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Effect of captopril on renal function in patients with congestive heart failure
Insights
Captopril, an angiotensin converting enzyme inhibitor, did not improve sodium excretion in patients with congestive heart failure. Close kidney function monitoring is essential, especially with falling blood pressure.
Area of Science:
- Nephrology
- Cardiology
- Pharmacology
Background:
- Angiotensin converting enzyme (ACE) inhibitors are known to improve hemodynamics in congestive heart failure (CHF) and enhance sodium excretion in hypertension.
- The specific effects of ACE inhibitors on renal function in patients with advanced CHF remain an area of clinical interest.
Purpose of the Study:
- To assess the effects of captopril on renal function in patients with stable New York Heart Association (NYHA) functional class 3 or 4 congestive heart failure.
- To evaluate captopril's impact on natriuresis and renal hemodynamics in this patient population.
Main Methods:
- A single-blinded, placebo-controlled study was conducted on nine patients with NYHA class 3 or 4 CHF.
- Patients received placebo, followed by captopril (25-100 mg TID), and then placebo again, with assessments of renal function and hemodynamics.
Main Results:
- Captopril administration led to a decrease in mean blood pressure without significant changes in heart rate or respiration.
- Serum urea levels slightly increased, and while mean creatinine clearance was unchanged, three patients experienced a >25% decrease.
- Urine output, sodium, and potassium excretion decreased during captopril treatment, particularly in patients with high baseline plasma renin activity and lower blood pressure.
Conclusions:
- Captopril failed to demonstrate a beneficial effect on natriuresis in patients with congestive heart failure.
- Close monitoring of renal function is crucial when administering captopril to CHF patients, especially when accompanied by a significant drop in blood pressure.
Abstract:
Angiotensin converting enzyme inhibitors can improve haemodynamics in patients with congestive heart failure and may enhance sodium excretion in hypertensive patients. In a metabolic unit we assessed the effects of one of these agents on renal function in nine patients with stable New York Heart Association functional class 3 or 4 congestive heart failure. Single blinded, the patients received placebo for three days, 25 to 100 mg of captopril three times a day for three days, and three more days of placebo. Mean blood pressure decreased during captopril, with little change in heart rate or respiration. Serum urea was slightly higher during captopril administration. The mean change in creatinine clearance during captopril was insignificant, but it decreased more than 25% in three of nine patients. Decreases in creatinine clearance correlated with lower blood pressure during captopril and were most obvious in patients with high baseline plasma renin activity. Urine output and both sodium and potassium excretion decreased during captopril. Thus captopril failed to improve natriuresis in patients with congestive heart failure and close monitoring of kidney function is necessary when using this agent in patients with congestive heart failure, particularly when blood pressure falls to lower levels.