Oxidative imbalance in idiopathic renal hypouricemia |
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Authors: | Kaneko Kazunari Taniguchi Naho Tanabe Yuko Nakano Takahide Hasui Masafumi Nozu Kandai |
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Institution: | (1) Department of Pediatrics, Kansai Medical University, 2-3-1 Shin-machi, Hirakata-shi, Osaka 573-1191, Japan;(2) Department of Pediatrics, Kobe University Graduate School of Medicine, Kobe, Japan |
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Abstract: | 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. |
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Keywords: | Antioxidant Exercise-induced acute renal failure Idiopathic renal hypouricemia Oxidative stress Urate transport URAT1 |
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