Chronic Laxative-Induced Hyperaldosteronism and Hypokalemia Simulating Bartter's Syndrome
- NORMAN FLEISCHER, M.D.;
- HAROLD BROWN, M.D., F.A.C.P.;
- DAVID Y. GRAHAM, M.D.; and
- SYLVIA DELEÑA, M.D.
- Requests for reprints should be addressed to Norman Fleischer, M.D., Department of Medicine, Baylor University College of Medicine, 1200 Moursund Ave., Houston, Tex. 77025
SUMMARY
A 47-year-old woman had a history of hypokalemia and laxative abuse throughout her adult life. She had markedly elevated renin and aldosterone secretion and juxtaglomerular hyperplasia on renal biopsy. The hyperaldosteronism played a major role in the genesis of her hypokalemia.
It is presumed that the juxtaglomerular hyperplasia and elevated renin and aldosterone secretion is the result of chronic diarrhea-induced sodium depletion. However, in acute studies she did not maximally retain dietary or infused sodium despite the capacity of her kidneys to retain sodium normally in response to dietary sodium depletion. Her vasculature was resistant to the pressor effects of angiotensin even after volume expansion. In addition, this patient was noted to develop hypercalcemia with dehydration and to have impaired glucose tolerance correctable with potassium supplementation.
Chronic diarrhea may simulate the clinical picture of Bartter's syndrome, and aldosterone antagonists may be therapeutically useful in hypokalemic states secondary to uncontrollable diarrhea.
Article and Author Information
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From the Department of Medicine, Baylor University College of Medicine; the Moody Clinical Research Unit, Methodist Hospital; and the Metabolic Research Laboratory, Veterans Administration Hospital; Houston, Tex.
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This study was supported in part by grants AM-05063, FR-00134, and HE-05435-P20, National Institutes of Health, Bethesda, Md.
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- Received October 16, 1968.
- Accepted November 20, 1968.
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