Acute Kidney Injury among Black Patients with Sickle Cell Trait and Sickle Cell Disease.
AKI
Black race
eGFR decline
hazard ratio
incidence
sickle cell disease
sickle cell trait
Journal
Clinical journal of the American Society of Nephrology : CJASN
ISSN: 1555-905X
Titre abrégé: Clin J Am Soc Nephrol
Pays: United States
ID NLM: 101271570
Informations de publication
Date de publication:
08 03 2021
08 03 2021
Historique:
received:
07
05
2020
accepted:
08
01
2021
pubmed:
3
3
2021
medline:
4
1
2022
entrez:
2
3
2021
Statut:
ppublish
Résumé
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. 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. 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 Sickle cell trait and disease are associated with higher risk of AKI, which is associated with accelerated decline in eGFR.
Sections du résumé
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 m
CONCLUSIONS
Sickle cell trait and disease are associated with higher risk of AKI, which is associated with accelerated decline in eGFR.
Identifiants
pubmed: 33648973
pii: 01277230-202103000-00006
doi: 10.2215/CJN.06960520
pmc: PMC8011026
doi:
Types de publication
Journal Article
Multicenter Study
Observational Study
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
348-355Subventions
Organisme : NIDDK NIH HHS
ID : R01 DK124453
Pays : United States
Informations de copyright
Copyright © 2021 by the American Society of Nephrology.
Références
Olaniran KO, Allegretti AS, Zhao SH, Achebe MM, Eneanya ND, Thadhani RI, Nigwekar SU, Kalim S: Kidney function decline among Black patients with sickle cell trait and sickle cell disease: An observational cohort study. J Am Soc Nephrol 31: 393–404, 2020 31810990
Naik RP, Derebail VK, Grams ME, Franceschini N, Auer PL, Peloso GM, Young BA, Lettre G, Peralta CA, Katz R, Hyacinth HI, Quarells RC, Grove ML, Bick AG, Fontanillas P, Rich SS, Smith JD, Boerwinkle E, Rosamond WD, Ito K, Lanzkron S, Coresh J, Correa A, Sarto GE, Key NS, Jacobs DR, Kathiresan S, Bibbins-Domingo K, Kshirsagar AV, Wilson JG, Reiner AP: Association of sickle cell trait with chronic kidney disease and albuminuria in African Americans. JAMA 312: 2115–2125, 2014 25393378
Hu J, Nelson DA, Deuster PA, Marks ES, O’Connor FG, Kurina LM: Sickle cell trait and renal disease among African American U.S. Army soldiers. Br J Haematol 185: 532–540, 2019 30859563
Bucknor MD, Goo JS, Coppolino ML: The risk of potential thromboembolic, renal and cardiac complications of sickle cell trait. Hemoglobin 38: 28–32, 2014 24099594
Rees DC, Williams TN, Gladwin MT: Sickle-cell disease. Lancet 376: 2018–2031, 2010 21131035
Piel FB, Steinberg MH, Rees DC: Sickle cell disease. N Engl J Med 376: 1561–1573, 2017 28423290
Powars DR, Elliott-Mills DD, Chan L, Niland J, Hiti AL, Opas LM, Johnson C: Chronic renal failure in sickle cell disease: Risk factors, clinical course, and mortality. Ann Intern Med 115: 614–620, 1991
Powars DR, Chan LS, Hiti A, Ramicone E, Johnson C: Outcome of sickle cell anemia: A 4-decade observational study of 1056 patients. Medicine (Baltimore) 84: 363–376, 2005 16267411
Chawla LS, Kimmel PL: Acute kidney injury and chronic kidney disease: An integrated clinical syndrome. Kidney Int 82: 516–524, 2012
Statius van Eps LW, Pinedo-Veels C, de Vries GH, de Koning J: Nature of concentrating defect in sickle-cell nephropathy. Microradioangiographic studies. Lancet 1: 450–452, 1970 4189754
Nath KA, Katusic ZS: Vasculature and kidney complications in sickle cell disease. J Am Soc Nephrol 23: 781–784, 2012 22440903
Nalichowski R, Keogh D, Chueh HC, Murphy SN: Calculating the benefits of a research patient data repository. AMIA Annu Symp Proc 2006: 1044, 2006
Nigwekar SU, Solid CA, Ankers E, Malhotra R, Eggert W, Turchin A, Thadhani RI, Herzog CA: Quantifying a rare disease in administrative data: The example of calciphylaxis. J Gen Intern Med 29[Suppl 3]: S724–S731, 2014 25029979
Kellum JA, Lameire N; KDIGO AKI Guideline Work Group: Diagnosis, evaluation, and management of acute kidney injury: A KDIGO summary (Part 1). Crit Care 17: 204, 2013 23394211
Freda BJ, Knee AB, Braden GL, Visintainer PF, Thakar CV: Effect of transient and sustained acute kidney injury on readmissions in acute decompensated heart failure. Am J Cardiol 119: 1809–1814, 2017
Inker LA, Schmid CH, Tighiouart H, Eckfeldt JH, Feldman HI, Greene T, Kusek JW, Manzi J, Van Lente F, Zhang YL, Coresh J, Levey AS; CKD-EPI Investigators: Estimating glomerular filtration rate from serum creatinine and cystatin C [published correction appears in N Engl J Med 367: 681, 2012]. N Engl J Med 367: 20–29, 2012
Levey AS, Stevens LA, Schmid CH, Zhang Y, Castro AF, Feldman HI, Kusek JW, Eggers P, Lente FV, Greene T, Coresh J: A new equation to estimate glomerular filtration rate. Ann Intern Med 150: 604–612, 2009
Olaniran KO, Eneanya ND, Allegretti AS, Zhao SH, Achebe MM, Thadhani RI: Cardiovascular outcomes in African Americans with sickle cell trait and chronic kidney disease. Am J Nephrol 49: 93–102, 2019 30625463
Ronco C, Bellomo R, Kellum JA: Acute kidney injury. Lancet 394: 1949–1964, 2019
Levey AS, James MT: Acute kidney injury [published correction appears in Ann Intern Med 168: 84, 2018 10.7326/L17-0682]. Ann Intern Med 167: ITC66–ITC80, 2017
Laird NM, Ware JH: Random-effects models for longitudinal data. Biometrics 38: 963–974, 1982 7168798
Grams ME, Waikar SS, MacMahon B, Whelton S, Ballew SH, Coresh J: Performance and limitations of administrative data in the identification of AKI. Clin J Am Soc Nephrol 9: 682–689, 2014
Nath KA, Vercellotti GM: Renal functional decline in sickle cell disease and trait. J Am Soc Nephrol 31: 236–238, 2020 31980590
Nath KA, Hebbel RP: Sickle cell disease: Renal manifestations and mechanisms. Nat Rev Nephrol 11: 161–171, 2015 25668001
Nath KA, Katusic ZS, Gladwin MT: The perfusion paradox and vascular instability in sickle cell disease. Microcirculation 11: 179–193, 2004
Choi JS, Kim YA, Kim MJ, Kang YU, Kim CS, Bae EH, Ma SK, Ahn YK, Jeong MH, Kim SW: Relation between transient or persistent acute kidney injury and long-term mortality in patients with myocardial infarction. Am J Cardiol 112: 41–45, 2013 23558040
Hoste EAJ, Kellum JA: AKI severity class doesn’t tell all: The case for transient AKI. Nephrol Dial Transplant 25: 1738–1739, 2010 20233738
Diaw M, Pialoux V, Martin C, Samb A, Diop S, Faes C, Mury P, Sall Diop N, Diop SN, Ranque B, Mbaye MN, Key NS, Connes P: Sickle cell trait worsens oxidative stress, abnormal blood rheology, and vascular dysfunction in type 2 diabetes. Diabetes Care 38: 2120–2127, 2015 26324331
Tripette J, Connes P, Hedreville M, Etienne-Julan M, Marlin L, Hue O, Hardy-Dessources MD: Patterns of exercise-related inflammatory response in sickle cell trait carriers. Br J Sports Med 44: 232–237, 2010 18499764
Monchanin G, Serpero LD, Connes P, Tripette J, Wouassi D, Francina A, Massarelli R, Gozal D, Thiriet P, Martin C: Plasma levels of adhesion molecules ICAM-1 and VCAM-1 in athletes with sickle cell trait with or without alpha-thalassemia during endurance exercise and recovery. Clin Hemorheol Microcirc 40: 89–97, 2008 19029634
Griffin PJ, Sebastiani P, Edward H, Baldwin CT, Gladwin MT, Gordeuk VR, Chui DHK, Steinberg MH: The genetics of hemoglobin A2 regulation in sickle cell anemia. Am J Hematol 89: 1019–1023, 2014
Akinsheye I, Alsultan A, Solovieff N, Ngo D, Baldwin CT, Sebastiani P, Chui DHK, Steinberg MH: Fetal hemoglobin in sickle cell anemia. Blood 118: 19–27, 2011
Yeruva SLH, Paul Y, Oneal P, Nouraie M: Renal failure in sickle cell disease: Prevalence, predictors of disease, mortality and effect on length of hospital stay. Hemoglobin 40: 295–299, 2016
Shah N, Bhor M, Xie L, Halloway R, Arcona S, Paulose J, Yuce H: Treatment patterns and economic burden of sickle-cell disease patients prescribed hydroxyurea: A retrospective claims-based study. Health Qual Life Outcomes 17: 155, 2019
Rifkin DE, Coca SG, Kalantar-Zadeh K: Does AKI truly lead to CKD? J Am Soc Nephrol 23:979–984, 2012
Arlet J-B, Ribeil J-A, Chatellier G, Eladari D, De Seigneux S, Souberbielle J-C, Friedlander G, de Montalembert M, Pouchot J, Prié D, Courbebaisse M: Determination of the best method to estimate glomerular filtration rate from serum creatinine in adult patients with sickle cell disease: A prospective observational cohort study. BMC Nephrol 13: 83, 2012 22866669
Ware RE, Rees RC, Sarnaik SA, Iyer RV, Alvarez OA, Casella JF, Shulkin BL, Shalaby-Rana E, Strife CF, Miller JH, Lane PA, Wang WC, Miller ST; BABY HUG Investigators: Renal function in infants with sickle cell anemia: Baseline data from the BABY HUG trial. J Pediatr 156: 66–70.e1, 2010 19880138
Yee MEM, Lane PA, Archer DR, Joiner CH, Eckman JR, Guasch A: Estimation of glomerular filtration rate using serum cystatin C and creatinine in adults with sickle cell anemia. Am J Hematol 92: E598–E599, 2017 28670697