ACE-INHIBITORS AND THE KIDNEY - A RISK-BENEFIT ASSESSMENT

ACE inhibitors effectively reduce systemic vascular resistance in pati ents with hypertension, heart failure or chronic renal disease. This a ntihypertensive efficacy probably accounts for an important part of th eir long term renoprotective effects in patients with diabetic and non -diabetic renal disease. The renal mechanisms underlying the renal adv erse effects of ACE inhibitors - intrarenal efferent vasodilation with a consequent fall in filtration pressure - are held to be involved in their renoprotective effects as well. The fall in filtration pressure presumably contributes to the antiproteinuric effect as well as to lo ng term renoprotection. The former is suggested by the positive correl ation between the fall in filtration fraction and the reduction in pro teinuria found during ACE inhibition. The latter is suggested by the c orrelation between the (slight) reduction in glomerular filtration rat e at onset of therapy and a more favourable course of renal function i n the long term. Such a fall in filtration rate at the onset of ACE in hibitor treatment is reversible after withdrawal, and can be considere d the trade-off for long term renal protection in patients with diabet ic and nondiabetic chronic renal disease. In conditions in which glome rular filtration is critically dependent on angiotensin II-mediated ef ferent vascular tone (such as a post-stenotic kidney, or patients with heart failure and severe depletion of circulating volume), ACE inhibi tion can induce acute renal failure, which is reversible after withdra wal of the drug. Systemic and renal haemodynamic effects of ACE inhibi tion, both beneficial and adverse, are potentiated by sodium depletion . Consequently, sodium repletion contributes to the restoration of ren al function in patients with ACE inhibitor-induced acute renal failure . On the other hand, co-treatment with diuretics and sodium restrictio n can improve therapeutic efficacy in patients in whom the therapeutic response of blood pressure or proteinuria is insufficient. Patients a t the greatest risk for renal adverse effects (those with heart failur e, diabetes mellitus and/or chronic renal failure) also can expect the greatest benefit. Therefore, ACE inhibitors should not be withheld in these patients, but dosages should be carefully titrated, with monito ring of renal function and serum potassium levels.