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[一名因尿酸分泌后重吸收缺陷导致特发性肾性低尿酸血症的男孩出现运动诱发的急性肾衰竭]

[Exercise-induced acute renal failure observed in a boy with idiopathic renal hypouricemia caused by postsecretary reabsorption defect of uric acid].

作者信息

Tazawa M, Morooka M, Takeichi S, Minowa S, Yasaki T

机构信息

Department of Pediatrics, Fujita Health University School of Medicine, Aichi, Japan.

出版信息

Nihon Jinzo Gakkai Shi. 1996 Sep;38(9):407-12.

PMID:8913093
Abstract

Acute renal failure without oliguria developed in an 11-year boy after running exercise. With improvement of his renal function, marked hypouricemia became apparent (0.8-0.9 mg/dl). Increased excretion of uric acid into the urine, increased clearance ratio of uric acid against creatinine (CUA/CCr), normal concentration of plasma xanthine and hypoxanthine, and suppression of CUA/CCr ratio by pyrazinamide loading but not by probenecid, were observed in the patient and his two siblings, suggesting that hereditary abnormalities of reabsorption of uric acid after secretion from the renal tubules resulted in the hypouricemia. The mechanism of acute renal failure in this disease remains unknown.

摘要

一名11岁男孩跑步锻炼后出现非少尿型急性肾衰竭。随着肾功能改善,明显出现显著低尿酸血症(0.8 - 0.9mg/dl)。在该患者及其两名同胞中观察到,尿酸尿排泄增加、尿酸对肌酐的清除率比值(CUA/CCr)升高、血浆黄嘌呤和次黄嘌呤浓度正常,以及吡嗪酰胺负荷试验可抑制CUA/CCr比值,而丙磺舒则无此作用,提示肾小管分泌后尿酸重吸收的遗传性异常导致了低尿酸血症。该疾病中急性肾衰竭的机制尚不清楚。

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[Renal hypouricemia].[肾性低尿酸血症]
Nihon Rinsho. 1996 Dec;54(12):3337-42.

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