Kidney Week

Abstract: SA-PO0493

Intersecting Risks: The Interaction of Social Risk and APOL1 Genetic Variants on Cardiometabolic Health in African Americans with CKD

Session Information

• CKM: Clinical - Screening, Population Management, Care Disparities, and Patient-Centered Outcomes
  October 24, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Cardiovascular-Kidney-Metabolic Health

• 602 Cardiovascular-Kidney-Metabolic Health: Clinical

Authors

• Ozieh, Mukoso N., Medical College of Wisconsin Department of Medicine, Milwaukee, Wisconsin, United States

Mukoso N. Ozieh, MD, MS

• Nagavally, Sneha, Medical College of Wisconsin, Center for Advancing Population Science, Milwaukee, Wisconsin, United States

Sneha Nagavally, MS, PhD

• Hawks, Laura C., Medical College of Wisconsin Department of Medicine, Milwaukee, Wisconsin, United States

Laura C. Hawks, MD, MPH

• Dawson, Aprill, Medical College of Wisconsin Department of Medicine, Milwaukee, Wisconsin, United States

Aprill Dawson, PhD, MPH

• Williams, Joni S., Medical College of Wisconsin Department of Medicine, Milwaukee, Wisconsin, United States

Joni S. Williams, MD, MPH

Background

Social risk exposure, including housing instability, food insecurity, and low socioeconomic status, are independently linked to adverse cardiometabolic health (CMH) and may modify the effects of genetic susceptibility. However, limited studies have examined whether social risk exposure differs by APOL1 genetic risk status or whether the association between genetic risk variants and CMH vary by social risk exposure.

Methods

We analyzed cross-sectional data from 154 Black adults aged 21 or older with non-dialysis CKD defined as eGFR <60 ml/min/1.73m² or UACR >30mg/g recruited from Southeast Wisconsin. We created a composite CMH score (primary outcome) of 0-100 based on a modified Life's Essential 8 score (diet, physical activity, smoking, BMI, blood pressure, and hemoglobin A1c), with higher scores indicating better CMH. APOL1 genetic risk was based on the presence of 2 genetic risk alleles, G1 and G2 (high-risk) and presence of 0 or 1 risk alleles (low-risk). Social risk exposure included housing insecurity, cost-related medication adherence, perceived stress, adverse childhood experiences, social support, health literacy, education, insurance, income, and employment status and was modeled as a continuous variable. Linear regression models were used to examine the association between genetic risk and CMH score and interaction term between genetic and social risk was included in the model. Statistical significance was defined at p-value< 0.05 and analyses were performed using R-4.1.3.

Results

The mean age was 62.1 ± 10.9, mean eGFR was 44.8 ± 19.0, mean CMH score was 55.4 ± 16.7, and mean social risk count was 4.7 ± 1.9 (5.2 ± 2.3 in those with high-risk genotype and 4.6 ± 1.8 in those with low-risk genotype, p = 0.16). The interaction term between genetic and social risk were statistically significant (p=0.017) hence stratified analyses were performed. Increasing social risk was associated with lower CMH scores among individuals with high-risk genotype (p=0.01) and no association was observed for low-risk genotype (p=0.72).

Conclusion

These findings suggest adverse social determinants may worsen CMH vulnerability among individuals with APOL1 high-risk genotype. Future longitudinal studies are warranted to investigate the potential effect modification relationship between APOL1 high-risk genotype, social risk exposure, and CMH.

Funding

• NIDDK Support