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Kidney Week

Abstract: FR-PO310

Interaction Between Apolipoprotein L1 (APOL1) Genetic Risk and Air Pollution for Kidney Disease in African Americans

Session Information

Category: CKD (Non-Dialysis)

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


  • Defelice, Nicholas B., Ichan School of Medicine, New York, New York, United States
  • Chan, Lili, Icahn School of Medicine at Mount Sinai, New York, New York, United States
  • Coca, Steven G., Icahn School of Medicine at Mount Sinai, New York, New York, United States
  • Horowitz, Carol, Icahn School of Medicine at Mount Sinai, New York, New York, United States
  • Cooper, Richard, Loyola University Chicago, Maywood, Illinois, United States
  • Nadkarni, Girish N., Ichan School of Medicine, New York, New York, United States

The APOL1 high-risk genotype is frequent in African Americans (AAs) and is associated with increased chronic kidney disease (CKD). However, only a fraction of individuals with APOL1 risk have CKD, indicating the presence of disease modifiers (‘second hits’). Air pollution, measured by particulate matter ≤2.5 micrometers (PM2.5) is an emerging risk factor for CKD and AAs are disproportionately exposed to higher levels. We assessed whether APOL1and environmental (PM2.5) risk interact.


We used data from an urban biobanked cohort (BioMe Biobank). This includes linked genotype, demographic and clinical data. . We geocoded address level data from initial enrollment date and assigned a census track to link PM2.5 estimates from EPAs Downscaler Model. We assigned annual average concentrations using daily PM2.5 exposure from the 365 days before enrollment. We considered CKD after enrollment and fit a logistic model accounting for APOL1, PM2.5 and their interaction, after adjusting for confounders .


We had data on 4800 AAs and 675 (14%) had APOL1 high-risk. Individuals with APOL1 high-risk had lower baseline eGFR vs. low risk (75 vs. 81 ml/min). There were no other significant differences. The median PM2.5 concentrations were 12.5 µg/m3 and did not differ by APOL1 risk. There were significant associations with CKD for both APOL1 (adjusted OR 1.5; 95% CI 1.2-1.8) and with PM2.5 (adjusted OR 1.09; 95% CI 1.08-1.10 per µg/m3 increase) in fully adjusted models. In models accounting for interaction between APOL1 and PM2.5, although both significantly were associated with CKD, there was a possible interaction (Pinteraction=0.06)


APOL1 and PM2.5 may interact for CKD. If validated , air pollution may be a novel environmental ‘second hit’ for baseline APOL1 genetic risk.

Table 1. Logistic Regression Model including APOL1 and Air Pollution
 Adjusted Odds Ratio (95% Confidence Interval)P Value
APOL1 Risk Genotype1.51 (1.20-1.81)<0.01
PM2.5 concentration (per µg/m3 increment)1.09 (1.08-1.10)<0.01
Interaction term between APOL1 and PM2.5 (continuous)0.83 (0.7-1.02)0.06
Age per year increment1.03 (1.02-1.04)<0.01
Body Mass Index per 1kg/m2 increment1.02 (1.01-1.03)<0.01
Baseline eGFR per 1ml/min decrease1.06 (1.05-1.07)<0.01
Education less than high school0.82 (0.62-1.10)0.19
African genetic ancestry0.93 (0.45-1.93)0.84


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