A Case of Exercise-Induced Acute Renal Failure in a Patient with Idiopathic Renal Hypouricemia Developed during Antihypertensive Therapy with Losartan and Trichlormethiazide.

Ito, Osamu; Sato, Kazuto; Mitsui, Hideaki; Yuda, Fumiaki; Sato, Hiroshi; Ito, Sadayoshi; Kudo, Ken Ichi

doi:10.1291/hypres.26.509

Cited by 14 publications

(8 citation statements)

References 19 publications

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“…There are only a small number of reports of kidney biopsy in similar cases. In early reports, the deposition of UA was found in kidney tissue [13], whereas later reports showed renal tubular necrosis, with the assumption that glomeruli had normal histology [14][15][16][17]. In our case, interstitial edema was apparent, although the shape of the renal tubules was maintained and there were no changes observed in the glomeruli.…”

Section: Discussionmentioning

confidence: 41%

A case of renal hypouricemia and a G774A gene mutation causing acute renal injury that was improved by hemodialysis

et al. 2012

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A 16-year-old man came to our hospital complaining of loin pain after a middle-distance race. Following admission, his renal dysfunction worsened rapidly, requiring several hemodialysis sessions. A renal biopsy showed no change in the glomeruli, although interstitial edema was observed. Following the recovery of renal function, we confirmed that his uric acid level was abnormally low and urate clearance was abnormality high. Gene analysis showed that he had a G774A mutation which dominated the SLC22A12 gene encoding the urate transporter 1.

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Section: Discussionmentioning

confidence: 41%

A case of renal hypouricemia and a G774A gene mutation causing acute renal injury that was improved by hemodialysis

et al. 2012

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“…Since then, more than 50 cases have been reported, mostly from Japan [4][5][6][7][8]. It is speculated that patients with idiopathic renal hypouricemia have a 200-fold greater predisposition to exercise-induced ARF than those without renal hypouricemia [6].…”

Section: Discussionmentioning

confidence: 99%

“…An important complication of this disorder is exerciseinduced acute renal failure (ARF) [4][5][6][7][8]. It has been suggested that decreased antioxidant potential in hypouricemia leads to kidney injury caused by reactive oxygen species (ROS) [9,10].…”

Section: Introductionmentioning

confidence: 99%

Oxidative imbalance in idiopathic renal hypouricemia

et al. 2009

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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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“…Losartan is not without side effects; a case of exercise-induced acute renal failure with hypouricemia, and acute tubular necrosis with interstitial necrosis has been reported [59]. The role of long-term fenofibrate therapy on hyperuricemia and attacks of gout in patients with hyperlipidemia is not yet determined.…”

Section: Fenofibrate Losartan and Amlodipinementioning

confidence: 99%

Serum uric acid-lowering therapies: Where are we heading in management of hyperuricemia and the potential role of uricase

Bomalaski

Clark²

2004

Curr Rheumatol Rep

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Although allopurinol has been available for approximately 50 years, hyperuricemia and its sequelae are not only prevalent, but the incidence and costs associated with this disorder continue to increase. However, several new therapies have been developed. Recombinant urate oxidase has been useful in the treatment of tumor lysis hyperuricemia, and pegylated urate oxidase shows promise in patients with hyperuricemia and gout. Febuxostat and Y-700 are new oral xanthine oxidase inhibitors that are in human clinical trials. Tailoring of antilipid therapy in selected hyperuricemic and hyperlipidemic patients with fenofibrate may be of benefit in lowering blood cholesterol and uric acid levels. Similarly, treatment of selected hyperuricemic patients who also are hypertensive with losartan or amlodipine may be beneficial in lowering blood pressure and hyperuricemia. Despite these advances, new treatments for hyperuricemia are needed.

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A Case of Exercise-Induced Acute Renal Failure in a Patient with Idiopathic Renal Hypouricemia Developed during Antihypertensive Therapy with Losartan and Trichlormethiazide.

Cited by 14 publications

References 19 publications

A case of renal hypouricemia and a G774A gene mutation causing acute renal injury that was improved by hemodialysis

A case of renal hypouricemia and a G774A gene mutation causing acute renal injury that was improved by hemodialysis

Oxidative imbalance in idiopathic renal hypouricemia

Serum uric acid-lowering therapies: Where are we heading in management of hyperuricemia and the potential role of uricase

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