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Selective Hypoaldosteronism with Hyperkalemia

GUIDO PEREZ, M.D.; LARRY SIEGEL, M.D.; and GEORGE E. SCHREINER, M.D., F.A.C.P.
[+] Article and Author Information

Supported in part by Clinical Study Unit Grant FR-60, the John A. Hartford Foundation, Inc., New York, N.Y., and the Georgetown University Kidney Foundation, Washington, D. C. Dr. Perez was supported by training grant 2T1 HE5256, U.S. Public Health Service, Washington, D.C.

▸Requests for reprints should be addressed to Larry Siegel, M.D., Georgetown University Nephrology Section, D.C. General Hospital, Box 303, Washington, D.C. 20003.


Washington, D.C.


Ann Intern Med. 1972;76(5):757-763. doi:10.7326/0003-4819-76-5-757
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A 59-year-old diabetic woman with moderate renal insufficiency had unexplained hyperkalemia, aggravated by sodium restriction and corrected with desoxycorticosterone acetate (Doca®) administration. Urinary aldosterone excretion was low and failed to increase despite several stimuli to its release; glucocorticoid excretion and response to adrenocorticotropic hormone stimulation were normal. Plasma renin activity in this patient was undetectable even after volume depletion and weight loss. We conclude that selective hypoaldosteronism in this case, unlike other reported cases, was caused by inadequate adrenal stimulation from the renin angiotensin system.

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