Akesson Agneta, Lundh Thomas, Vahter Marie, Bjellerup Per, Lidfeldt Jonas, Nerbrand Christina, Samsioe Göran, Strömberg Ulf, Skerfving Staffan
Institute of Environmental Medicine, Division of Metals and Health, Karolinska Institutet, Stockholm, Sweden.
Environ Health Perspect. 2005 Nov;113(11):1627-31. doi: 10.1289/ehp.8033.
Cadmium is a well-known nephrotoxic agent in food and tobacco, but the exposure level that is critical for kidney effects in the general population is not defined. Within a population-based women's health survey in southern Sweden (Women's Health in the Lund Area, WHILA), we investigated cadmium exposure in relation to tubular and glomerular function, from 1999 through early 2000 in 820 women (71% participation rate) 53-64 years of age. Multiple linear regression showed cadmium in blood (median, 0.38 microg/L) and urine (0.52 microg/L; density adjusted = 0.67 microg/g creatinine) to be significantly associated with effects on renal tubules (as indicated by increased levels of human complex-forming protein and N-acetyl-beta-D-glucosaminidase in urine), after adjusting for age, body mass index, blood lead, diabetes, hypertension, and regular use of nephrotoxic drugs. The associations remained significant even at the low exposure in women who had never smoked. We also found associations with markers of glomerular effects: glomerular filtration rate and creatinine clearance. Significant effects were seen already at a mean urinary cadmium level of 0.6 microg/L (0.8 microg/g creatinine). Cadmium potentiated diabetes-induced effects on kidney. In conclusion, tubular renal effects occurred at lower cadmium levels than previously demonstrated, and more important, glomerular effects were also observed. Although the effects were small, they may represent early signs of adverse effects, affecting large segments of the population. Subjects with diabetes seem to be at increased risk.
镉是食品和烟草中一种广为人知的肾毒性物质,但对于一般人群肾脏产生影响的关键暴露水平尚未明确。在瑞典南部一项基于人群的女性健康调查(隆德地区女性健康调查,WHILA)中,我们于1999年至2000年初对820名53 - 64岁的女性(参与率71%)的镉暴露与肾小管和肾小球功能的关系进行了调查。多元线性回归显示,在调整了年龄、体重指数、血铅、糖尿病、高血压以及是否经常使用肾毒性药物后,血液中镉(中位数为0.38微克/升)和尿液中镉(0.52微克/升;密度校正后为0.67微克/克肌酐)与肾小管效应显著相关(尿液中人类复合蛋白和N - 乙酰 - β - D - 氨基葡萄糖苷酶水平升高表明了这一点)。即使在从不吸烟女性的低暴露水平下,这种关联仍然显著。我们还发现了与肾小球效应标志物的关联:肾小球滤过率和肌酐清除率。在平均尿镉水平为0.6微克/升(0.8微克/克肌酐)时就已观察到显著影响。镉增强了糖尿病对肾脏的影响。总之,肾小管效应在比之前所证明的更低的镉水平下就已出现,更重要的是,还观察到了肾小球效应。尽管这些影响较小,但它们可能代表了不良影响的早期迹象,影响着很大一部分人群。糖尿病患者似乎风险更高。