Kidney Week

Abstract: TH-PO0104

Genome-Wide Association Study of Diabetic Kidney Disease in Stroke Survivors

Session Information

• Integrative Genomics and Multi-Omics in Noncystic Genetic Kidney Disease
  October 22, 2026 | Location: Exhibit Hall A, Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Genetic Diseases of the Kidneys

• 1202 Genetic Diseases of the Kidneys: Non-Cystic (Complex and Non-Cystic Monogenic)

Authors

• Wu, Yu, Beijing Tiantan Hospital Affiliated to Capital Medical University, Beijing, China

Yu Wu, MD, PhD

• Li, Mengshi, Beijing Tiantan Hospital Affiliated to Capital Medical University, Beijing, China

Mengshi Li, PhD

• Zhou, Yi-Lun, Beijing Tiantan Hospital Affiliated to Capital Medical University, Beijing, China

Yi-Lun Zhou, MD

Background

Despite a substantial heritable background for diabetic kidney disease (DKD), its genetic architecture in relation to stroke remains elusive. Therefore, this study aimed to investigate whether the genetic predisposition to DKD influences stroke prognosis in patients with type 2 diabetes (T2DM).

Methods

A genome-wide association study (GWAS) of DKD was conducted in patients with T2DM and stroke (case=1,089 and control=2,230). DKD was defined as decreased estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m². Using summary statistics from two independent cohorts with T2DM-induced DKD, variables that reached suggestive results (P < 5× 10^–6) were further assessed. A hierarchical computational framework was used to rank functional variants and determine regulatory implications. The DKD GWAS study yielded polygenic risk scores (PRSs), which were subjected to regression analyses to assess the correlation between PRSs and stroke prognosis at 1 year.

Results

Four suggestive loci were identified, with the strongest signal detected at rs78539902 within BICD Cargo Adaptor 1 (BICD1) (OR 0.13, 95% CI 0.06-0.27, P=8.15×10^-8). According to functional analysis, rs78539902 might change the binding affinities of transcription factors (ZBTB12, MEF2C, MEF2A, and FOXI1), thus influencing the aberrant expression of BICD1 during renal injury. Individuals in the top 50% of the DKD PRS distribution were more likely than those in the lower 50% to have a poor post stroke functional outcome in multivariable-adjusted models (OR=1.37, 95% CI 1.10–1.71, P=0.004).

Conclusion

Hereditary sensitivity to microvascular injury may influence the progression of both renal and cerebrovascular disease, supporting a shared polygenic background between DKD and impaired stroke recovery.

Funding

• Government Support – Non-U.S.