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Reversible Renal Insufficiency due to Angiotensin Converting Enzyme Inhibitors in Hypertensive Nephrosclerosis

Robert D. Toto, MD; Helen C. Mitchell, MD; Hing-Chung Lee, MD, PhD; Cynthia Milam, RN; and William A. Pettinger, MD
[+] Article and Author Information

Grant Support: By grants from Merck Sharp & Dohme and the National Heart, Lung, and Blood Institutes #R01-HL30339.

Requests for Reprints: Robert D. Toto, MD, Division of Nephrology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75235-8856.

Current Author Addresses: Drs. Toto and Mitchell and Ms. Milam: Division of Nephrology, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Boulevard, Dallas, TX 75235-8856. Drs. Lee and Pettinger: Midwest Hypertension Research Institute, Creighton University Medical Center, 601 North 30th Street, Omaha, NE 68131-2197.


© 1991 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1991;115(7):513-519. doi:10.7326/0003-4819-115-7-513
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Objective: To review the incidence of reversible renal insufficiency in patients with hypertensive nephrosclerosis undergoing antihypertensive therapy.

Design: Retrospective analysis of 73 patients in a long-term blood pressure control study that compared the effects of an angiotensin converting enzyme (ACE) inhibitor plus conventional antihypertensive agents compared with placebo plus antihypertensive agents.

Setting: Hospital-based outpatient treatment center.

Interventions: Patients were divided into group 1, which received enalapril plus conventional antihypertensives, and group 2, which received placebo plus conventional antihypertensives.

Measurements: Blood pressure and serum creatinine levels were measured, and imaging studies of the main renal arteries were done.

Main Results: In group 1, eight of 42 patients (19%, 95% Cl, 9% to 34%) developed reversible renal insufficiency, defined as an unexpected increase in serum creatinine of 88 μmol/L or higher. Six episodes of reversible renal insufficiency occurred during July and August when temperatures were 32.2 °C to 37.8 °C (90 °F to 100 °F). Renal artery stenosis was excluded by renal arteriogram or ultrasonic duplex scanning. All eight group-1 patients had a significant decrease in mean arterial pressure below their baseline level during reversible renal insufficiency (mean change, - 28 ± 10 mm Hg, P < 0.001). The increase in the serum creatinine level was inversely correlated with the decrease in the mean arterial pressure (r= - 0.68, P < 0.01). Reversible renal insufficiency was successfully managed by withdrawing or reducing enalapril as well as other antihypertensive agents. Subsequently, enalapril was tolerated by seven of the eight patients without recurrence of renal insufficiency. In contrast, none of 31 (Cl, 0% to 11%) patients in group 2 developed reversible renal insufficiency despite the fact that both the incidence of decreases in mean arterial pressure in 6 of 31 patients (19%) and the magnitude of the decreases in mean arterial pressure (mean change, - 33 ± 16 mm Hg) were similar to those observed in group 1.

Conclusions: Reversible renal insufficiency in hypertensive nephrosclerosis associated with ACE inhibitor therapy correlates with relative hypotension, is not dependent on renal artery stenosis, and can usually be managed by dose reduction.

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