Angiotensin-converting enzyme inhibitors and renal function in heart failure

Abstract Patients with severe heart failure often exhibit signs of an impaired renal function. As judged from serum urea and creatinine concentrations, renal function may deteriorate further after the addition of angiotensin-converting enzyme (ACE) inhibitors to therapy. The beneficial effect of unloading the failing heart by reducing the systemic outflow resistance is opposed by a potentially harmful effect of unloading the kidney by preferentially reducing the outflow resistance of the glomerulus. However, development of functional renal insufficiency is unlikely and is a rare cause for withdrawing ACE inhibitors when certain precautions are considered: (1) The initial dose of the ACE inhibitor has to be reduced with increasing severity of heart failure (the titration period thereafter should be monitored carefully); (2) an increase in serum creatinine not exceeding 30% of the basal value may be taken as evidence for a beneficial action of the drug, which in addition to altering cardiac function alters kidney function (when the increase in serum creatinine is considered to be of clinical significance, it seems wise to reduce the dose of diuretics first—thereby neuroendocrine stimulation can be attenuated and the dependency of renal filtration from angiotensin II-induced efferent vasoconstriction can be reduced); and (3) the coadministration of inhibitors of prostaglandin synthesis (e.g., acetylsalicylic acid) appears to be associated with a higher risk of impairing renal function: the decrease in glomerular filtration rate is more marked and the compensatory increase in renal plasma flow following ACE inhibition is no longer observed.