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Abstract: TH-PO467

APOL1 Genotypes and Vascular and Endothelial Function in the Multi-Ethnic Study of Atherosclerosis (MESA)

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
  • Katz, Ronit, University of Washington, Seattle, Washington, United States
  • Estrella, Michelle M., University of California, San Francisco and San Francisco VA Medical Center, San Francisco, California, United States
  • Post, Wendy S., Johns Hopkins University, Baltimore, Maryland, United States
  • Kramer, Holly J., Loyola University Medical Center, Maywood, Illinois, United States
  • Rotter, Jerome I., LABioMed at Harbor-UCLA Medical Center, Torrance, California, United States
  • Tayo, Bamidele O., Loyola University Chicago Stritch School of Medicine, Maywood, Illinois, United States
  • Mychaleckyj, Josyf, University of Virginia, Charlottesville, Virginia, United States
  • Wassel, Christina, Premier, Inc, Charlotte, North Carolina, United States
  • Peralta, Carmen A., University of California San Francisco/SFVAMC, San Francisco, California, United States
Background

The APOL1 high-risk genotypes, present in 13% of U.S. blacks, are associated with an increased risk for hypertension-attributed kidney disease. Biopsy studies show differences in kidney vasculature by APOL1 status, but less is known about the variants' associations with systemic vascular and endothelial function.

Methods

Using a recessive genetic model, we examined the cross-sectional associations of APOL1 risk genotypes (high=2 risk alleles; low=0-1 risk allele) with subclinical measures of vascular and endothelial function in MESA. Outcomes included measures of vascular (small and large arterial elasticity [SAE, LAE] by HDI PulseWave CR-2000 and ascending aortic distensibility [AAD] by magnetic resonance imaging) and endothelial (by brachial artery Doppler flow-mediated dilation [FMD]) function. We constructed linear regression models, adjusting for age, sex, and genetic global ancestry.

Results

We included African-American MESA participants with available APOL1 genotyping and measurements of SAE (n=1586), LAE (n=1586), AAD (n=985), and FMD (n= 777) at Exam 1 (2000-2002). Mean age was 62 years, 54% were female, 59% had hypertension, mean systolic blood pressure was 131 ± 22 mmHg, and mean eGFRCysC was 90 ± 20 ml/min/1.73 m2. Mean (SD) SAE, LAE, AAD, and FMD were 4.2 (2.5) ml/mmHg*100, 13.5 (5.8) ml/mmHg*100, 1.7 (1.3) 1/mmHg*1000, and 0.2 (0.1) mm, respectively. In linear regression models, the APOL1 high-risk genotypes were not associated with SAE, LAE, AAD, or FMD, though there was a trend of lower AAD among APOL1 high- vs. low-risk individuals (Table).

Conclusion

Among African Americans in MESA, the APOL1 high-risk genotypes were not associated with subclinical measures of vascular or endothelial function. Further studies are needed to clarify the potential role of APOL1 in vascular changes.

Funding

  • NIDDK Support