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Pediatr Nephrol. 2009 Apr;24(4):869-71. doi: 10.1007/s00467-008-1032-6. Epub 2008 Oct 21.

Oxidative imbalance in idiopathic renal hypouricemia.

Author information

1
Department of Pediatrics, Kansai Medical University, 2-3-1 Shin-machi, Hirakata-shi, Osaka 573-1191, Japan. kanekok@hirakata.kmu.ac.jp

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.

PMID:
18936980
DOI:
10.1007/s00467-008-1032-6
[Indexed for MEDLINE]

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