Kidney Week

Abstract: FR-PO0265

Biomarkers of Tubular Injury and Immune Activation Across APOL1 Genotypes

Session Information

• CKD: Omics, Systemic Stressors, and Targeted Pharmacotherapy
  October 23, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

• 2201 CKD (Non-Dialysis): Epidemiology, Risk Factors, and Prevention

Authors

• Slear, Jessica Hope King, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, United States

Jessica Hope King Slear

• Kizza, Timothy, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, United States

Timothy Kizza, MPH

• Zhao, Runqi, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, United States

Runqi Zhao, MS

• Omotoso, Bolanle Aderonke, Obafemi Awolowo University Teaching Hospital Complex, Ife, Osun, Nigeria

Bolanle Aderonke Omotoso, MBChB

• Arogundade, Fatiu Abiola, Obafemi Awolowo University Teaching Hospital Complex, Ife, Osun, Nigeria

Fatiu Abiola Arogundade, MD

• Mamven, Manmak, University of Abuja, Abuja, FCT, Nigeria

Manmak Mamven, MBBS

• Kamboj, Kajal, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, United States

Kajal Kamboj, PhD

• Huynh, Courtney, Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, United States

Courtney Huynh, MS

• Amira, Christiana Oluwatoyin, University of Lagos College of Medicine, Lagos, Nigeria

Christiana Oluwatoyin Amira, MD

• Solarin, Adaobi, Lagos State University Teaching Hospital, Lagos, Nigeria

Adaobi Solarin, MBBS

• Umeizudike, Theophilus I., Lagos State University Teaching Hospital, Lagos, Nigeria

Theophilus I. Umeizudike, MBBS, MSc

• Ulasi, Ifeoma I., University of Nigeria, Nsukka, Enugu, Nigeria

Ifeoma I. Ulasi, MBBS, MS, MSc

• Raji, Yemi R., University of Ibadan College of Medicine, Ibadan, Oyo, Nigeria

Yemi R. Raji, MBChB

• Kwakyi, Edward Papa Kwabena, University of Ghana Medical School, Accra, Greater Accra Region, Ghana

Edward Papa Kwabena Kwakyi, MD, FASN

• Adu, Dwomoa, University of Ghana Medical School, Accra, Greater Accra Region, Ghana

Dwomoa Adu, MD

• Waikar, Sushrut S., Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, United States

Sushrut S. Waikar, MD, MPH

• Ilori, Titilayo O., Boston University Chobanian & Avedisian School of Medicine, Boston, Massachusetts, United States

Titilayo O. Ilori, MD, MS, MSc, FASN

Background

Biomarkers of kidney injury and immune activation may help identify those at highest risk of CKD progression. We examined the association of APOL1 genotypes with urinary kidney injury molecule-1 (KIM-1), a marker of tubular injury, and plasma soluble tumor necrosis factor receptor 1 (sTNFR1), a marker of immune activation.

Methods

We performed a cross-sectional analysis of West African CKD participants (n=609) in the Diet, CKD, and Apolipoprotein L1 (DCA) Study. We measured urine KIM-1 and plasma sTNFR1 using the Meso Scale Discovery platform. Inter-assay imprecision was determined using internal quality control (QC) and blind replicates (BR). The intraassay coefficient of variation (CV) across KIM-1 duplicates was 3.62%, interassay QC CVs were 12% and BR CVs were 2.91%. The intraassay CV across sTNFR1 duplicates was 2.34%, interassay QC CVs were 18.45% and BR CVs were 2.55%. High-risk APOL1 genotypes were 2 risk alleles (n=191) and low-risk were 0-1 allele (n=418). The primary outcome was log-transformed, creatinine-normalized urine KIM-1 and plasma sTNFR1. To estimate the association of genotypes with the biomarkers, we conducted linear mixed-effects regression models with the clinical site as a random effect, adjusting for key covariates.

Results

Mean age in high- vs. low-risk genotypes was 48 vs. 50 years; eGFR was 61 vs. 70 mL/min per 1.73 m², and 54% were male. Mean urine KIM-1 levels in high- vs. low-risk APOL1 genotypes were 14.1 ± 92.5 vs. 16.2 ± 143 pg/mL and showed no significant association after adjustment (Table 1). Mean plasma sTNFR1 was higher in the high-risk group with 382 ± 2008 vs. 188 ± 302 pg/mL. After adjustment for age, sex, and BMI, sTNFR1 was 26% higher in those with high- vs. low-risk genotypes (Exp(β)=1.26, 95% CI: 1.06–1.49, p = 0.01). This association was attenuated and no longer statistically significant after adjusting for eGFR (Exp(β)=1.11, 95% CI: 0.95–1.30, p = 0.18) (Table 1).

Conclusion

In West African participants with CKD, urine KIM-1 levels were no different at enrollment in those with high- vs. low-risk APOL1 genotype. Plasma sTNFR1 levels were higher, but this finding was confounded by eGFR, suggesting that immune activation is a reflection of CKD severity rather than an independent genotype marker.

Funding

• NIDDK Support