Abstract

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 (E<inf>alb</inf>) and β<inf>2</inf>-microglobulin (E<inf>β2M</inf>) in 65 diabetics and 72 controls. Excretion of Cd (E<inf>Cd</inf>) was a measure of exposure, while excretion of N-acetylglucosaminidase (E<inf>NAG</inf>) reflected the extent of kidney tubular cell injury. In participants with an elevated excretion of E<inf>β2M</inf>, 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 E<inf>alb</inf> among diabetics could be explained by female gender (η² = 0.176), E<inf>NAG</inf> (η² = 0.162), hypertension (η² = 0.146), smoking (η² = 0.107), and body mass index (η² = 0.097), while the direct contribution of E<inf>Cd</inf> to E<inf>alb</inf> 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 β<inf>2</inf>M.