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Glucose-Induced Hyperkalemia in Diabetic Subjects
Giorgio L. Nicolis, MD, PhD;
Thomas Kahn, MD;
Ariel Sanchez, MD;
J. Lester Gabrilove, MD
Arch Intern Med. 1981;141(1):49-53.
Abstract
• Four insulin-deprived patients with diabetes mellitus and normal baseline potassium and aldosterone levels became hyperkalemic when given 100 g of glucose orally. The increases in plasma potassium concentrations averaged 1.3 mEq/L (range, 0.7 to 1.8 mEq/L) and were accompanied by increases in plasma aldosterone level. Four other insulin-deprived diabetics had normal plasma potassium and aldosterone responses when given 50 mEq of potassium chloride orally. These findings suggest that glucose-induced hyperkalemia is not infrequent in diabetics and that it is not usually associated with hypoaldosteronism. The acute suppression of aldosterone biosynthesis with aminoglutethimide did not lead to increased plasma potassium levels following oral potassium loads. This suggests that the acute responses of aldosterone to potassium loads may not be important in preventing postprandial hyperkalemia.
(Arch Intern Med 141:49-53, 1981)
Author Affiliations
From the Departments of Medicine, Veterans Administration Hospital, Bronx, NY (Drs Nicolis, Kahn, and Sanchez), and Mount Sinai Hospital and School of Medicine, City University of New York, New York (Drs Nicolis, Kahn, Sanchez, and Gabrilove).
Footnotes
Accepted for publication Feb 15, 1980.
Read in part before the 61st annual meeting of the Endocrine Society, Anaheim, Calif, June 14, 1979.
Reprint requests to Endocrinology and Metabolism Section, Veterans Administration Medical Center, 130 W Kingsbridge Rd, Bronx, NY 10468 (Dr Nicolis).
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