Back
For best output, select "Paper Size" as "A4" and "Margin" as "0" or "None".
To save or print to PDF, please select Print Destination > Save as PDF, enable Background Graphics under "More Settings", then click "Save".
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.
Dotinurad is a novel selective urate reabsorption inhibitor that potently and selectively inhibits urate transporter 1 (URAT1) in the kidney. In addition to its urate-lowering action, recent studies have suggested its potential renoprotective effects, including reductions in urinary albumin excretion. However, clinical data on long-term renal outcomes remain limited. We aimed to evaluate the effects of dotinurad on renal function decline and proteinuria in patients with hyperuricemia.
We conducted a single-center, retrospective cohort study including 34 patients treated with dotinurad. The mean age was 72.5 ± 15.5 years, baseline serum uric acid (UA) 9.0 ± 2.4 mg/dL, estimated Glomerular Filtration Rate (eGFR) 26.4 ± 10.1 mL/min/1.73m 2 , and urinary protein 1.2 ± 2.3 g/gCr. Using SPSS version 29.0.2.0, paired-samples t-tests were performed to compare baseline and post-treatment values. The slopes of estimated glomerular filtration rate (eGFR) before and after dotinurad administration were also analyzed.
After two years of treatment, UA levels significantly decreased from 8.4 ± 1.5 to 6.2 ± 1.4 mg/dL (p < 0.001). eGFR decreased modestly from 29.1 ± 10.2 to 25.8 ± 13.7 mL/min/1.73m 2 (p = 0.017). Urinary protein excretion showed no significant change (0.8 ± 1.6 vs 0.5 ± 0.5 g/gCr, p = 0.34). Regarding renal function trajectory, the eGFR slope significantly improved after initiation of dotinurad: from –7.25 mL/min/1.73 m² per two years to –2.70 mL/min/1.73 m² per two years (p = 0.018). Similarly, comparison over one-year intervals demonstrated improvement from –6.32 mL/min/1.73 m² per year to –1.48 mL/min/1.73 m² per year (p = 0.009). These findings indicate that dotinurad significantly attenuated the rate of eGFR decline despite the absence of a significant reduction in proteinuria.
In this retrospective cohort, dotinurad treatment was associated with a significant suppression of eGFR decline over one and two years, suggesting a potential renoprotective effect beyond urate lowering. However, no improvement in proteinuria was observed. Given the single-center design and small sample size, further multicenter prospective studies are warranted to confirm these findings and elucidate the mechanisms underlying the renoprotective effects of dotinurad.
