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Acute Hyperkalemia Induced by Hyperglycemia: Hormonal Mechanisms

[+] Article, Author, and Disclosure Information

Grant support: By U.S. Public Health Service Training Grant #AM 05634-05; Veterans Administration Renal Training Program #204; U.S. Public Health Service Research Grants AMHL 17344-04 and HL 00340-25; U.S. Public Health Service CRC Grant #RR 00040; and the Philadelphia Veterans Administration Hospital (103.14M).

A preliminary report of this paper was presented before the Annual Meeting of the American College of Physicians, San Francisco, California, April 1975.

▸Requests for reprints should be addressed to Stanley Goldfarb, M.D., Hospital of the University of Pennsylvania, 860 Gates Pavilion, Philadelphia, PA 19104.

Philadelphia, Pennsylvania

Ann Intern Med. 1976;84(4):426-432. doi:10.7326/0003-4819-84-4-426
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Two insulin-requiring diabetics with isolated hyporeninemic hypoaldosteronism spontaneously developed hyperkalemia that was aggravated whenever blood glucose concentration rose. Acute glucose infusions raised the serum potassium concentration in these patients with combined insulin and aldosterone deficiency but lowered, or did not change, the serum potassium concentration in normal subjects and in patients with either aldosterone or insulin deficiency alone. The paradoxical hyperkalemic response to glucose in patients with combined hormonal deficiency was blunted by prior administration of desoxycorticosterone acetate and abolished by prior administration of insulin. Our studies emphasize the crucial roles played by insulin and aldosterone in regulating the serum potassium concentration in man, and the need to avoid hyperglycemia in patients with combined insulin and aldosterone deficiency.





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