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Diabetes and the Kidney |
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* Research Division, Joslin Diabetes Center,
Department of Medicine, Harvard Medical School,
Massachusetts General Hospital Cancer Center, and ¶ School of Public Health, Boston University, Boston, Massachusetts;
Division of Endocrinology and Metabolism, University of Toronto, Toronto, Ontario, Canada; and || Division of Internal Medicine and Hypertension, Warsaw Medical University, Warsaw, Poland
Address correspondence to: Dr. Andrzej S. Krolewski, Section on Genetics & Epidemiology, Joslin Diabetes Center, One Joslin Place, Room 368, Boston, MA 02215. Phone: 617-732-2668; Fax: 617-732-2667; E-mail: andrzej.krolewski{at}joslin.harvard.edu
The aims of this study were to assess the frequency and determinants of (1) treatment with angiotensin-converting enzyme inhibitors (ACE-I) and (2) progression to proteinuria in the presence of ACE-I treatment in patients with type 1 diabetes and microalbuminuria. A clinic-based cohort study of patients with type 1 diabetes was begun in 1991. The patients who were included in this study (n = 373) are the cohort members who received a diagnosis of microalbuminuria during a 2-yr baseline observation and were followed for 10 yr with frequent assessments of urinary albumin excretion and biennial examinations. Progression to proteinuria occurred when the median urinary albumin excretion during a 2-yr interval exceeded 299 µg/min. During the decade-long study, the proportion of patients who had a history of microalbuminuria and were treated with ACE-I rose from 17 to 67%. Patients who started this treatment had (on average) higher BP, higher urinary albumin excretion, and longer diabetes duration than those who did not. Microalbuminuria often progressed to proteinuria (6.3/100 person-years) in those who were treated. Poor glycemic control and elevated serum cholesterol were the major determinants/predictors of this progression. Although treatment with ACE-I increased during the past decade, it was not completely effective, because microalbuminuria progressed to proteinuria in many treated patients. Poor glycemic control and elevated serum cholesterol were the major determinants/predictors for progression while on ACE-I treatment. The mechanisms that are responsible for the frequent failure of ACE-I to prevent progression of microalbuminuria to proteinuria in a clinical setting are not clear.
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Clin. J. Am. Soc. Nephrol. 2007 2: 407-409.
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