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CKD Progression and Mortality among Hispanics and Non-Hispanics

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posted on 30.01.2017, 00:00 by Michael J. Fischer, Jesse Y. Hsu, Claudia M. Lora, Ana C. Ricardo, Amanda H. Anderson, Lydia Bazzano, Magdalena M. Cuevas, Chi-yuan Hsu, John W. Kusek, Amada Renteria, Akinlolu O. Ojo, Dominic S. Raj, Sylvia E. Rosas, Qiang Pan, Kristine Yaffe, Alan S. Go, James P. Lash
Although recommended approaches to CKD management are achieved less often in Hispanics than in non-Hispanics, whether long-term outcomes differ between these groups is unclear. In a prospective longitudinal analysis of participants enrolled into the Chronic Renal Insufficiency Cohort (CRIC) and Hispanic-CRIC Studies, we used Cox proportional hazards models to determine the association between race/ethnicity, CKD progression (50% eGFR loss or incident ESRD), incident ESRD, and all-cause mortality, and linear mixed-effects models to assess differences in eGFR slope. Among 3785 participants, 13% were Hispanic, 43% were non-Hispanic white (NHW), and 44% were non-Hispanic black (NHB). Over a median follow-up of 5.1 years for Hispanics and 6.8 years for non-Hispanics, 27.6% of all participants had CKD progression, 21.3% reached incident ESRD, and 18.3% died. Hispanics had significantly higher rates of CKD progression, incident ESRD, and mean annual decline in eGFR than did NHW (P<0.05) but not NHB. Hispanics had a mortality rate similar to that of NHW but lower than that of NHB (P<0.05). In adjusted analyses, the risk of CKD progression did not differ between Hispanics and NHW or NHB. However, among nondiabetic participants, compared with NHB, Hispanics had a lower risk of CKD progression (hazard ratio, 0.61; 95% confidence interval, 0.39 to 0.95) and incident ESRD (hazard ratio, 0.50; 95% confidence interval, 0.30 to 0.84). At higher levels of urine protein, Hispanics had a significantly lower risk of mortality than did non-Hispanics (P<0.05). Thus, important differences in CKD progression and mortality exist between Hispanics and non-Hispanics and may be affected by proteinuria and diabetes.

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Funding

Funding for the Chronic Renal Insufficiency Cohort Study was obtained under a cooperative agreement from the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) (U01DK060990, U01DK060984, U01DK061022, U01DK061021, U01DK061028, U01DK060980, U01DK060963, and U01DK060902). In addition, this work was supported in part by: the Perelman School of Medicine at the University of Pennsylvania Clinical and Translational Science Award and the National Institutes of Health (NIH)/ National Center for Advancing Translational Sciences (NCATS) (UL1 TR-000003), Johns Hopkins University (UL1 TR-000424), University of Maryland General Clinical Research Center (M01 RR-16500), Clinical and Translational Science Collaborative of Cleveland, UL1 TR-000439 from the NCATS component of the NIH and NIH roadmap for Medical Research, Michigan Institute for Clinical and Health Research (UL1 TR-000433), University of Illinois at Chicago Clinical and Translational Science Award (UL1 RR-029879), Tulane University Translational Research in Hypertension and Renal Biology (P30GM103337), and Kaiser Permanente NIH/National Center for Research Resources, University of California-San Francisco Clinical & Translational Science Institute (UL1 RR-024131). Additional support was provided by the National Center for Minority Health and Health Disparities, the NIH, and Department of Veterans Affairs Health Services Research and Development Service (to M.J.F.). Support was provided from NIH/NIDDK K24-DK092290 (to J.P.L.), K23 DK091313 (to C.M.L.), K23 DK094829 (to A.C.R.).

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Publisher Statement

This is a copy of an article published in the Journal of the American Society of Nephrology Copyright © 2016 by the American Society of Nephrology

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American Society of Nephrology

issn

1046-6673

Issue date

25/03/2016

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