Sakemi T, Ohchi N, Sanai T, Rikitake O, Maeda T
Department of Internal Medicine, Saga Medical School, Japan.
Am J Nephrol. 1988;8(3):245-8. doi: 10.1159/000167591.
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 When captopril was withdrawn, elevated serum potassium levels and metabolic acidosis returned to normal.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.
一名接受卡托普利治疗的34岁高血压女性被诊断为高肾素性低醛固酮血症。肾活检显示为IgA肾病晚期，其肌酐清除率为40 ml/分钟。卡托普利治疗后，血清钾从4.7 mEq/升升至5.8 mEq/升，并出现高氯性代谢性酸中毒，实验室检查结果为pH 7.285、HCO3- 13.5 mEq/升、Na 141和Cl 114 mEq/升。停用卡托普利后，血清钾水平升高和代谢性酸中毒恢复正常。再次使用卡托普利导致血浆醛固酮水平降低、血浆肾素活性增加，并出现高钾性、高氯性代谢性酸中毒，补充盐皮质激素后可纠正。该病例研究表明，卡托普利可导致高肾素性低醛固酮血症，并伴有高钾性、高氯性代谢性酸中毒的实验室检查结果。
