ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on Twitter

Kidney Week

Abstract: TH-PO1043

Explaining Racial Inequality in Albuminuria Through Multiple Mediators

Session Information

Category: CKD (Non-Dialysis)

  • 1901 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

  • Lopes, Marcelo, University of Michigan, Ann Arbor, Michigan, United States
  • Morgenstern, Hal, University of Michigan, Ann Arbor, Michigan, United States
  • Bragg-Gresham, Jennifer L., University of Michigan, Ann Arbor, Michigan, United States
  • Crews, Deidra C., Johns Hopkins University School of Medicine, Baltimore, Maryland, United States
  • Powe, Neil R., Priscilla Chan and Mark Zuckerberg San Francisco Gen Hosp & UCSF, San Francisco, California, United States
  • Burrows, Nilka Rios, Centers for Disease Control and Prevention, Atlanta, Georgia, United States
  • Saran, Rajiv, University of Michigan, Ann Arbor, Michigan, United States
Background

Previous studies have shown that blacks have a higher prevalence of albuminuria than whites and that certain risk factors may account for that racial inequality. No research, however, has assessed the role of multiple risk factors collectively as mediators of the race effect.

Methods

Using cross-sectional data from the 2007-2010 National Health And Nutrition Examination Surveys for 6700 non-Hispanic black and white adults, ages 20+, we applied flexible mediation analysis (medflex, R package) to decompose the total effect of black race on albuminuria prevalence (albumin/creatinine ratio ≥30 mg/g) into direct and indirect (mediated) effects for combinations of 4 potential mediators: diabetes; hypertension; obesity (body mass index ≥30 kg/m2), and low vitamin D level (25[OH]D3 <50 nmol/L). For each set of mediators, we estimated odds ratios (OR; 95% CI) for the direct, indirect and total effects and the percentage of the total effect that was mediated; ORs were adjusted for age, sex and non-mediating confounders.

Results

The weighted mean albuminuria level was 32 mg/g in blacks and 23 mg/g in whites; the adjusted OR for the total effect of black race on albuminuria was 1.61 (1.23, 2.11). The % mediated by each risk factor treated separately was 50% for low vitamin D, 44% for diabetes, 27% for hypertension, and 12% for obesity. When all 4 mediators were analyzed jointly, the direct-effect OR was 1.10 (0.65, 1.86), the indirect-effect OR was 1.46 (1.23, 1.74), and 84% of the total effect was mediated by these 4 risk factors. Excluding low vitamin D reduced the percentage mediated to 46%; doing the same with the other 3 mediators reduced the percentage mediated to no less than 70%.

Conclusion

The 4 risk factors treated as mediators in this study—especially low vitamin D and diabetes—appear to explain most of the racial difference in albuminuria prevalence in the United States. Although causal inference is limited by the cross-sectional design and possible residual confounding, the findings suggest that much of the racial inequality may be preventable through improvement of the risk-factor profile in blacks. As we learn more about how to control vitamin D level, the long-term impact on the incidence of chronic and end-stage renal disease could be appreciable.

Funding

  • Other U.S. Government Support