Oxidative Imbalance in Acute Renal Failure after Exercise without Renal Hypouricemia

Abstract

Acute renal failure (ARF) induced by anaerobic exercise is an important complication of idiopathic renal hypouricemia. It has been suggested that decreased antioxidant potential in hypouricemia leads to kidney injury caused by reactive oxygen species (ROS). However, the mecha- nisms involved in the development of exercise-induced ARF, especially in patients without renal hypouricemia, have not been fully clarified. We demonstrated the oxidative imbalance after exercise stress testing in a boy with exercise-induced ARF without hypouricemia. Materials and Methods: A 13-year-old Japanese boy was transferred to our hospital for evaluation of ARF that developed after anaerobic exercise. Routine laboratory tests revealed 350.9 mumol/l of serum creatinine and 12.8 mg/dl of serum uric acid, respectively. Contrast enhanced computerized tomography identified a patchy wedge-shaped enhancement on both kidneys 24 h after injection of contrast media. These results indicated a diagnosis of exercise-induced ARF. After obtaining informed consent from the patient' parents, we subjected the patient to a period of strenuous exercise on a treadmill. For comparison, a healthy male volunteer in his twenties was tested in the same manner. Serum concentrations of ROS and biological antioxidant potentials (BAP) were measured by spectrophotometric methods using commercially available kits (d-ROMs and BAP test, respectively). Exerciseinduced alterations in renal blood flow were investigated with an ultrasound scan. Results: Before exercise the patient was completely asymptomatic, but headache and abdominal pain developed 1 h after anaerobic stress. There was a negligible difference in the serum concentrations of ROS before and after exercise in both the patient and the volunteer. In contrast, the serum level of BAP in the patient was reduced soon after the initiation of anaerobic stress, whereas that of the volunteer was elevated. Therefore, the ratio of ROS to BAP was increased in the patient (before, 0.20; after, 0.39) but decreased in the volunteer (before, 0.17; after, 0.12). Furthermore, renal blood flow after exercise was remarkably reduced in the patient. Conclusion: These data suggested that an oxidative imbalance resulting from a decreased antioxidant capability is involved in the pathogenesis of exercise-induced ARF. Uric acid may be an important antioxidant in patients with idiopathic renal hypouricemia; patients with exerciseinduced ARF without hypouricemia could lack another antioxidant factor. The oxidant imbalance in patients with exercise-induced ARF without hypouricemia may lead to renal vasoconstriction and renal injury