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Published ahead of print on September 17, 2009
J Am Soc Nephrol 20: 2214-2222, 2009
© 2009 American Society of Nephrology
doi: 10.1681/ASN.2008090980

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CLINICAL EPIDEMIOLOGY

Method of Glomerular Filtration Rate Estimation Affects Prediction of Mortality Risk

Brad C. Astor*,{dagger},{ddagger}, Andrew S. Levey§, Lesley A. Stevens§, Frederick Van Lente||, Elizabeth Selvin*,{dagger} and Josef Coresh*,{dagger},{ddagger}

*Welch Center for Prevention, Epidemiology and Clinical Research, Departments of
{dagger}Epidemiology and
Biostatistics, Bloomberg School of Public Health, and
{ddagger}Department of Medicine, School of Medicine, Johns Hopkins University, Baltimore, Maryland;
§Division of Nephrology, Tufts Medical Center, Boston, Massachusetts; and
||Cleveland Clinic Lerner College of Medicine, Cleveland, Ohio

Correspondence: Dr. Brad C. Astor, Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, 2024 E. Monument Street, Suite 2-600, Baltimore, MD 21287. Phone: 410-502-2779; Fax: 410-955-0476; E-mail: bastor{at}jhsph.edu

Received for publication September 17, 2008. Accepted for publication June 3, 2009.

Decreased kidney function, determined using a serum creatinine–based estimation of GFR, is associated with a higher risk for mortality from cardiovascular disease. Equations incorporating cystatin C improve the estimation of GFR, but whether this improves the prediction of risk for mortality is unknown. We measured cystatin C on 6942 adult participants in the Third National Health and Nutrition Examination Survey Linked Mortality File, including all participants who had high serum creatinine (>1.2 mg/dl for men; >1.0 mg/dl for women) or were older than 60 yr and 25% random sample of participants who were younger than 60 yr. We estimated GFR using equations that included standardized serum creatinine, cystatin C, or both. Participant data were linked to the National Death Index. A total of 1573 (22.7%) deaths (713 deaths from cardiovascular disease) occurred during a median of 8 yr. Lower estimated GFR based on cystatin C was strongly associated with higher risk for overall and cardiovascular mortality across the range of normal to moderately decreased estimated GFR. Creatinine-based estimates of GFR resulted in weaker associations, with the association between estimated GFR and all-cause mortality reversed at higher levels of estimated GFR. An equation using both creatinine and cystatin C (in addition to age, race, and gender) resulted in weaker associations than equations using only cystatin C (with or without age, race, and gender). In conclusion, despite better performance in terms of estimating GFR, equations based on both cystatin C and creatinine do not predict mortality as well as equations based on cystatin C alone.


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