Gargah Tahar, Essid Afif, Labassi Aymen, Hamzaoui Mourad, Lakhoua Mohamed Rachid
Department of Pediatrics, Charles Nicolle Hospital, Bab Saadoun, Tunisia.
Saudi J Kidney Dis Transpl. 2010 Mar;21(2):328-31.
Hereditary xanthinuria type I, a defect of purine metabolism, results from a genetic deficiency of xanthine oxidase. It is an uncommon cause of stone formation in children. We report here two children with xanthine urolithiasis. The first patient was an 8-year-old boy who presented with repeated episodes of hematuria evaluated with excretory urography, which demonstrated radio-lucent pelvic stone in the right kidney, causing hydronephrosis. He had pyelolithotomy, and the extracted stone consisted of pure xanthine. Family study revealed an asymptomatic xanthinuria in younger brother. The second patient was a 5-year-old boy who had a 2-week history of abdominal pain and gross hematuria. Conventional excretory intravenous urography showed a non-functioning right kidney. Nephrectomy was performed, and histology revealed end-stage pyelonephritis. The calculi consisted of pure xanthine. In both patients, plasma and urinary concentrations of uric acid were low but xanthine and hypoxanthine concentrations were markedly elevated. Xanthine urolithiasis is usually a benign condition, easy to prevent or cure by appropriate alkalinization, forced hydration and restriction of dietary purines. However asymptomatic, and therefore undiagnosed, stones may invade the kidney and urinary tract, resulting in destruction of parenchyma, nephrectomy and renal failure.
I型遗传性黄嘌呤尿症是一种嘌呤代谢缺陷病,由黄嘌呤氧化酶的基因缺陷引起。它是儿童结石形成的罕见原因。我们在此报告两例患有黄嘌呤尿路结石的儿童。首例患者为一名8岁男孩,因反复血尿就诊,经排泄性尿路造影评估,显示右肾有透光性肾盂结石,导致肾积水。他接受了肾盂切开取石术,取出的结石为纯黄嘌呤结石。家族研究显示其弟弟有无症状性黄嘌呤尿症。第二例患者为一名5岁男孩,有2周腹痛和肉眼血尿病史。传统的排泄性静脉尿路造影显示右肾无功能。进行了肾切除术切除术切除术,组织学检查显示为终末期肾盂肾炎。结石由纯黄嘌呤组成。两名患者的血浆和尿液尿酸浓度均较低,但黄嘌呤和次黄嘌呤浓度明显升高。黄嘌呤尿路结石通常是一种良性疾病,通过适当的碱化、强制水化和限制饮食中的嘌呤,易于预防或治愈。然而,无症状且因此未被诊断出的结石可能会侵犯肾脏和尿路,导致实质破坏、肾切除和肾衰竭。