ArticleJournal of diabetes research2025
Benzbromarone Inhibits Renal URAT1 and Attenuates Renal Damage in Streptozotocin-Induced Diabetic Rats, Independent of Its Uricosuric Effects.
Article in Journal of diabetes research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Polydatin alleviates adenine-induced nephropathy in mice.Renal failure · 2026Article
- Association Between Time-Averaged Serum Uric Acid and Renal Outcomes in Patients with Type 2 Diabetes Mellitus with Chronic Kidney Disease: A Multicenter Retrospective Cohort Study.Diabetes therapy : research, treatment and education of diabetes and related disorders · 2026Article
- Allopurinol Beyond Gout: Targeting Oxidative Stress and Metabolic Inflammation in Diabetes and Its Complications.International journal of rheumatic diseases · 2026Article
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Authors and funding
5 authors.
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Abstract
Background: Hyperuricemia remains a critical risk factor for diabetic kidney disease (DKD) currently. Recent studies have confirmed that allopurinol, an inhibitor of xanthine oxidase (XO), does not have any beneficial effects on DKD. However, it is still unclear how uricosurics, such as benzbromarone (BZ), affect the progression of DKD. Methods: STZ-induced diabetic and control rats were treated with BZ for 8 weeks. Blood samples were collected to measure fasting blood glucose (FBG), serum uric acid (SUA), serum creatinine (SCr), and blood urea nitrogen (BUN). Simultaneously, urinary samples were tested, and the daily urinary amounts of albumin (UAE), uric acid (UUA), creatinine (UCr), urea nitrogen (UUN), were calculated. Gene expressions of XO, urate transporter 1 (URAT1), and glucose transporter 9 (GLUT9) in the kidney, as well as XO, uricase, and GLUT9 in the liver, were detected. Results: (1) Compared with normal rats, diabetic rats exhibited significant increases in FBG, BUN, UUN, UAE, UUA, while SUA was significantly decreased. BZ significantly decreased UAE and increased SUA over 8 weeks in diabetic rats. (2) Diabetic rats developed noticeable hyaline degeneration, and a slight decrease in mean glomerular area. BZ treatment significantly attenuated tubular damage in diabetic rats without affecting glomerular morphology. (3) In the kidney, gene expression of XO was increased, while URAT1 and GLUT9 were unchanged in diabetic rats. BZ treatment had no effect on GLUT9 and XO gene expression but significantly inhibited URAT1 expression in diabetic rats. (4) In the liver, gene expression of XO, uricase, and GLUT9 did not differ between diabetic and normal rats. BZ treatment significantly inhibited GLUT9 expression but had no effect on XO and uricase expression in diabetic rats. Conclusions: BZ treatment significantly protects against renal damage in STZ-induced diabetic rats independent of its uricosuric effects, possibly because of its inhibition of renal URAT1.
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