The kidney disease of diabetes mellitus (ie, diabetic nephropathy) is a clinical syndrome characterized by albuminuria, hypertension, and inexorably progressive renal insufficiency.1-3 The magnitude of this problem can be gauged by the realization that approximately 30% of new cases of end-stage renal disease in the United States are attributable to diabetic nephropathy, making it one of the two most common causes of renal failure in this country.4 The role of pharmacologic interventions to ameliorate or retard the progression of such diabetic nephropathy has not been established.
Over the past several years, angiotensin converting enzyme (ACE) inhibitors have been advocated as being advantageous in patients with diabetic nephropathy. The observations from Brenner's laboratory5-7 have provided a theoretic framework for therapeutic interventions with an ACE inhibitor in patients with diabetes mellitus. These theoretical observations, coupled with the relative paucity of side effects of these agents, have eventuated in an
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