期刊
INTERNATIONAL JOURNAL OF NEPHROLOGY
卷 2012, 期 -, 页码 -出版社
HINDAWI LTD
DOI: 10.1155/2012/748984
关键词
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资金
- NIGMS/MBRS/SCORE Program [S06GM008016-320107, S06GM008016-380111]
- National Center for Research Resources, a component of the National Institutes of Health [2M01RR010284]
- Intramural Research Program of the National Human Genome Research Institute in the Center for Research in Genomics and Global Health [CRGGH-Z01HG200362]
- National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)
- Center for Information Technology
- Office of the Director at the National Institutes of Health
- National Institute on Minority Health and Health Disparities
- NIDDK
- NHGRI
Low levels of high-density cholesterol (HDLc) accompany chronic kidney disease, but the association between HDLc and the estimated glomerular filtration rate (eGFR) in the general population is unclear. We investigated the HDLc-eGFR association in nondiabetic Han Chinese (HC, n - 1100), West Africans (WA, n - 1497), and African Americans (AA, n - 1539). There were significant differences by ancestry: HDLc was positively associated with eGFR in HC (beta = 0.13, P < 0.0001), but negatively associated among African ancestry populations (WA: -0.19, P < 0.0001; AA: -0.09, P = 0.02). These differences were also seen in nationally-representative NHANES data (among European Americans: 0.09, P = 0.005; among African Americans -0.14, P = 0.03). To further explore the findings in African ancestry populations, we investigated the role of an African ancestryspecific nephropathy risk variant, rs73885319, in the gene encoding HDL-associated APOL1. Among AA, an inverse HDLc-eGFR association was observed only with the risk genotype (-0.38 versus 0.001; P = 0.03). This interaction was not seen in WA. In summary, counter to expectation, an inverse HDLc-eGFR association was observed among those of African ancestry. Given the APOL1 x HDLc interaction among AA, genetic factors may contribute to this paradoxical association. Notably, these findings suggest that the unexplained mechanism by which APOL1 affects kidney-disease risk may involve HDLc.
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