Renal functional alterations induced by angiotensin-converting enzyme inhibitors in heart failure.

OBJECTIVE

To review the effects of angiotensin-converting enzyme (ACE) inhibitors on renal pathophysiology and the compensatory mechanisms involved in heart failure. A clinical application of the use of these agents in the setting of concomitant heart failure and renal insufficiency also is presented.

DATA SOURCES

A MEDLINE search was conducted using the terms heart failure, congestive; renal insufficiency; and angiotensin-converting enzyme inhibitors.

STUDY SELECTION

All applicable animal and human trials were reviewed.

DATA SYNTHESIS

Advances in the management of heart failure have led to new insights into the complex pathophysiology of this condition, particularly the favorable clinical effects noted with the ACE inhibitors. The net effect of ACE inhibitors on the renin-angiotensin system in patients with heart failure is to augment renal blood flow to a greater extent than cardiac output. Glomerular filtration rate is either unchanged or decreased by ACE inhibition. Sodium excretion is augmented primarily by alterations in glomerular hemodynamic parameters. ACE inhibitors may alter renal tubular function, both directly and indirectly, leading to increased diuresis and natriuresis.

CONCLUSIONS

Although ACE inhibitors exert beneficial pharmacodynamic effects on the renal bed in patients with heart failure, clinical consideration of volume and neurohormonal status prior to institution of therapy is prudent.