February 1983

Glucose-Induced Hyperkalemia During Captopril Treatment

Arch Intern Med. 1983;143(2):389. doi:10.1001/archinte.1983.00350020219048

To the Editor.  —Suppression of aldosterone production with slight increases in serum potassium levels have been reported during captopril treatment.1 However, clinically important hyperkalemia resulting from captopril administration is rare.2 I recently treated a patient in whom glucose-induced hyperkalemia (GIH) was observed during captopril therapy without consistent elevations of the baseline serum potassium levels.

Report of a Case.  —A 72-year-old man was admitted to the hospital because of hypertensive emergencies. His BP at the time of admission was 300/150 mm Hg. Within three hours of receiving hydralazine hydrochloride and furosemide therapy, the patient's BP was reduced to 175/80 mm Hg. Important laboratory study values included the following: serum urea nitrogen, 49 mg/dL; creatinine clearance, 15 mL/min; serum sodium, 141 mEq/L; serum potassium, 3.3 mEq/L; and serum chloride, 86 mEq/L. The patient was discharged on a daily regimen of 80 mg of furosemide, 1.2 mg of clonidine hydrochloride, and

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