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In a cohort of black patients having sickle cell trait and sickle cell disease was associated with a significantly faster annual eGFR decline, and eGFR declined significantly faster in patients with sickle cell disease than in those with sickle cell trait. Male sex, diabetes mellitus, and high baseline GFRs were associated with faster eGFR decline in both phenotypes. In sickle cell trait, high hemoglobin S and elevated hemoglobins F and A\n                      <jats:sub>2<\/jats:sub>\n                      were associated with a slower eGFR decline. Physicians caring for black patients need to consider sickle cell trait and sickle cell disease status and interactions with comorbidities when evaluating CKD risk.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Sickle cell trait and sickle cell disease are thought to be independent risk factors for CKD, but the trajectory and predictors of kidney function decline in patients with these phenotypes are not well understood.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Our multicenter, observational study used registry data (collected January 2005 through June 2018) and included adult black patients with sickle cell trait or disease (exposures) or normal hemoglobin phenotype (reference) status (ascertained by electrophoresis) and at least 1 year of follow-up and three eGFR values. We used linear mixed models to evaluate the difference in the mean change in eGFR per year.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We identified 1251 patients with sickle cell trait, 230 with sickle cell disease, and 8729 reference patients, with a median follow-up of 8 years. After adjustment, eGFR declined significantly faster in patients with sickle cell trait or sickle cell disease compared with reference patients; it also declined significantly faster in patients with sickle cell disease than in patients with sickle cell trait. Male sex, diabetes mellitus, and baseline eGFR \u226590 ml\/min per 1.73 m\n                      <jats:sup>2<\/jats:sup>\n                      were associated with faster eGFR decline for both phenotypes. In sickle cell trait, low hemoglobin S and elevated hemoglobin A were associated with faster eGFR decline, but elevated hemoglobins F and A\n                      <jats:sub>2<\/jats:sub>\n                      were renoprotective.\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 faster eGFR decline in black patients, with faster decline in sickle cell disease. Low hemoglobin S was associated with faster eGFR decline in sickle cell trait but may be confounded by concurrent hemoglobinopathies. Prospective and mechanistic studies are needed to develop best practices to attenuate eGFR decline in such patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2019050502","type":"journal-article","created":{"date-parts":[[2019,12,6]],"date-time":"2019-12-06T16:15:17Z","timestamp":1575648917000},"page":"393-404","source":"Crossref","is-referenced-by-count":55,"title":["Kidney Function Decline among Black Patients with Sickle Cell Trait and Sickle Cell Disease: An Observational Cohort Study"],"prefix":"10.1681","volume":"31","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 Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;"},{"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":"Maureen M.","family":"Achebe","sequence":"additional","affiliation":[{"name":"Hematology Division, Brigham and Women\u2019s Hospital, Harvard Medical School, Boston, Massachusetts;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Nwamaka D.","family":"Eneanya","sequence":"additional","affiliation":[{"name":"Renal-Electrolyte and Hypertension Division, Perelman School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania; and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ravi I.","family":"Thadhani","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, Massachusetts;"},{"name":"Department of Biomedical Sciences, Cedars-Sinai Medical Center, Los Angeles, California"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6750-0072","authenticated-orcid":false,"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 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