title: Sickle Cell Trait and the Risk of ESRD in Blacks.
abstract: Blacks, compared with whites, have an increased risk of progression to end-stage renal disease (ESRD). Emerging evidence suggests that, in addition toAPOL1high-risk genotypes, hemoglobin variants, including sickle cell trait (SCT) and hemoglobin C trait, have a role in kidney disease in blacks. However, the association between these hemoglobin traits and ESRD remains unknown. In a large population-based cohort, the REasons for Geographic and Racial Differences in Stroke (REGARDS) study, we evaluated 9909 self-reported blacks (739 with SCT and 243 with hemoglobin C trait). Incident ESRD occurred in 40 of 739 (5.4%) individuals with SCT, six of 243 (2.5%) individuals with hemoglobin C trait, and 234 of 8927 (2.6%) noncarriers. The incidence rate for ESRD was 8.5 per 1000 person-years for participants with SCT and 4.0 per 1000 person-years for noncarriers. Compared with individuals without SCT, individuals with SCT had a hazard ratio for ESRD of 2.03 (95% confidence interval, 1.44 to 2.84). Hemoglobin C trait did not associate with prevalent CKD or ESRD. The incidence rate for ESRD among participants withAPOL1high-risk genotypes was 6.6 per 1000 person-years, with a hazard ratio for ESRD of 1.77 (95% confidence interval, 1.31 to 2.38) for participants with, compared with those without,APOL1high-risk genotypes. In this cohort, SCT strongly associated with risk of progression to ESRD in blacks, and this degree of risk for ESRD was similar to that conferred byAPOL1high-risk genotypes. These results may have important public policy implications for genetic counseling of SCT carriers.
authors.affiliation: Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland; rakhi@jhmi.edu.
authors.forename: Rakhi P
authors.initials: RP
authors.lastname: Naik
authors.affiliation: Departments of Medicine and Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama.
authors.forename: Marguerite R
authors.initials: MR
authors.lastname: Irvin
authors.affiliation: Departments of Medicine and Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama.
authors.forename: Suzanne
authors.initials: S
authors.lastname: Judd
authors.affiliation: Departments of Medicine and Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama.
authors.forename: Orlando M
authors.initials: OM
authors.lastname: Gutiérrez
authors.affiliation: Departments of Medicine and.|Pathology and Laboratory Medicine, Larner College of Medicine at the University of Vermont, Burlington, Vermont.
authors.forename: Neil A
authors.initials: NA
authors.lastname: Zakai
authors.affiliation: Division of Nephrology and Hypertension, Department of Medicine, University of North Carolina Kidney Center, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina.
authors.forename: Vimal K
authors.initials: VK
authors.lastname: Derebail
authors.affiliation: Department of Medicine, San Francisco Veterans Affairs Medical Center, University of California San Francisco, San Francisco, California.
authors.forename: Carmen
authors.initials: C
authors.lastname: Peralta
authors.affiliation: Pathology and Laboratory Medicine, Larner College of Medicine at the University of Vermont, Burlington, Vermont.
authors.forename: Michael R
authors.initials: MR
authors.lastname: Lewis
authors.affiliation: Departments of Medicine and Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama.
authors.forename: Degui
authors.initials: D
authors.lastname: Zhi
authors.affiliation: College of Public Health, University of Kentucky, Lexington, Kentucky.
authors.forename: Donna
authors.initials: D
authors.lastname: Arnett
authors.affiliation: Department of Epidemiology, Emory University School of Public Health, Atlanta, Georgia.
authors.forename: William
authors.initials: W
authors.lastname: McClellan
authors.affiliation: Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi.
authors.forename: James G
authors.initials: JG
authors.lastname: Wilson
authors.affiliation: Department of Epidemiology, University of Washington School of Public Health, Seattle, Washington.
authors.forename: Alexander P
authors.initials: AP
authors.lastname: Reiner
authors.affiliation: Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland; and.
authors.forename: Jeffrey B
authors.initials: JB
authors.lastname: Kopp
authors.affiliation: Basic Research Laboratory, National Cancer Institute, Leidos Biomedical Research, Frederick National Laboratory, Frederick, Maryland.
authors.forename: Cheryl A
authors.initials: CA
authors.lastname: Winkler
authors.affiliation: Departments of Medicine and.|Pathology and Laboratory Medicine, Larner College of Medicine at the University of Vermont, Burlington, Vermont.
authors.forename: Mary
authors.initials: M
authors.lastname: Cushman
mesh_terms: D000075944:Apolipoprotein L1; D001053:Apolipoproteins / Q000235:genetics; D044383:Black People; D005260:Female; D006801:Humans; D015994:Incidence; D007676:Kidney Failure, Chronic / Q000453:epidemiology* / Q000209:etiology* / Q000235:genetics; D008075:Lipoproteins, HDL / Q000235:genetics; D008297:Male; D008875:Middle Aged; D051436:Renal Insufficiency, Chronic; D018570:Risk Assessment; D012805:Sickle Cell Trait / Q000150:complications* / Q000235:genetics
chemical_list: C108666:APOL1 protein, human; D000075944:Apolipoprotein L1; D001053:Apolipoproteins; D008075:Lipoproteins, HDL
keywords: end stage kidney disease; epidemiology and outcomes; genetic renal disease