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一名患有肾性低尿酸血症的日本相扑选手运动后出现急性肾衰竭。

Acute renal failure after exercise in a Japanese sumo wrestler with renal hypouricemia.

作者信息

Mima Akira, Ichida Kimiyoshi, Matsubara Takeshi, Kanamori Hiroshi, Inui Emi, Tanaka Misa, Manabe Yumi, Iehara Noriyuki, Tanaka Yoshinori, Yanagita Motoko, Yoshioka Atsuko, Arai Hidenori, Kawamura Masashi, Usami Katsumasa, Hosoya Tatsuo, Kita Toru, Fukatsu Atsushi

机构信息

Department of Nephrology, Kyoto University Graduate School of Medicine, and Department of Internal Medicine, Ijinkai Takeda General Hospital, Kyoto, Japan.

出版信息

Am J Med Sci. 2008 Dec;336(6):512-4. doi: 10.1097/MAJ.0b013e318164717f.

Abstract

Familial renal hypouricemia is a hereditary disease characterized by extraordinary high renal uric acid clearance and is associated with acute renal failure (ARF). An 18-year-old sumo wrestler developed ARF after anaerobic exercise. Several hours after the exercise, he had a pain in the loins with oliguria, headache, and nausea. On admission, his serum uric acid was decreased despite the elevation of serum creatinine (9.5 mg/dL). The level of creatine kinase was normal and there was no myoglobinuria or urolithiasis. Magnetic resonance imaging showed no significant abnormality. Renal function improved completely within 2 weeks of hydration treatment. After remission, hypouricemia became obvious (1.0 mg/dL) from the initial level of uric acid (6.1 mg/dL) and fractional excretion of uric acid was 49%. Polymerase chain reaction of a urate anion exchanger known to regulate blood urate level (SLC22A12 gene: URAT1) demonstrated that homozygous mutations in exon 4 (W258X). Both parents showed heterozygous mutation of the URAT1 gene, but both siblings showed no mutation. Thus, we describe a Japanese sumo wrestler of familial renal hypouricemia complicated with anaerobic exercise-induced ARF, with definite demonstration of genetic abnormality in the responsible gene, URAT1.

摘要

家族性肾性低尿酸血症是一种遗传性疾病,其特征为肾脏尿酸清除率异常增高,并与急性肾衰竭(ARF)相关。一名18岁的相扑选手在无氧运动后发生了ARF。运动数小时后,他出现腰部疼痛,伴有少尿、头痛和恶心。入院时,尽管血清肌酐升高(9.5mg/dL),但其血清尿酸降低。肌酸激酶水平正常,无肌红蛋白尿或尿路结石。磁共振成像未显示明显异常。经补液治疗2周内肾功能完全恢复。缓解后,尿酸血症从初始尿酸水平(6.1mg/dL)明显降低至1.0mg/dL,尿酸分数排泄率为49%。对已知调节血尿酸水平的尿酸阴离子交换体(SLC22A12基因:URAT1)进行聚合酶链反应,结果显示外显子4存在纯合突变(W258X)。父母双方均显示URAT1基因杂合突变,但两个兄弟姐妹均未显示突变。因此,我们描述了一名患有家族性肾性低尿酸血症并合并无氧运动诱发ARF的日本相扑选手,并明确证实了致病基因URAT1存在基因异常。

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