Diabetic Kidney Disease Associated with Chronic Exposure to Low Doses of Environmental Cadmium

Accumulating evidence suggests that exposure to pollution from environmental cadmium (Cd) contributes to diabetic kidney disease as indicated by albuminuria and a progressive decrease in the estimated glomerular filtration rate (eGFR). This study examined the effects of Cd exposure on eGFR and the excretion rates of albumin (Ealb) and β2-microglobulin (Eβ2M) in 65 diabetics and 72 controls. Excretion of Cd (ECd) was a measure of exposure, while excretion of N-acetylglucosaminidase (ENAG) reflected the extent of kidney tubular cell injury. In participants with an elevated excretion of Eβ2M, the prevalence odds ratios (POR) for a reduced eGFR rose 6.4-fold, whereas the POR for albuminuria rose 4.3-fold, 4.1-fold, and 2.8-fold in those with a reduced eGFR, diabetes, and hypertension, respectively. Using covariance analysis, which adjusted for the interactions, 43% of the variation in Ealb among diabetics could be explained by female gender (η2 = 0.176), ENAG (η2 = 0.162), hypertension (η2 = 0.146), smoking (η2 = 0.107), and body mass index (η2 = 0.097), while the direct contribution of ECd to Ealb variability was minimal (η2 = 0.005). Results from a mediating-effect analysis imply that Cd could contribute to albuminuria and a falling eGFR through inducing tubular cell injury, leading to reduced reabsorption of albumin and β2M.