Captopril-induced metabolic acidosis with hyperkalemia.
Hyperreninemic hypoaldosteronism was diagnosed in a 34-year-old woman with hypertension who was receiving captopril therapy. Renal biopsy revealed an advanced stage of IgA nephropathy, and her creatinine clearance was 40 ml/min. Elevation of serum potassium from 4.7 to 5.8 mEq/l and development of hyperchloremic metabolic acidosis with laboratory findings of pH 7.285, HCO3- 13.5 mEq/l, Na 141, and Cl 114 mEq/l were observed after captopril therapy. When captopril was withdrawn, elevated serum potassium levels and metabolic acidosis returned to normal. Challenge with captopril resulted in a decrease in plasma aldosterone levels, an increase in plasma renin activity, and development of hyperkalemic, hyperchloremic metabolic acidosis which is corrected with mineralocorticoid replacement. This case study demonstrates that captopril can cause hyperreninemic hypoaldosteronism with the laboratory finding of hyperkalemic, hyperchloremic metabolic acidosis.
Sakemi
T
T
Department of Internal Medicine, Saga Medical School, Japan.
Ohchi
N
N
Sanai
T
T
Rikitake
O
O
Maeda
T
T
D000138:Acidosis / Q000139:chemically induced*; D000328:Adult; D002216:Captopril / Q000009:adverse effects*; D002712:Chlorides / Q000097:blood; D005260:Female; D006801:Humans; D006947:Hyperkalemia / Q000139:chemically induced*; D006994:Hypoaldosteronism / Q000150:complications
D002712:Chlorides; D002216:Captopril