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Diabetes Care 28:2525-2530, 2005
© 2005 by the American Diabetes Association, Inc.


Metabolic Syndrome/Insulin Resistance Syndrome/Pre-Diabetes
Original Article

Urinary Albumin Excretion and Its Relation With C-Reactive Protein and the Metabolic Syndrome in the Prediction of Type 2 Diabetes

Auke H. Brantsma, MD1, Stephan J.L. Bakker, MD, PHD2, Hans L. Hillege, MD, PHD3, Dick de Zeeuw, MD, PHD4, Paul E. de Jong, MD, PHD1, Ronald T. Gansevoort, MD, PHD1 the PREVEND Study Group

1 Division of Nephrology, Department of Medicine, University Medical Center Groningen, Groningen, the Netherlands
2 Department of Medicine, University Medical Center Groningen, Groningen, the Netherlands
3 Trial Coordination Center, Department of Cardiology, University Medical Center Groningen, Groningen, the Netherlands
4 Department of Clinical Pharmacology, University Medical Center Groningen, Groningen, the Netherlands

Address correspondencereprint requests to Ronald T. Gansevoort, MD, PhD, Division of Nephrology, Dept. of Medicine, University Medical Center Groningen, P.O. Box 30,001, 9700 RB, Groningen, Netherlands. E-mail: r.t.gansevoort{at}int.umcg.nl

OBJECTIVE—To investigate urinary albumin excretion (UAE) and its relation with C-reactive protein (CRP) and the metabolic syndrome in the prediction of the development of type 2 diabetes.

RESEARCH DESIGN AND METHODS—We used data from the Prevention of Renal and Vascular End Stage Disease (PREVEND) study, an ongoing, community-based, prospective cohort study initiated in 1997 in the Netherlands. The initial cohort consisted of 8,592 subjects. After 4 years, 6,894 subjects participated in a follow-up survey. Subjects with diabetes at baseline or missing data on fasting glucose were excluded, leaving 5,654 subjects for analysis. The development of type 2 diabetes, defined as a fasting glucose ≥7.0 mmol/l and/or the use of antidiabetic medication, was used as the outcome measure. UAE was calculated as the mean UAE from two consecutive 24-h urine collections. Logistic regression models were used, with the development of type 2 diabetes as the dependent variable.

RESULTS—Of the 5,654 subjects for whom data were analyzed, 185 (3.3%) developed type 2 diabetes during a mean follow-up period of 4.2 years. UAE, CRP, and the presence of the metabolic syndrome at baseline were significantly associated with the incidence of type 2 diabetes (P < 0.001 for all variables). In a univariate model, the odds ratio (OR) for UAE was 1.59 (95% CI 1.42–1.79). In our full model, adjusted for age, sex, number of criteria of metabolic syndrome, and other known risk factors for the development of type 2 diabetes (including fasting insulin), the association between UAE and type 2 diabetes remained significant (OR 1.53, 95% CI 1.25–1.88, P < 0.001). There was a significant interaction between UAE and CRP (P = 0.002). After CRP was stratified into tertiles, the ORs for the association between baseline UAE and the development of type 2 diabetes were 2.2 (1.47–3.3), 1.33 (0.96–1.84), and 1.04 (0.83–1.31) for the lowest to highest tertiles, respectively.

CONCLUSIONS—UAE predicts type 2 diabetes independent of the metabolic syndrome and other known risk markers of development of type 2 diabetes. The predictive value of UAE was modified by the level of CRP.

Abbreviations: AUC, area under the curve • CRP, C-reactive protein • PREVEND, Prevention of Renal and Vascular End Stage Disease • UAE, urinary albumin excretion


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