{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,21]],"date-time":"2026-10-21T11:34:49Z","timestamp":1792582489912,"version":"4.5.0"},"reference-count":27,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"7","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2017,7]]},"abstract":"\n Blacks, compared with whites, have an increased risk of progression to end-stage renal disease (ESRD). Emerging evidence suggests that, in addition to\n APOL1<\/jats:italic>\n high-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 with\n APOL1<\/jats:italic>\n high-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,\n APOL1<\/jats:italic>\n high-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 by\n APOL1<\/jats:italic>\n high-risk genotypes. These results may have important public policy implications for genetic counseling of SCT carriers.\n <\/jats:p>","DOI":"10.1681\/asn.2016101086","type":"journal-article","created":{"date-parts":[[2017,3,9]],"date-time":"2017-03-09T20:25:29Z","timestamp":1489091129000},"page":"2180-2187","source":"Crossref","is-referenced-by-count":90,"title":["Sickle Cell Trait and the Risk of ESRD in Blacks"],"prefix":"10.1681","volume":"28","author":[{"given":"Rakhi P.","family":"Naik","sequence":"first","affiliation":[{"name":"Division of Hematology, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marguerite R.","family":"Irvin","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Suzanne","family":"Judd","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Orlando M.","family":"Guti\u00e9rrez","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Neil A.","family":"Zakai","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"},{"name":"Pathology and Laboratory Medicine, Larner College of Medicine at the University of Vermont, Burlington, Vermont;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Vimal K.","family":"Derebail","sequence":"additional","affiliation":[{"name":"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;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Carmen","family":"Peralta","sequence":"additional","affiliation":[{"name":"Department of Medicine, San Francisco Veterans Affairs Medical Center, University of California San Francisco, San Francisco, California;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michael R.","family":"Lewis","sequence":"additional","affiliation":[{"name":"Pathology and Laboratory Medicine, Larner College of Medicine at the University of Vermont, Burlington, Vermont;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Degui","family":"Zhi","sequence":"additional","affiliation":[{"name":"Departments of Medicine and Epidemiology, University of Alabama at Birmingham, Birmingham, Alabama;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Donna","family":"Arnett","sequence":"additional","affiliation":[{"name":"College of Public Health, University of Kentucky, Lexington, Kentucky;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William","family":"McClellan","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, Emory University School of Public Health, Atlanta, Georgia;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"James G.","family":"Wilson","sequence":"additional","affiliation":[{"name":"Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, Mississippi;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alexander P.","family":"Reiner","sequence":"additional","affiliation":[{"name":"Department of Epidemiology, University of Washington School of Public Health, Seattle, Washington;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey B.","family":"Kopp","sequence":"additional","affiliation":[{"name":"Kidney Diseases Branch, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, Maryland; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cheryl A.","family":"Winkler","sequence":"additional","affiliation":[{"name":"Basic Research Laboratory, National Cancer Institute, Leidos Biomedical Research, Frederick National Laboratory, Frederick, Maryland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mary","family":"Cushman","sequence":"additional","affiliation":[{"name":"Departments of Medicine and"},{"name":"Pathology and Laboratory Medicine, Larner College of Medicine at the University of Vermont, Burlington, Vermont;"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2017,3,9]]},"reference":[{"key":"B2-20230829","doi-asserted-by":"crossref","first-page":"2902","DOI":"10.1097\/01.ASN.0000091586.46532.B4","article-title":"Racial differences in the progression from chronic renal insufficiency to end-stage renal disease in the United States.","volume":"14","author":"Hsu","year":"2003","journal-title":"J Am Soc Nephrol"},{"key":"B3-20230829","doi-asserted-by":"crossref","first-page":"1710","DOI":"10.1681\/ASN.2005111200","article-title":"Racial differences in the prevalence of chronic kidney disease among participants in the Reasons for Geographic and Racial Differences in Stroke (REGARDS) Cohort Study.","volume":"17","author":"McClellan","year":"2006","journal-title":"J Am Soc Nephrol"},{"key":"B4-20230829","doi-asserted-by":"crossref","first-page":"2363","DOI":"10.1097\/01.ASN.0000026493.18542.6A","article-title":"Excess risk of chronic kidney disease among African-American versus white subjects in the United States: A population-based study of potential explanatory factors.","volume":"13","author":"Tarver-Carr","year":"2002","journal-title":"J Am Soc Nephrol"},{"key":"B5-20230829","doi-asserted-by":"crossref","first-page":"2183","DOI":"10.1056\/NEJMoa1310345","article-title":"APOL1 risk variants, race, and progression of chronic kidney disease.","volume":"369","author":"Parsa","year":"2013","journal-title":"N Engl J Med"},{"key":"B6-20230829","doi-asserted-by":"crossref","first-page":"2115","DOI":"10.1001\/jama.2014.15063","article-title":"Association of sickle cell trait with chronic kidney disease and albuminuria in African Americans.","volume":"312","author":"Naik","year":"2014","journal-title":"JAMA"},{"key":"B7-20230829","doi-asserted-by":"crossref","first-page":"457","DOI":"10.1016\/S1473-3099(12)70055-5","article-title":"Haemoglobinopathies and the clinical epidemiology of malaria: A systematic review and meta-analysis.","volume":"12","author":"Taylor","year":"2012","journal-title":"Lancet Infect Dis"},{"issue":"3","key":"B8-20230829","doi-asserted-by":"crossref","first-page":"413","DOI":"10.1681\/ASN.2009070705","article-title":"High prevalence of sickle cell trait in African Americans with ESRD","volume":"21","author":"Derebail","journal-title":"J Am Soc Nephrol"},{"key":"B9-20230829","doi-asserted-by":"crossref","first-page":"1339","DOI":"10.1038\/ki.2011.286","article-title":"Sickle cell trait is not independently associated with susceptibility to end-stage renal disease in African Americans.","volume":"80","author":"Hicks","year":"2011","journal-title":"Kidney Int"},{"key":"B10-20230829","doi-asserted-by":"crossref","first-page":"1484","DOI":"10.1681\/ASN.2013010113","article-title":"APOL1 variants associate with increased risk of CKD among African Americans.","volume":"24","author":"Foster","year":"2013","journal-title":"J Am Soc Nephrol"},{"key":"B11-20230829","doi-asserted-by":"crossref","first-page":"134","DOI":"10.1053\/j.semperi.2009.12.006","article-title":"History and current status of newborn screening for hemoglobinopathies.","volume":"34","author":"Benson","year":"2010","journal-title":"Semin Perinatol"},{"key":"B12-20230829","doi-asserted-by":"crossref","first-page":"160","DOI":"10.1182\/asheducation-2015.1.160","article-title":"Sickle cell trait diagnosis: clinical and social implications.","volume":"2015","author":"Naik","year":"2015","journal-title":"Hematology (Am Soc Hematol Educ Program)"},{"key":"B13-20230829","doi-asserted-by":"crossref","first-page":"2842","DOI":"10.1681\/ASN.2015070763","article-title":"Race, APOL1 risk, and eGFR decline in the general population.","volume":"27","author":"Grams","year":"2016","journal-title":"J Am Soc Nephrol"},{"key":"B14-20230829","doi-asserted-by":"crossref","first-page":"910","DOI":"10.1056\/NEJM199204023261402","article-title":"Prevalence and pathologic features of sickle cell nephropathy and response to inhibition of angiotensin-converting enzyme.","volume":"326","author":"Falk","year":"1992","journal-title":"N Engl J Med"},{"key":"B15-20230829","doi-asserted-by":"crossref","first-page":"1847","DOI":"10.1681\/ASN.2014111126","article-title":"Six months of hydroxyurea reduces albuminuria in patients with sickle cell disease.","volume":"27","author":"Bartolucci","year":"2015","journal-title":"J Am Soc Nephrol"},{"key":"B16-20230829","doi-asserted-by":"crossref","first-page":"450","DOI":"10.1016\/S0140-6736(70)90836-6","article-title":"Nature of concentrating defect in sickle-cell nephropathy. Microradioangiographic studies.","volume":"1","author":"Statius van Eps","year":"1970","journal-title":"Lancet"},{"key":"B17-20230829","doi-asserted-by":"crossref","first-page":"781","DOI":"10.1681\/ASN.2011101019","article-title":"Vasculature and kidney complications in sickle cell disease.","volume":"23","author":"Nath","year":"2012","journal-title":"J Am Soc Nephrol"},{"key":"B18-20230829","doi-asserted-by":"crossref","first-page":"194","DOI":"10.1053\/snep.2003.50017","article-title":"Hyperfiltration and glomerulosclerosis.","volume":"23","author":"Hostetter","year":"2003","journal-title":"Semin Nephrol"},{"key":"B19-20230829","doi-asserted-by":"crossref","first-page":"386","DOI":"10.1111\/j.1365-2141.2011.08832.x","article-title":"MYH9 and APOL1 are both associated with sickle cell disease nephropathy.","volume":"155","author":"Ashley-Koch","year":"2011","journal-title":"Br J Haematol"},{"key":"B20-20230829","doi-asserted-by":"crossref","first-page":"114","DOI":"10.1038\/ki.2012.263","article-title":"Apolipoprotein L1 gene variants associate with hypertension-attributed nephropathy and the rate of kidney function decline in African Americans.","volume":"83","author":"Lipkowitz","year":"2013","journal-title":"Kidney Int"},{"key":"B21-20230829","doi-asserted-by":"crossref","first-page":"266","DOI":"10.1097\/MNH.0b013e3283600f8c","article-title":"Rethinking hypertensive kidney disease: Arterionephrosclerosis as a genetic, metabolic, and inflammatory disorder.","volume":"22","author":"Kopp","year":"2013","journal-title":"Curr Opin Nephrol Hypertens"},{"key":"B22-20230829","doi-asserted-by":"crossref","first-page":"1963","DOI":"10.1172\/JCI115521","article-title":"Effects of alpha-thalassemia and sickle polymerization tendency on the urine-concentrating defect of individuals with sickle cell trait.","volume":"88","author":"Gupta","year":"1991","journal-title":"J Clin Invest"},{"key":"B23-20230829","doi-asserted-by":"crossref","first-page":"171","DOI":"10.1016\/S0002-9343(96)00407-X","article-title":"Natural history of blood pressure in sickle cell disease: Risks for stroke and death associated with relative hypertension in sickle cell anemia.","volume":"102","author":"Pegelow","year":"1997","journal-title":"Am J Med"},{"key":"B24-20230829","doi-asserted-by":"crossref","first-page":"135","DOI":"10.1159\/000086678","article-title":"The reasons for geographic and racial differences in stroke study: Objectives and design.","volume":"25","author":"Howard","year":"2005","journal-title":"Neuroepidemiology"},{"key":"B25-20230829","doi-asserted-by":"crossref","first-page":"136","DOI":"10.3389\/fgene.2015.00136","article-title":"PCSK9 variation and association with blood pressure in African Americans: preliminary findings from the HyperGEN and REGARDS studies.","volume":"6","author":"Tran","year":"2015","journal-title":"Front Genet"},{"key":"B26-20230829","doi-asserted-by":"crossref","first-page":"904","DOI":"10.1038\/ng1847","article-title":"Principal components analysis corrects for stratification in genome-wide association studies.","volume":"38","author":"Price","year":"2006","journal-title":"Nat Genet"},{"key":"B27-20230829","doi-asserted-by":"crossref","first-page":"604","DOI":"10.7326\/0003-4819-150-9-200905050-00006","article-title":"A new equation to estimate glomerular filtration rate.","volume":"150","author":"Levey","year":"2009","journal-title":"Ann Intern Med"},{"key":"B28-20230829","doi-asserted-by":"crossref","first-page":"1545","DOI":"10.1001\/jama.2011.468","article-title":"Detection of chronic kidney disease with creatinine, cystatin C, and urine albumin-to-creatinine ratio and association with progression to end-stage renal disease and mortality.","volume":"305","author":"Peralta","year":"2011","journal-title":"JAMA"}],"container-title":["Journal of the American Society of Nephrology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/www.ovid.com\/00001751-201707000-00024","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2026,8,7]],"date-time":"2026-08-07T19:28:53Z","timestamp":1786130933000},"score":1,"resource":{"primary":{"URL":"https:\/\/www.ovid.com\/00001751-201707000-00024"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[2017,3,9]]},"references-count":27,"journal-issue":{"issue":"7","published-print":{"date-parts":[[2017]]}},"URL":"https:\/\/doi.org\/10.1681\/asn.2016101086","relation":{},"ISSN":["1046-6673","1533-3450"],"issn-type":[{"value":"1046-6673","type":"print"},{"value":"1533-3450","type":"electronic"}],"subject":[],"published":{"date-parts":[[2017,3,9]]}}}