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尿钙作为镉暴露普通人群肾功能障碍的生物标志物。

Urinary calcium as a biomarker of renal dysfunction in a general population exposed to cadmium.

作者信息

Wu X, Jin T, Wang Z, Ye T, Kong Q, Nordberg G

机构信息

Department of Occupational Health, School of Public Health, Fudan University, 138# Yixue Yuan Road, Shanghai 200032 China.

出版信息

J Occup Environ Med. 2001 Oct;43(10):898-904. doi: 10.1097/00043764-200110000-00009.

Abstract

Urinary beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase have been recommended as sensitive indicators of renal dysfunction induced by cadmium. However, an increase in urinary calcium in early renal damage induced by cadmium has been reported both in humans and in animal experiments. To investigate the feasibility of using urinary calcium as a biomarker of renal dysfunction induced by cadmium, two areas were selected in this study, namely, a polluted area with a 3.71 mg/kg cadmium concentration in rice and a control area with a 0.07 mg/kg cadmium concentration. The total number of participants was 499, made up of 252 in the control group and 247 from the cadmium-polluted area. Urinary cadmium, urinary calcium, and zinc concentrations were measured by atomic absorption spectrometry, and beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase in urine were analyzed. The levels of urinary cadmium and urinary calcium in persons from the exposed area were significantly higher (P < 0.05) than those in the control area for both men and women, but there was no significant difference regarding urinary zinc between the two areas. A significant dose-response relationship between the prevalence of hypercalciuria and the excretion of urinary cadmium was observed, and a significantly increased prevalence of calciuria was found when excretion of urinary cadmium exceeded 2 micrograms/g creatinine. The findings were similar to those for excess urinary secretion of beta 2-microglobulin and N-acetyl-beta-D-glucosaminidase. Because cadmium can affect Ca2+ uptake by tubular cells, with decreased renal Ca2+ reabsorption, calciuria may reflect tubular cell damage caused by cadmium. It was concluded that cadmium exposure can result in increased excretion of urinary calcium in a general population and that there is a significant dose-response relationship. Urinary calcium can therefore be used as a biomarker of renal dysfunction induced by cadmium.

摘要

尿β2-微球蛋白和N-乙酰-β-D-氨基葡萄糖苷酶已被推荐作为镉诱导的肾功能障碍的敏感指标。然而,在人类和动物实验中均报告了镉诱导的早期肾损伤中尿钙增加。为了研究将尿钙用作镉诱导的肾功能障碍生物标志物的可行性,本研究选择了两个地区,即大米中镉浓度为3.71mg/kg的污染区和镉浓度为0.07mg/kg的对照区。参与者总数为499人,其中对照组252人,镉污染区247人。采用原子吸收光谱法测定尿镉、尿钙和锌浓度,并分析尿中β2-微球蛋白和N-乙酰-β-D-氨基葡萄糖苷酶。暴露区人群的尿镉和尿钙水平在男性和女性中均显著高于对照区(P<0.05),但两区尿锌水平无显著差异。观察到高钙尿患病率与尿镉排泄之间存在显著的剂量反应关系,当尿镉排泄超过2μg/g肌酐时,发现钙尿患病率显著增加。这些发现与β2-微球蛋白和N-乙酰-β-D-氨基葡萄糖苷酶尿分泌过多的情况相似。由于镉可影响肾小管细胞对Ca2+的摄取,导致肾脏Ca2+重吸收减少,钙尿可能反映了镉引起的肾小管细胞损伤。得出的结论是镉暴露可导致普通人群尿钙排泄增加,且存在显著的剂量反应关系。因此,尿钙可作为镉诱导的肾功能障碍的生物标志物。

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