Angiotensin-converting enzyme inhibitors and renal function.

The effects of angiotensin-converting enzyme (ACE) inhibitors on renal hemodynamics vary widely depending on the preexisting physiologic and pathologic state of the kidneys. Although some studies of ACE inhibitors in primary essential hypertension have demonstrated increases in glomerular filtration rate (GFR) and effective renal plasma flow in patients with renal impairment, other studies have not shown these same beneficial results. The difference may involve the choice of ACE inhibitor used in the investigations, but controlled comparison trials are needed to determine whether this is the case. The use of ACE inhibitors in renovascular hypertension remains controversial. ACE inhibition can interfere with the autoregulation of GFR mediated by angiotensin II and may lead to deterioration of renal function, especially in patients with bilateral renal artery stenosis or stenosis of a solitary kidney. Additionally, ACE inhibitors have been shown to cause a decline in GFR in the kidney affected by the stenosis, whether or not clinically apparent renal insufficiency occurs. Although the functional impairment associated with ACE inhibitors in renal artery stenosis has generally been reversible following removal of the drug, the consequences of a long-term reduction in GFR are unknown. Treatment of stable congestive heart failure (CHF) with ACE inhibitors can result in enhancement of GFR and reduction of sodium and fluid retention, thus improving the clinical state. However, in patients with decompensated cardiac failure, renal perfusion pressures may already be at or near the autoregulatory breakpoint and ACE inhibition may cause deterioration of renal function. In general, ACE inhibitors can be used safely in CHF if they are initiated cautiously, with adjustment of ACE inhibitor and diuretic dosages to avoid systemic hypotension and sodium and fluid depletion. In studies comparing the agents, enalapril and lisinopril have both been shown to cause higher incidences of renal function deterioration than has captopril. These findings suggest that the more complete or sustained ACE inhibition seen with the longer-acting agents may be detrimental to renal function in patients with CHF. The use of ACE inhibitors in the treatment of proteinuria is the newest area of research with these agents. At present it appears that ACE inhibitors reduce urinary protein excretion the most effectively in diabetic patients with mild proteinuria and in hypertensive patients with renal insufficiency and proteinuria due to glomerular disorders. More study is needed to determine whether these agents can reduce the rate of renal failure progression and to define the patient populations expected to benefit most.(ABSTRACT TRUNCATED AT 400 WORDS)