Background: The pivotal role of transforming growth factor-β1 (TGF-β1)-induced tubulointerstitial fibrosis in the progression of chronic kidney disease is an active topic of research. Recent evidence indicates that hyperuricemia is associated with increased TGF-β1 and progressive tubulointerstitial injury. We examined the hypothesis that lowering serum uric acid attenuates TGF-β1-induced profibrogenic tubular change in type 2 diabetic nephropathy. Methods: KK-Ay/Ta mice, an animal model of type 2 diabetes, were provided access to either regular drinking water or drinking water containing 10 mg/dl of allopurinol. Normal rat kidney epithelial cells were cultured and stimulated with 5 m
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