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Low level kidney cadmium and effects on urinary alpha-1-microgloblin

机译:低水平的肾脏镉及其对尿中α-1-微球蛋白的影响

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Background: Cadmium (Cd) can cause renal damage after high-level exposure. Recently such effects have been shown also at low-level exposure, as measured by Cd in blood or urine. Using urinary Cd may, however, result in erroneous conclusions. Associations with Cd in kidney biopsies from a healthy population have not been examined previously. As cadmium damages the proximal tubular cells, the reabsorption of low-molecular-weight (LMW) proteins is decreased and results in increased urinary excretion. One of the most commonly used biomarkers linked to cadmium nephrotoxicity is the LMW protein alpha-1-microglobulin (A1M). Aims: The aim of this study was to explore the relation between kidney Cd and urinary excretion of alpha-1-microglobulin in kidney donors, representing the healthy part of the general population Methods: Cd was determined in kidney cortex biopsies from 109 living kidney donors. A1M and creatinine was analyzed in overnight and 24-hour urine samples. Correlations between single variables were assessed by Spearman correlation coefficients. Associations between urinary A1M and kidney Cd and background variables were assessed using multiple linear regression with backward elimination. Results: In spite of relatively low kidney Cd levels (median 13 μg/g, range 1.5-55 μg/g) kidney Cd and urinary A1M were positively associated, with significant correlations both in 24-hour and overnight samples. In multivariate analyses, there were significant associations between kidney Cd and creatinine-adjusted A1M in never-smokers, both in 24-hour and overnight urine, in a model including age, sex and weight. Conclusions: This study provides support for an association in the general population between kidney Cd levels and urinary excretion of A1M, a biomarker for kidney damage. The results further confirm the importance of preventing environmental pollution by cadmium.
机译:背景:镉(Cd)在高水平暴露后会导致肾脏损害。最近,在血液或尿液中的Cd含量低的情况下,也显示出这种影响。但是,使用尿镉可能会得出错误的结论。先前尚未检查健康人群肾脏活检中镉与镉的关联。由于镉损害近端肾小管细胞,低分子量(LMW)蛋白的重吸收减少,并导致尿排泄增加。 LMW蛋白α-1-微球蛋白(A1M)是与镉的肾毒性相关的最常用的生物标记物之一。目的:本研究的目的是探讨代表正常人群的肾脏供体中肾脏镉与尿中α-1-微球蛋白排泄之间的关系。方法:从109个活体肾脏供体的肾皮质活检组织中测定镉。在过夜和24小时尿液样本中分析了A1M和肌酐。通过Spearman相关系数评估单个变量之间的相关性。使用多元线性回归与向后消除方法评估尿中A1M与肾脏Cd和背景变量之间的关联。结果:尽管肾脏Cd水平较低(中位数13μg/ g,范围1.5-55μg/ g),肾脏Cd和尿A1M仍呈正相关,在24小时和过夜样品中均具有显着相关性。在多变量分析中,在包括年龄,性别和体重的模型中,从不吸烟者的24小时和过夜尿液中,肾脏Cd和肌酐校正后的A1M之间存在显着相关性。结论:这项研究为一般人群中肾脏Cd水平与尿液A1M排泄之间的联系提供了支持,A1M是肾脏损害的生物标志物。结果进一步证实了防止镉污染环境的重要性。

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