THE CLINICAL USES of captopril and the other angiotensin converting enzyme (ACE) inhibitors have increased steadily since their introduction. Captopril has proven to be effective therapy for hypertension of all degrees of severity and in all subpopulations of patients.(1,2) ACE inhibition results in sustained improvement in congestive heart failure(3,4) and scleroderma-related renal crisis.(5) In addition, some believe that ACE inhibitors have a therapeutic advantage over other antihypertensive agents in the treatment of patients with progressive renal failure.(6) Clinical trials with captopril consistently document low side-effect profiles and excellent patient compliance.(1,2,7) Hyperkalemia is an anticipated adverse effect of captopril therapy because of the reproducible fall in aldosterone levels during ACE inhibition.(8,9) Potassium elevation in the normal range(7,10,11) and mild hyperkalemia(12-16) have been reported during ACE inhibition. In general, the rises in potassium in these cases were limited and easily reversible. There have been rare reports of life-threatening hyperkalemia associated with the use of ACE inhibitors, none requiring extracorporeal therapy.(17,18) We describe here a patient who required acute hemodialysis because of severe, life-threatening hyperkalemia associated with captopril.