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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.
Background: Accumulating evidences have suggested that hyperuricemia is associated with aggravation of chronic kidney disease (CKD). Treatment guidelines propose, the administration of a uric acid production inhibitor to achieve serum uric level below 6 mg / dL in CKD patients with hyperuricemia; however, the success rate is not satisfactory. Amidst this, the uric acid-lowering agent dotinurad was newly launched in 2020. This selectively inhibits URAT-1 in the proximal tubule, suppressing uric acid reabsorption. Aim: Investigation of the effects of dotinurad in non-dialysis CKD patients. Design: Case collection. Subjects: Six non-dialysis CKD patients attending our department.
Methods: Before administering dotinurad, we confirmed the absence of kidney stones by ultrasound and encouraged patients to drink 2 L of water per day. The dose of uric acid production inhibitors already being taken was kept constant. Serum uric acid levels, uric acid clearance/creatinine clearance ratio (CUA/CCr), urine pH, renal function (eGFR), and urinary protein (random urine protein g/gCr) were investigated before and after dotinurad administration at 1 month, 3 months, 6 months, 9 months, and 12 months. Dotinurad was initiated at 0.5 mg/day and increased to 1 mg/day depending on the case. Comparisons were performed using paired t-tests, with p < 0.05 considered significant. At the same time, age, sex, medical history (disease that caused CKD, history of gout, hypertension, diabetes), and medications affecting uric acid metabolism were investigated from the medical records.
Results: The patients were all males, aged 74.5 ± 7.2 years. Renal function was assessed by eGFR; 31.3±11.9 mL/min/1.73m2, proteinuria was 0.85 ± 0.68 g/gCr, and CKD status was A1-A3G3a-G4. Two patients had a history of gout, four were taking uric acid inhibitors, two were taking ARBs, and two were taking diuretics. During the observation period, no change was made to concomitant medications that affect the metabolism of uric acid. The dose of dotinurad was increased to 1 mg/day in two patients; one patient increased the dose at 4 months, and the other at 8 months. One patient discontinued the treatment after 10 days. Serum uric acid levels improved over 12 months in all patients, decreasing significantly from 7.58 ± 0.47 mg/dL to 6.10 ± 0.29 mg/dL and 5.75 ± 0.78 mg/dL at 1 month and 12 months, respectively. CUA/CCr increased from 5.0 ± 1.8% to 7.3 ± 2.6% (p=0.10) after 1 month, 7.1 ± 2.1% (p<0.05) after 6 months, and 9.0 ± 4.7% (p=0.18) after 12 months. Urinary pH increased in all patients, from 5.8 ± 0.9 to 6.6 ± 0.9 (p<0.05) and 6.0 ± 0.9 (p=0.71) at 1 month and 12 months, respectively. No change was observed in eGFR or proteinuria. No new onset of gout attack did not appear.
Conclusion: A small dose of dotinurad administered for 12 months improved CKD symptoms in all patients, resulting in an increase in uric acid excretion into urine. Interestingly, the urine became alkalized, indicating that this agent may also inhibit the production of urinary stones. In the future, we need to increase the number of people involved and conduct further research.
