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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.
Ann Intern Med. 1969;70(4):791-798. doi:10.7326/0003-4819-70-4-791
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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.

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