Aminoaciduria and glycosuria following severe childhood lead poisoning
Aminoaciduria and glycosuria following severe childhood lead poisoning
复制标题
DOI：
10.1007/s004670050441
复制
发表时间：
1998-04-01
影响因子：
3
通讯作者：
Loghman-Adham, M
中科院分区：
文献类型：
--
作者：
Loghman-Adham, M
为了确定铅中毒后肾功能异常的发生率，我们评估了134名儿童和年轻人在重度铅中毒螯合治疗后8-13年的肾小管功能参数。通过血清肌酐（Cr）浓度评估，无高血压或肾功能降低的证据。与19名年龄匹配的健康对照组相比，尿α-氨基氮（U-aan）浓度显著升高。94名儿童（70%）有氨基酸尿（U-aan/Cr > 0.23）。尿糖排泄也显著高于2个历史对照。32名儿童（24%）有糖尿（> 125 mg/24 h）。所有儿童的磷酸盐排泄分数均正常。我们的结论是，部分范可尼综合征可以持续长达13年后，儿童铅中毒。
To determine the incidence of renal functional abnormalities after lead poisoning, we evaluated the parameters of renal tubular function in 134 children and young adults, 8-13 years after chelation therapy for severe lead poisoning. There was no evidence of hypertension or reduced kidney function as assessed by serum creatinine (Cr) concentrations. Urinary alpha-amino nitrogen (U-aan) concentrations were significantly increased compared with 19 healthy age-matched controls. Ninety-four children (70%) had aminoaciduria (U-aan/Cr > 0.23). Urinary glucose excretion was also significantly higher than that of 2 historical controls. Thirty-two children (24%) had glycosuria (> 125 mg/24 h). Fractional excretion of phosphate was normal in all children. We conclude that a partial Fanconi syndrome can persist up to 13 years after childhood lead poisoning.