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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
The clinical appropriateness of urate-lowering therapy in patients with hyperuricemia and chronic kidney disease (CKD) remains controversial due to the bidirectional relationship between serum uric acid (sUA) and renal function. It is unclear whether elevated sUA contributes to renal impairment or if reduced kidney function leads to hyperuricemia. Ethical limitations hinder prospective interventional studies to resolve this issue. Although recent guidelines, such as those from KDIGO, suggest limited evidence supporting urate-lowering therapy for CKD prevention, genetic predisposition—particularly in populations with high prevalence of urate transporter variants—offers a unique opportunity to infer causality through Mendelian Randomization (MR). In Japanese populations, ABCG2 gene variants (rs2231142 and rs72552713) are more common and strongly associated with hyperuricemia. This study aimed to determine whether genetically elevated sUA due to ABCG2-related SNPs causally affects renal function, measured by estimated glomerular filtration rate (eGFR), using MR analysis.
A retrospective genetic association study was conducted in 8,277 Japanese individuals. A two-step analytical approach was used. First, multiple linear regression analyses assessed the association between four SNPs—rs2231142 and rs72552713 (ABCG2), rs3775948 (SLC2A9), and rs55975541 (CDC42BPG)—and sUA levels to validate their use as genetic instruments. Second, MR analysis using the inverse-variance weighted (IVW) method estimated the causal effect of sUA on eGFR. ABCG2 variants were selected as primary instruments based on biological relevance and statistical strength. Exploratory MR analyses were also performed using the other two SNPs.
ABCG2 variants rs2231142 and rs72552713 were significantly associated with elevated sUA levels and demonstrated strong instrument strength (F-statistic = 23.9). MR analysis revealed a significant inverse causal effect of sUA on eGFR (Estimate = -4.892; 95% CI: -9.172 to -0.612; p = 0.025), with low heterogeneity (I² = 11.5%). In contrast, MR analyses using rs3775948 and rs55975541 showed no significant causal effect (Estimate = -1.102, p = 0.41; Estimate = 0.763, p = 0.58, respectively), while these SNPs were significantly associated with sUA levels. Of all four SNPs investigated in the present study, only ABCG2-related variants demonstrated a causal link to renal function, suggesting transporter-specific mechanisms in urate-mediated kidney injury.
This study provides genetic evidence supporting a causal relationship between elevated sUA levels and reduced renal function mediated by ABCG2-related SNPs in a Japanese population. These findings underscore the utility of MR in clarifying complex pathophysiological relationships and suggest that urate transporter genotypes may inform individualized risk assessment for CKD progression.
