{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,23]],"date-time":"2026-08-23T17:03:05Z","timestamp":1787504585712,"version":"build-2736575974"},"reference-count":24,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"3","funder":[{"DOI":"10.13039\/100001463","name":"American Society of Nephrology","doi-asserted-by":"publisher","award":["Ben J. Lipps Research Fellowship"],"award-info":[{"award-number":["Ben J. Lipps Research Fellowship"]}],"id":[{"id":"10.13039\/100001463","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":["CJASN"],"published-print":{"date-parts":[[2021,3]]},"abstract":"<jats:sec>\n                    <jats:title>Background and objectives<\/jats:title>\n                    <jats:p>Sickle cell trait and sickle cell disease are associated with faster GFR decline compared with normal hemoglobin phenotypes. We sought to compare the AKI risk in sickle cell trait\/disease to normal hemoglobin phenotypes and investigate the association between AKI and GFR decline in sickle cell trait\/disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Design, setting, participants, &amp; measurements<\/jats:title>\n                    <jats:p>This multicenter observational study used registry data (January 2005\u2013June 2018) of adult Black patients with sickle cell trait\/disease (exposures) and normal hemoglobin phenotype (reference) ascertained by hemoglobin electrophoresis. Outcomes of interest (incident AKI [1.5 times baseline serum creatinine or higher], incident severe AKI [doubling of baseline serum creatinine or higher], and incident sustained AKI [AKI persisting for \u226572 hours]) were adjudicated by chart review and evaluated by Cox regression. The association between AKI and GFR decline (linear mixed models) was also investigated.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified 8968 reference patients, 1279 patients with sickle cell trait, and 254 patients with sickle cell disease with a median follow-up of 7.6 years and mean baseline serum creatinine of 0.8 mg\/dl. We observed 796 AKI events, 452 sustained AKI events, and 466 severe AKI events. Compared with people with a normal hemoglobin phenotype, sickle cell trait was associated with higher risk for sustained AKI (adjusted hazard ratio, 1.64; 95% confidence interval, 1.27 to 2.11), but not AKI (adjusted hazard ratio, 1.11; 95% confidence interval, 0.91 to 1.36) or severe AKI (adjusted hazard ratio, 1.26; 95% confidence interval, 0.96 to 1.64). Sickle cell disease was associated with AKI (adjusted hazard ratio, 2.85; 95% confidence interval, 2.13 to 3.81), severe AKI (adjusted hazard ratio, 2.38; 95% confidence interval, 1.65 to 3.42), and sustained AKI (adjusted hazard ratio, 2.50; 95% confidence interval, 1.68 to 3.71). Post-AKI GFR decline was significantly faster in sickle cell trait (0.37 ml\/min per 1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      per year faster,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.01) and disease (1.69 ml\/min per 1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      per year faster,\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      &lt;0.01) compared with the reference.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Sickle cell trait and disease are associated with higher risk of AKI, which is associated with accelerated decline in eGFR.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.2215\/cjn.06960520","type":"journal-article","created":{"date-parts":[[2021,3,1]],"date-time":"2021-03-01T10:22:16Z","timestamp":1614594136000},"page":"348-355","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":24,"title":["Acute Kidney Injury among Black Patients with Sickle Cell Trait and Sickle Cell Disease"],"prefix":"10.2215","volume":"16","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1785-960X","authenticated-orcid":false,"given":"Kabir O.","family":"Olaniran","sequence":"first","affiliation":[{"name":"Division of Nephrology, Department of Internal Medicine, University of Texas Southwestern, Dallas, Texas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrew S.","family":"Allegretti","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophia H.","family":"Zhao","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sagar U.","family":"Nigwekar","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sahir","family":"Kalim","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2021,3,1]]},"reference":[{"key":"B1-20241015","doi-asserted-by":"crossref","first-page":"393","DOI":"10.1681\/ASN.2019050502","article-title":"Kidney function decline among Black patients with sickle cell trait and sickle cell disease: An observational cohort study","volume":"31","author":"Olaniran","year":"2020","journal-title":"J Am Soc Nephrol"},{"key":"B2-20241015","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":"B3-20241015","doi-asserted-by":"crossref","first-page":"532","DOI":"10.1111\/bjh.15820","article-title":"Sickle cell trait and renal disease among African American U.S. Army soldiers","volume":"185","author":"Hu","year":"2019","journal-title":"Br J Haematol"},{"key":"B4-20241015","doi-asserted-by":"crossref","first-page":"28","DOI":"10.3109\/03630269.2013.832689","article-title":"The risk of potential thromboembolic, renal and cardiac complications of sickle cell trait","volume":"38","author":"Bucknor","year":"2014","journal-title":"Hemoglobin"},{"key":"B5-20241015","doi-asserted-by":"crossref","first-page":"2018","DOI":"10.1016\/S0140-6736(10)61029-X","article-title":"Sickle-cell disease","volume":"376","author":"Rees","year":"2010","journal-title":"Lancet"},{"key":"B6-20241015","doi-asserted-by":"crossref","first-page":"1561","DOI":"10.1056\/NEJMra1510865","article-title":"Sickle cell disease","volume":"376","author":"Piel","year":"2017","journal-title":"N Engl J Med"},{"key":"B8-20241015","doi-asserted-by":"crossref","first-page":"363","DOI":"10.1097\/01.md.0000189089.45003.52","article-title":"Outcome of sickle cell anemia: A 4-decade observational study of 1056 patients","volume":"84","author":"Powars","year":"2005","journal-title":"Medicine (Baltimore)"},{"key":"B10-20241015","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. 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