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Abstract: TH-PO709

APOL1 Risk Variants, Subclinical Cardiovascular Disease, and Mortality in African Americans Initiating Hemodialysis

Session Information

Category: Hypertension and CVD

  • 1401 Hypertension and CVD: Epidemiology, Risk Factors, and Prevention

Authors

  • Chen, Teresa K., Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Fitzpatrick, Jessica, The Hospital for Sick Children, Toronto, Ontario, Canada
  • Winkler, Cheryl Ann, NCI, NIH, Frederick National Laboratory, Frederick, Maryland, United States
  • Binns-Roemer, Elizabeth A., LEIDOS, Frederick, Maryland, United States
  • Corona villalobos, Celia Pamela, Johns Hopkins University, Baltimore, Maryland, United States
  • Jaar, Bernard G., Johns Hopkins University and Nephrology Center of Maryland, Baltimore, Maryland, United States
  • Sozio, Stephen M., Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Parekh, Rulan S., The Hospital for Sick Children, Toronto, Ontario, Canada
  • Estrella, Michelle M., University of California, San Francisco and San Francisco VA Medical Center, San Francisco, California, United States
Background

The role of APOL1 risk variants in cardiovascular disease (CVD) remains unclear, especially among ESRD patients. We evaluated associations of APOL1 with subclinical CVD and mortality in a cohort of African Americans (AA) initiating hemodialysis (HD) in the Predictors of Arrhythmic and Cardiovascular Risk in End-Stage Renal Disease (PACE) Study.

Methods

APOL1 risk variants and ancestry markers were genotyped using custom Taqman assays and Infinium QC array kits. We defined APOL1 risk status by a recessive genetic model (high=2 risk alleles; low=0-1 risk allele). We studied associations of APOL1 high-risk status with baseline subclinical CVD (left ventricular [LV] hypertrophy, LV mass, ejection fraction, coronary artery calcification [CAC], pulse wave velocity) using logistic/linear regression and time to all-cause or CVD mortality using Cox hazards models, adjusting for age, sex and ancestry. In sensitivity analyses, we further adjusted for systolic blood pressure (SBP) and Charlson Comorbidity Index (CCI).

Results

Of 267 AA participants successfully genotyped, 27% were APOL1 high-risk. At baseline, mean age was 53 years, 41% were female, 56% had diabetes, and mean SBP was 138 mmHg. In cross-sectional analyses, APOL1 high- vs. low-risk status was independently associated with lower odds of LV hypertrophy and CAC, and lower LV mass. These associations remained robust upon further adjustment for CCI, but were attenuated when adjusted for SBP (Table). Over a mean follow-up of 2.5 years, APOL1 risk status was not associated with all-cause or CVD mortality.

Conclusion

Among AA incident HD patients, APOL1 high-risk status was associated with better subclinical measures of CVD, but these did not translate to improved survival. Future studies are needed to clarify the clinical implications of APOL1 risk variants in AA with ESRD.

Funding

  • NIDDK Support –