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Asymmetric Dimethylarginine and Mortality in Stages 3 to 4 Chronic Kidney Disease

Jill Melendez Young^*, Norma Terrin, Xuelei Wang, Tom Greene, Gerald J. Beck, John W. Kusek^||, Allan J. Collins^¶, Mark J. Sarnak^*, and Vandana Menon^*

^* Department of Medicine, Division of Nephrology, and Institute for Clinical Research and Health Policy Studies, Tufts Medical Center, Boston, Massachusetts; Department of Biostatistics and Epidemiology, Cleveland Clinic Foundation, Cleveland, Ohio; Division of Clinical Epidemiology, University of Utah, Salt Lake City, Utah; ^|| National Institutes of Health, Bethesda, Maryland; and ^¶ Division of Nephrology, Hennepin County Medical Center, Minneapolis, Minnesota

Correspondence: Dr. Vandana Menon, Division of Nephrology, Department of Medicine, 750 Washington Street, #391, Boston, MA 02111. Phone: 617-636-8791; Fax: 617-636-8329; E-mail: vmenon{at}tufts-nemc.org

Background and objectives: Asymmetric dimethylarginine (ADMA), an endogenous inhibitor of nitric oxide synthase, reduces bioavailability of nitric oxide and induces endothelial dysfunction. This dimethylated amino acid accumulates in chronic kidney disease and may be involved in the pathophysiology of cardiovascular disease (CVD) in this population.

Design, settings, participants, & methods: The Modification of Diet in Renal Disease Study was a randomized, controlled trial conducted between 1989 and 1993. We measured ADMA in frozen samples collected at baseline (n = 820) and obtained survival status, up to December 31, 2000, from the National Death Index. We examined the relationship of ADMA with prevalent CVD and performed multivariable Cox models to examine the relationship of ADMA with all-cause and CVD mortality.

Results: Mean (SD) age was 52 (12) yr, GFR was 32 ± 12 ml/min per 1.73 m², and ADMA was 0.70 ± 0.25 µmol/L. A 1-SD increase in ADMA was associated with a 31% increased odds of prevalent CVD in an adjusted logistic regression model. During the 10-yr follow-up period, 202 (25%) participants died of any cause, 122 (15%) from CVD, and 545 (66%) reached kidney failure. In multivariable Cox models, a 1-SD increase in ADMA was associated with a 9% increased risk for all-cause and 19% increased risk for CVD mortality.

Conclusions: In this cohort of patients with predominantly nondiabetic, stages 3 to 4 chronic kidney disease, there was a strong association of ADMA with prevalent CVD and a modest association with all-cause and CVD mortality.

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