Captopril-induced metabolic acidosis with hyperkalemia

Area of Science:

• Nephrology
• Endocrinology

Background:

• Hypertension management often involves angiotensin-converting enzyme inhibitors like captopril.
• IgA nephropathy is a common cause of chronic kidney disease.

Observation:

• A patient with IgA nephropathy developed hyperreninemic hypoaldosteronism while on captopril.
• Captopril withdrawal normalized potassium and corrected metabolic acidosis.
• Rechallenge with captopril precipitated similar electrolyte abnormalities.

Findings:

• Captopril induced hyperkalemic, hyperchloremic metabolic acidosis.
• This was associated with suppressed aldosterone and elevated renin activity.
• Mineralocorticoid replacement corrected the induced acidosis and hyperkalemia.

Implications:

• Captopril can unmask or cause hyperreninemic hypoaldosteronism in susceptible individuals, particularly those with kidney disease.
• Monitoring electrolytes, especially potassium, is crucial during captopril therapy.
• This case highlights the importance of considering iatrogenic causes of electrolyte disturbances.