Overt proteinuria is often accompanied by hypercholesterolemia and is associated with increased lipoprotein(a) levels. These lipid abnormalities are probably involved in the high incidence of macrovascular complications associated with diabetic nephropathy and possibly other kinds of non-diabetic proteinuric renal disease. Over the last decade many studies have shown that ACE inhibitors can reduce urinary protein excretion but little attention was paid to the impact of this form of therapeutic intervention on the lipid profile. In this article we review our recent data showing that fosinopril administration was associated with significant decreases in both urinary protein excretion, serum total cholesterol levels, and plasma lp(a) levels. The use of ACE inhibitors in patients with renal impairment can result in the development of hyperkalemia as a result of suppression of angiotensin II-driven aldosterone secretion by the adrenal gland. Inhibition of aldosterone secretion may depend on the degree of inhibition of angiotensin II formation in the circulation and also locally in the adrenal gland. Because the various ACE inhibitors exhibit different degrees of ACE inhibition at the tissue level, we have postulated that angiotensin II-dependent aldosterone production will be inhibited to a lesser degree by agents that have low tissue affinity for the adrenal gland. The implication of this theoretical concept for the development of hyperkalemia in patients with impaired renal function treated with ACE inhibitors is discussed.