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Functional Renal Insufficiency During Long-Term Therapy with Captopril and Enalapril in Severe Chronic Heart Failure

MILTON PACKER, M. D.; WAI HUNG LEE, M.D.; NORMA MEDINA, R.N.; MADELINE YUSHAK, R.N.; and PAUL D. KESSLER, M.D.
[+] Article and Author Information

Grant support: by grants ROl-HL-25055, K04-HL-01229, and T32-HL-07347 from the National Heart, Lung, and Blood Institute. Dr. Packer is the recipient of a Research Career Development Award from the National Institutes of Health.

▸Requests for reprints should be addressed to Milton Packer, M.D.; Division of Cardiology, The Mount Sinai Medical Center. One Gustave Levy Place; New York, NY 10029.


New York, New York


© 1987 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1987;106(3):346-354. doi:10.7326/0003-4819-106-3-346
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Renal function was evaluated in 104 patients with severe chronic heart failure whom we treated with Captopril or enalapril. Seventy patients showed no change or an improvement in renal function (group A)1 and 34 patients developed functional renal insufficiency (group B). Before converting-enzyme inhibition, group B patients received higher doses of furosemide (p < 0.02) and had lower central venous pressures (p < 0.05) than group A patients. After 1 to 3 months of converting-enzyme inhibition, an excessive reduction in left ventricular filling pressure (to less than 15 mm Hg) or mean arterial pressure (to less than 60 mm Hg) was noted in 28 of 34 (82%) patients in group B but in only 22 of 70 patients in group A (31%) (p < 0.001). At the end of the study, drug-induced azotemia resolved after a reduction in the dosage of diuretics, despite unaltered treatment with Captopril and enalapril. Hence, the deterioration of renal function after converting-enzyme inhibition in heart failure is not a toxic or immunologic reaction to therapy but results from specific hemodynamic events that can be ameliorated by sodium repletion.

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