PDF(Pubmed)
Abstract：
Kidney disease associated with chronic cadmium (Cd) exposure is primarily due to proximal tubule cell damage. This results in a sustained decline in glomerular filtration rate (GFR) and tubular proteinuria. Similarly, diabetic kidney disease (DKD) is marked by albuminuria and a declining GFR and both may eventually lead to kidney failure. The progression to kidney disease in diabetics exposed to Cd has rarely been reported. Herein, we assessed Cd exposure and the severity of tubular proteinuria and albuminuria in 88 diabetics and 88 controls, matched by age, gender and locality. The overall mean blood and Cd excretion normalized to creatinine clearance (Ccr) as ECd/Ccr were 0.59 µg/L and 0.0084 µg/L filtrate (0.96 µg/g creatinine), respectively. Tubular dysfunction, assessed by β2-microglobulin excretion rate normalized to Ccr(Eβ2M/Ccr) was associated with both diabetes and Cd exposure. Doubling of Cd body burden, hypertension and a reduced estimated GFR (eGFR) increased the risks for a severe tubular dysfunction by 1.3-fold, 2.6-fold, and 84-fold, respectively. Albuminuria did not show a significant association with ECd/Ccr, but hypertension and eGFR did. Hypertension and a reduced eGFR were associated with a 3-fold and 4-fold increases in risk of albuminuria. These findings suggest that even low levels of Cd exposure exacerbate progression of kidney disease in diabetics.
摘要：
与慢性镉（Cd）暴露相关的肾脏疾病主要是由于近端小管细胞损伤。这导致肾小球滤过率(GFR)和肾小管性蛋白尿的持续下降。同样，糖尿病肾病(DKD)以蛋白尿和GFR下降为特征,两者都可能最终导致肾衰竭.很少报道暴露于Cd的糖尿病患者向肾脏疾病的进展。在这里，我们评估了88位糖尿病患者和88位对照者的Cd暴露和肾小管蛋白尿和白蛋白尿的严重程度，与年龄相匹配,性别和地域。按ECd/Ccr归一化为肌酐清除率（Ccr）的总平均血液和Cd排泄为0.59µg/L和0.0084µg/L滤液（0.96µg/g肌酐），分别。肾小管功能障碍,通过标准化为Ccr（Eβ2M/Ccr）的β2-微球蛋白排泄率评估与糖尿病和Cd暴露有关。镉的身体负担加倍，高血压和估计GFR（eGFR）降低使严重肾小管功能障碍的风险增加1.3倍，2.6折,84倍，分别。白蛋白尿与ECd/Ccr无显著相关性，但高血压和eGFR确实如此。高血压和eGFR降低与蛋白尿风险增加3倍和4倍相关。这些发现表明，即使低水平的Cd暴露也会加剧糖尿病患者肾脏疾病的进展。
