Effects of ACE inhibitors and calcium antagonists on progression of chronic renal disease

Abstract

The declining mortality due to coronary heart disease and stroke has been attributed in part to improved effectiveness and application of antihypertensive therapy and the successful identification and treatment of the population at risk. In striking contrast, end-stage renal disease (ESRD) attributed to hypertension has increased annually for the last decade and will probably worsen at least through the year 2000. Taken together, patients with diabetic nephropathy and patients with hypertensive renal disease account for the majority of new cases annually. The reasons for the striking dissociation between our success with coronary heart disease and stroke on the one hand and our inability to lessen the incidence of ESRD on the other remain to be clarified. Evidence reveals that all levels of untreated hypertension are associated with potentially declining renal function. Data from the Hypertension Detection and Follow-up Program and other studies suggest that antihypertensive treatment can prevent or retard development of progressive renal failure. Although the importance of blood pressure control is implicit, a theoretic framework based on data derived from experimental animal suggests that ACE-inhibitors and perhaps calcium antagonists may exert specific renoprotective effects beyond those achieved by blood pressure reduction per se. The results of recent long-term prospective studies are consistent with such a formulation. In view of the increasing importance of ACE-inhibitors and calcium antagonists in the antihypertensive armamentarium, additional prospective randomized studies are required to delineate further the effects of these agents on the progression of chronic renal insufficiency.