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Glucose-Induced Hyperkalemia During Captopril Treatment

Janos P. Rado, MD
Arch Intern Med. 1983;143(2):389. doi:10.1001/archinte.1983.00350020219048.
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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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