TY - JOUR
T1 - Acute kidney injury among black patients with sickle cell trait and sickle cell disease
AU - Olaniran, Kabir O.
AU - Allegretti, Andrew S.
AU - Zhao, Sophia H.
AU - Nigwekar, Sagar U.
AU - Kalim, Sahir
N1 - Funding Information:
A. Allegretti reports consultancy agreements with Mallinckrodt Pharmaceuticals. S. Kalim reports being supported by National Institutes of Health award K23 DK 106479. S. Nigwekar reports having consultancy agreements with Allena Pharma, Becker Professional Education, Epizon Pharma, and Laboratoris Sanifit; reports receiving research funding from Allena Pharma and Hope Pharma; reports being supported by the American Heart Associa-tionCareerDevelopmentAward18CDA34110131;reportsreceiving honoraria from Guidpoint and Sanofi-Aventis; reports serving as a scientific advisor or member of Vifor Pharma; and reports being supported by the National Center for Research Program Winter 2015 Fellow-to-Faculty Transition Award 15FTF25980003 from the American Heart Association and by the KL2/Catalyst Medical Research Investigator Training award TR001100 (an appointed KL2
Funding Information:
award) from Harvard Catalyst, The Harvard Clinical and Translational Science Center (National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health). All remaining authors have nothing to disclose.
Funding Information:
K. Olaniran was supported by the American Society of Nephrology Ben J. Lipps Research Fellowship Award.
Publisher Copyright:
© 2021 by the American Society of Nephrology.
PY - 2021
Y1 - 2021
N2 - Background and objectives 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. Design, setting, participants, & measurements This multicenter observational study used registry data (January 2005–June 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 ≥72 hours]) were adjudicated by chart review and evaluated by Cox regression. The association between AKI and GFR decline (linear mixed models) was also investigated. Results 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 m2 per year faster, P<0.01) and disease (1.69 ml/min per 1.73 m2 per year faster, P<0.01) compared with the reference. Conclusions Sickle cell trait and disease are associated with higher risk of AKI, which is associated with accelerated decline in eGFR.
AB - Background and objectives 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. Design, setting, participants, & measurements This multicenter observational study used registry data (January 2005–June 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 ≥72 hours]) were adjudicated by chart review and evaluated by Cox regression. The association between AKI and GFR decline (linear mixed models) was also investigated. Results 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 m2 per year faster, P<0.01) and disease (1.69 ml/min per 1.73 m2 per year faster, P<0.01) compared with the reference. Conclusions Sickle cell trait and disease are associated with higher risk of AKI, which is associated with accelerated decline in eGFR.
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U2 - 10.2215/CJN.06960520
DO - 10.2215/CJN.06960520
M3 - Article
C2 - 33648973
AN - SCOPUS:85102721767
SN - 1555-9041
VL - 16
SP - 348
EP - 355
JO - Clinical Journal of the American Society of Nephrology
JF - Clinical Journal of the American Society of Nephrology
IS - 3
ER -