemodynamic effects of Captopril were studied prospectively in a patient with


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