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The Effect of Angiotensin-Converting Enzyme Inhibitors on the Progression of Nondiabetic Renal Disease: A Pooled Analysis of Individual-Patient Data from 11 Randomized, Controlled Trials

Robert W. Schrier, MD; and Raymond O. Estacio, MD
[+] Article and Author Information

Dr. Schrier: University of Colorado Health Sciences Center, Denver, CO 80262 Dr. Estacio: Denver Health, Denver, CO 80204


Requests for Single Reprints: Robert W. Schrier, MD, University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Room 6403, Denver, CO 80262; e-mail, Robert.Schrier@uchsc.edu.

Current Author Addresses: Dr. Schrier: University of Colorado Health Sciences Center, 4200 East Ninth Avenue, Room 6403, Denver, CO 80206.

Dr. Estacio: Denver Health c/o Westside Health Center, 1100 Federal Building, Denver, CO 80204.


Ann Intern Med. 2001;135(2):138-139. doi:10.7326/0003-4819-135-2-200107170-00015
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An increase in the incidence of end-stage renal disease (ESRD) in most developed countries around the world has been due in part to the increasing incidence of diabetes mellitus worldwide. However, it is clear that at least 50% of the new cases of ESRD are not secondary to diabetes. While the success of renal replacement in patients with ESRD, using either a variety of dialytic approaches or kidney transplantation, is clearly one of the major advances in modern medicine, the ultimate goal must be to prevent the progression to ESRD. In recent years, results from randomized clinical trials have demonstrated how that goal might be achieved. The use of the angiotensin-converting enzyme (ACE) inhibitor captopril in patients with type 1 diabetes mellitus and nephropathy clearly slows the progression to ESRD (1). Similarly, tight blood glucose control in patients with type 1 diabetes has been shown to slow the increase of albuminuria, an important surrogate measure of progressing renal disease (2). Emerging results from clinical trials in patients with type 2 diabetes have emphasized the importance of tight blood glucose (3) and blood pressure control, as well as a potential protective role of ACE inhibitors (45).

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