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Abstract: PO1543

APOL1 High-Risk Genotype Is Associated with Worse Renal Outcomes in Black Patients with Membranous Nephropathy

Session Information

Category: Glomerular Diseases

  • 1203 Glomerular Diseases: Clinical, Outcomes, and Trials

Authors

  • Chen, Dhruti P., University of North Carolina System, Chapel Hill, North Carolina, United States
  • Henderson, Candace Dione, University of North Carolina System, Chapel Hill, North Carolina, United States
  • Aiello, Claudia, University of North Carolina System, Chapel Hill, North Carolina, United States
  • Hu, Yichun, University of North Carolina System, Chapel Hill, North Carolina, United States
  • Hogan, Susan L., University of North Carolina System, Chapel Hill, North Carolina, United States
  • Falk, Ronald J., University of North Carolina System, Chapel Hill, North Carolina, United States
Background

Black patients have a higher propensity for progression to end-stage kidney disease (ESKD) and this disparity persists in glomerular diseases studied thus far. Genetic variants in the Apolipoprotein L1 (APOL1) gene contribute to kidney disease burden in those with African ancestry. To date, there are no data on the role of APOL1 risk alleles in outcomes among black patients with membranous nephropathy (MN).

Methods

Sanger sequencing for APOL1 risk allele genotyping was completed on patients of African-American ancestry (self or clinician reported) with diagnosis of MN enrolled in the Glomerular Disease Collaborative Network (GDCN) or Cure Glomerulonephropathy Network (CureGN) with DNA samples available were included. White patients from CureGN were included for comparison. Data from CureGN or chart abstraction for GDCN patients were used to determine demographics, diagnosis, disease onset, and ESKD (dialysis initiation or transplantation). Fisher’s exact, Wilcoxon rank, and Kaplan-Meier curves with log rank tests were used to evaluate differences between high risk (2 variants) and low risk (0/1 variant) and white population.

Results

There were 106 African American patients with diagnosis of MN in our study. Of these, 15 patients (14%) were high risk (two risk alleles of APOL1) and the remaining 91 patients (86%) were low risk (0/1 risk alleles of APOL1). Data were available for 493 white patients. Hazard ratio for composite outcome of ESKD/death was 4.21 (95% CI 1.54,11.51) among African Americans (high risk vs. low risk) and 6.37 (95% CI 2.74, 14.80) compared to white population. Time to endpoint was significantly faster in those with high risk APOL1 genotype (Figure), p<0.0001.

Conclusion

High-risk APOL1 genotype in African Americans is associated with faster time to ESKD/death compared to low-risk AA or white patients with MN.

Funding

  • NIDDK Support