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Angiotensin-Receptor Blockers in the Prevention or Treatment of Microalbuminuria

Patrick S. Parfrey, MD
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From Health Sciences Centre, Memorial University, St. John's, Newfoundland A1B 3V6, Canada.

Potential Financial Conflicts of Interest:Consultancies: Amgen, Ortho Biotech, Roche. Grants received: Amgen, Ortho Biotech, Merck & Co. Other: Dr. Parfrey has served with Dr. H.H. Parving, a DIRECT Steering Committee member, on the executive committee of a randomized, controlled trial funded by Amgen.

Requests for Single Reprints: Patrick S. Parfrey, MD, Health Sciences Centre, Memorial University, St. John's, Newfoundland A1B 3V6, Canada; e-mail, pparfrey@mun.ca.

Ann Intern Med. 2009;151(1):63-65. doi:10.7326/0003-4819-151-1-200907070-00011
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Type 1 and type 2 diabetes mellitus are the most frequent causes of end-stage renal disease in the United States (1). The natural history of diabetic nephropathy starts with microalbuminuria, which may progress to macroalbuminuria, gradual deterioration in glomerular filtration rate (GFR), and eventually end-stage kidney disease. Microalbuminuria in diabetes strongly predicts end-stage renal disease and adverse cardiovascular events (24). Although inhibitors of the renin–angiotensin system (RAS) have become the mainstays of treating established diabetic nephropathy (5), the role of these agents in the early phases of diabetic nephropathy is unclear. Kidney damage may occur in diabetics who do not have albuminuria. We do not know whether patients with a high burden of vascular disease but no albuminuria are less likely to develop renal disease if they take RAS-blocking agents. Two articles in this issue examine the effect of angiotensin-receptor blockers (ARBs) on microalbuminuria in 2 different patient groups: diabetics at an early phase of nephropathy (6) and adults with known cardiovascular disease or diabetes with end-organ damage but no albuminuria at baseline (7).

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