Glucose-induced hyperkalemia in diabetic subjects.
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.
D000328:Adult; D000450:Aldosterone / Q000097:blood*; D000616:Aminoglutethimide / Q000494:pharmacology; D003920:Diabetes Mellitus / Q000378:metabolism*; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D006947:Hyperkalemia / Q000139:chemically induced*; D008297:Male; D008875:Middle Aged; D011188:Potassium / Q000097:blood
D000616:Aminoglutethimide; D000450:Aldosterone; D005947:Glucose; D011188:Potassium