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Abstract: TH-PO1041

APOL1 Risk Alleles in Glomerular Diseases

Session Information

Category: Glomerular Diseases

  • 1203 Glomerular Diseases: Clinical, Outcomes, and Trials

Authors

  • Henderson, Candace Dione, UNC Kidney Center, Chapel Hill, North Carolina, United States
  • Anguiano, Jaeline, UNC Kidney Center, Chapel Hill, North Carolina, United States
  • Chen, Dhruti P., UNC Kidney Center, Chapel Hill, North Carolina, United States
  • Jain, Koyal, UNC Kidney Center, Chapel Hill, North Carolina, United States
  • Hu, Yichun, UNC Kidney Center & Divisions of Nephrology & Hypertension, Chapel Hill, North Carolina, United States
  • Hogan, Susan L., University of North Carolina, Chapel Hill, North Carolina, United States
  • Falk, Ronald J., UNC Kidney Center, Chapel Hill, North Carolina, United States
Background

Impact of APOL1 variants in glomerular diseases is not well described. In published studies, 0 or 1 risk variant in APOL1 do not influence progression to end stage renal disease (ESRD), but two risk variants increase risk. We examined APOL1 variant association with developing ESRD in patients with glomerular disease.

Methods

The Glomerular Disease Collaborative Network (GDCN) is a large registry in southeastern US of patients with glomerular diseases including ANCA vasculitis, membranous glomerulopathy (MN), focal segmental glomerulosclerosis (FSGS), minimal change disease (MCD), and lupus. African-American patients with DNA samples from the GDCN were evaluated. 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). Proportional hazards models adjusted for age were used to evaluate time to ESRD by high vs. low risk variant with hazards ratios and 95% confidence intervals reported (HR, 95% CI).

Results

Two APOL1 variants were observed in 27% of 252 patients across all diseases except MCD, and most frequently in FSGS (50/93=54%), Table. Those with high risk variant were 1.9 times more likely to progress to ESRD (95% CI 1.2-3.0). In FSGS, high and low risk variants progressed similarly to ESRD (HR 1.0, 95% CI 0.5-1.7), but in other glomerular diseases those with the high risk variant were 2.5 times more likely to progress to ESRD (95% CI 1.2-5.1), Figure.

Conclusion

High-risk variants were present in most glomerular diseases studied, and common in FSGS. However, impact on progression to ESRD was not evident in FSGS, but influential in other glomerular diseases.