Oxidative imbalance in idiopathic renal hypouricemia
Oxidative imbalance in idiopathic renal hypouricemia
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DOI：
10.1007/s00467-008-1032-6
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发表时间：
2009-04-01
影响因子：
3
通讯作者：
Nozu, Kandai
中科院分区：
文献类型：
--
作者：
Kaneko, Kazunari;Taniguchi, Naho;Nozu, Kandai
特发性肾性低尿酸血症的一个重要并发症是运动诱发的急性肾功能衰竭（ARF）。对这种并发症最合理的解释是抗氧化能力降低导致活性氧（ROS）肾损伤。我们证明了这种氧化失衡的ROS生产和抗氧化系统的能力在一个15岁的女孩与特发性肾性低尿酸血症引起的突变尿酸转运蛋白（URAT 1）基因的伴随评估。她的血清活性氧水平增加，抗氧化能力下降后不久，开始无氧应激，由于跑步机运动。此后，血清活性氧水平和抗氧化潜力表现出平行的过程，在运动后240分钟恢复到基线值。一些特发性肾性低尿酸血症患者在运动后不久表现出氧化失衡，易患运动诱发的急性肾衰竭。抗氧化特性可以通过增强抗氧化活性来改变这种不平衡。
An important complication of idiopathic renal hypouricemia is exercise-induced acute renal failure (ARF). The most plausible explanation for this complication is that decreased antioxidant potential leads to kidney injury by reactive oxygen species (ROS). We demonstrated this oxidative imbalance by a concomitant assessment of ROS production and antioxidant system capability in a 15- year-old girl with idiopathic renal hypouricemia caused by a mutation in the urate transporter (URAT1) gene. Her serum level of ROS increased with decreasing antioxidant potential capacity soon after the initiation of anaerobic stress due to treadmill exercise. Thereafter, serum levels of ROS and antioxidant potential showed a parallel course, returning to the baseline values at 240 min after exercise. Some patients with idiopathic renal hypouricemia demonstrate oxidative imbalance soon after exercise with a predisposition to exercise-induced acute renal failure. Antioxidant properties may alter this imbalance by augmenting the antioxidant activity.