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Epidemiology and Outcomes |
,







,
* Department of Medicine,
Division of Nephrology,
Department of Epidemiology and Biostatistics, ** Department of Biopharmaceutical Sciences, and 
Center for Human Genetics, Department Dermatology, and Cardiovascular Research Institute, University of California at San Francisco, 
Lung Biology Center, San Francisco General Hospital, and
General Internal Medicine Section, San Francisco Veterans Affairs Medical Center, San Francisco, California; || Collaborative Health Studies Coordinating Center, Department of Biostatistics, ¶ Departments of Epidemiology and Laboratory Medicine, and |||| Departments of Medicine, Epidemiology, and Health Services, Cardiovascular Health Research Unit, University of Washington, Seattle, Washington; and 
Renal Section, VA Pittsburgh Healthcare System, and Renal-Electrolyte Division, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania
Address correspondence to: Dr. Michael G. Shlipak, General Internal Medicine Section 111A1, VA Medical Center, 4150 Clement Street, San Francisco, CA 94124. Phone: 415-221-4810, ext. 3381; Fax: 415-379-5573; E-mail: shlip{at}itsa.ucsf.edu
Received for publication May 18, 2006. Accepted for publication September 7, 2006.
Kidney disease is a major public health problem in the United States that affects African Americans disproportionately. The relative contribution of environmental and genetic factors to the increased burden of kidney disease among African Americans is unknown. The associations of genetic African ancestry and socioeconomic status with kidney function were studied cross-sectionally and longitudinally among 736 community-dwelling African Americans who were aged >65 yr and participating in the Cardiovascular Health Study. Genetic African ancestry was determined by genotyping 24 biallelic ancestry-informative markers and combining this information statistically to generate an estimate of ancestry for each individual. Kidney function was evaluated by cystatin C and estimated GFR (eGFR) using the Modification of Diet in Renal Disease equation. Longitudinal changes in serum creatinine and eGFR were estimated using baseline and follow-up values. In cross-sectional analyses, there was no association between genetic African ancestry and either measure of kidney function (P = 0.36 for cystatin C and 0.68 for eGFR). African ancestry was not associated with change in serum creatinine
0.05 mg/dl per yr (odds ratio [OR] 0.94; 95% confidence interval [CI] 0.83 to 1.06) or with change in eGFR
3 ml/min per 1.73 m2 per yr (OR 1.02; 95% CI 0.92 to 1.13). In contrast, self reported African-American race was strongly associated with increased risk for kidney disease progression compared with white individuals for change in creatinine (OR 1.77; 95% CI 1.33 to 2.36) and for change in eGFR (OR 3.21; 95% CI 2.54 to 4.06). Among self-identified African Americans, low income (<$8000/yr) was strongly associated with prevalent kidney dysfunction by cystatin C >1.29 g/dl (adjusted OR 2.7; 95% CI 1.0 to 7.5) or by eGFR <60 ml/min per 1.73 m2 (adjusted OR 3.2; 95% CI 1.1 to 9.4) compared with those with incomes >$35,000/yr. Alleles that are known to be present more frequently in the African ancestral group were not associated with kidney dysfunction or kidney disease progression. Rather, kidney dysfunction in elderly African Americans seems more attributable to differences in environmental and social factors.
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