Elucidation of mechanism for exercise-induced acute renal failure in urate transporter deficient mice

运动诱发急性肾功能衰竭（EIARF）是肾性低尿酸血症的重要并发症。提出了EIARF的两种机制。一种假设是，由于血管收缩导致的肾再灌注损伤是由于运动诱导的氧自由基增加和缺乏尿酸盐、自由基清除剂所致。另一种假设是尿酸盐肾病是由于运动引起的ATP分解导致尿酸产生增加。我们研究了尿酸盐重吸收转运蛋白URAT 1缺陷小鼠的肾损伤，这些小鼠喂食尿酸盐和oxonate。从我们的结果来看，肾再灌注损伤是可以接受的。

Exercise induced acute renal failure (EIARF) are significant complications of renal hypouricemia. Two mechanisms for EIARF were proposed. One hypothesis is that renal reperfusion injury due to vasoconstriction results from an exercise-induced increase in oxygen free radicals and a lack of urate, free radical scavengers. The other hypothesis is that urate nephropathy results from an increase in uric acid production by exercise induced ATP breakdown. We examined renal injury of mice deficient in urate reabsorption transporter, URAT1, fed with urate and oxonate. Renal reperfusion injury was acceptable from our results.