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Renal effects of ACE inhibitors in heart failure

Wilson S Colucci, MD
Section Editors
Richard H Sterns, MD
Stephen S Gottlieb, MD
Deputy Editor
John P Forman, MD, MSc


Angiotensin-converting enzyme (ACE) inhibitors are widely used in the treatment of heart failure. These agents decrease the formation of angiotensin II, thereby decreasing both arteriolar and venous resistance. This vasodilator effect causes immediate improvement in the symptoms of heart failure by decreasing left ventricular afterload, thereby increasing cardiac output and decreasing left and right heart filling pressures, which ameliorates pulmonary and systemic venous congestion. Due to their pleiotropic effects on various target organs including the heart, vasculature, and kidneys, ACE inhibitors slow the rate of progressive cardiac dysfunction and produce an approximately 25 percent reduction in cardiovascular mortality at one to three years [1-4]. In addition, the administration of an ACE inhibitor after an acute myocardial infarction can preserve cardiac function (as evidenced by an increased ejection fraction and slowed ventricular enlargement) and improve long-term survival [5]. (See "ACE inhibitors in heart failure with reduced ejection fraction: Therapeutic use" and "Angiotensin converting enzyme inhibitors and receptor blockers in acute myocardial infarction: Recommendations for use".)

An ACE inhibitor given with a loop diuretic may have the additional advantage of raising the plasma sodium concentration in patients with heart failure and hyponatremia [6]. This synergism may reflect factors that result in an increase in free water excretion. (See "Hyponatremia in patients with heart failure".)

In addition to a possible elevation in free water excretion, ACE inhibitors have other renal actions in heart failure, including changes in the glomerular filtration rate (GFR), reduced potassium excretion that can lead to hyperkalemia, and variable effects on the natriuretic response to diuretics.


In view of the improvement in cardiac output and in renal blood flow, it might be assumed that ACE inhibitors would also increase the glomerular filtration rate (GFR). However, this expected response occurs in only 10 to 25 percent of patients, while an increase in the plasma creatinine concentration is a more common finding [7-9]. As an example, the Cooperative North Scandinavian Enalapril Survival Study (CONSENSUS) trial of patients with severe heart failure noted a mean elevation in the plasma creatinine concentration of 0.1 to 0.2 mg/dL (10 to 20 micromol/L); furthermore, 11 percent of patients had more than a 100 percent rise in the plasma creatinine concentration [8]. This usually modest decline in GFR occurs within the first week; renal function then tends to be stable unless a complicating factor, such as worsening of cardiac function, is superimposed [8].

A reduction in GFR in heart failure is most likely to occur in those settings in which maintenance of the GFR is dependent upon high ambient angiotensin II levels [6-10]:

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Literature review current through: Nov 2017. | This topic last updated: Jul 11, 2017.
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