Aminoaciduria and glycosuria following severe childhood lead poisoning

被引:30
作者
Loghman-Adham, M [1 ]
机构
[1] Univ Utah, Sch Med, Dept Internal Med, Div Nephrol & Hypertens, Salt Lake City, UT 84132 USA
关键词
lead poisoning; proximal tubule; Fanconi syndrome;
D O I
10.1007/s004670050441
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
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.
引用
收藏
页码:218 / 221
页数:4
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