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Abstract: FR-OR056

Sickle Cell Trait (SCT) and CKD Progression Among African Americans in the Chronic Renal Insufficiency Cohort (CRIC) Study

Session Information

Category: CKD (Non-Dialysis)

  • 2101 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention


  • Derebail, Vimal K., University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States
  • Hsu, Jesse Yenchih, University of Pennsylvania, Philadelphia, Pennsylvania, United States
  • Kshirsagar, Abhijit V., University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States
  • Key, Nigel S., University of North Carolina at Chapel Hill, Chapel Hill, North Carolina, United States
  • Navaneethan, Sankar D., Baylor College of Medicine, Sugar Land, Texas, United States
  • Hsu, Chi-yuan, University of California San Francisco, San Francisco, California, United States
  • Hyacinth, Hyacinth I., Aflac Cancer and Blood Disorder Center, Emory University., Atlanta, Georgia, United States
  • Liang, Yulan, University of Maryland, Baltimore, Maryland, United States
  • Feldman, Harold I., University of Pennsylvania, Philadelphia, Pennsylvania, United States

SCT has been identified as a risk factor for CKD in prior epidemiologic cohort studies. The influence of SCT upon progression of established CKD has not been previously evaluated.


SCT was imputed from genetic data in AA CRIC participants. We excluded those with hemoglobin C trait. Mixed effects models were used to analyze estimated glomerular filtration rate (eGFR) decline. Association of SCT and the CRIC composite renal outcome (end-stage renal disease or halving of eGFR) was assessed by Cox regression. Models were constructed in stepwise fashion and included demographics, African ancestry, clinical site, baseline eGFR, education, income, insurance status, nephrologist use, ACE-I/ARB use, systolic blood pressure, body mass index, diabetes, hemoglobin A1c, smoking and 24-hour urine protein. Analyses were also stratified by APOL1 risk status.


We included 1,468 participants, of whom 218 (14.9%) had SCT. Median follow up was 8.6 years (IQR 6.7 - 9.6). Baseline characteristics including eGFR were similar between the SCT and non-SCT groups (TABLE) as was the unadjusted eGFR decline (-1.37 [1.43] v. -1.44 [1.55]). In the fully adjusted model, no difference was noted in eGFR slope comparing SCT to non-SCT (-0.031 [-0.567, 0.504] ml/min/1.73m2/year, p=0.91). SCT was not associated with the composite renal outcome (HR 1.19 [95% CI 0.89 - 1.61], p=0.24). When stratified by APOL1, no association was noted between SCT and the outcomes of interest.


SCT is present in 8-10% of the general AA population but was enriched among AAs in the CRIC Study suggesting it may confer risk for developing CKD. In contrast to prior findings in population-based cohorts, SCT was not associated with progression of renal disease when evaluated in individuals with CKD.

CharacteristicsNon-SCT AA
Age (years)57.4 (10.8)58.9 (10.3)
Female sex631 (50.5%)117 (53.7%)
Hypertension1165 (93.2%)198 (90.8%)
Diabetes638 (51%)116 (53.2%)
Baseline eGFR (ml/min/1.73m2) - Mean (SD)44.2 (16.5)42.1 (15.0)
24hr Urine Protein (g/24hr) - Median (IQR)0.25 (0.08 - 1.10)0.23 (0.07 - 0.90)
eGFR slope per year - Mean (SD)-1.44 (1.55)-1.37 (1.43)
APOL1 high risk allele226 (19.4%)36 (17.2%)


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