Dysfunction on tubular protein reabsorption in Cadmium-induced Acute Kidney Injury

Cadmium (Cd2+) is a transition heavy metal widely distributed in the environment being a health public problem. Humans keep in touch with this metal by various sources such as cigarettes, galvanizing industry and products, batteries, water contaminated and seafood. The long-term exposure of Cd2+ causes tissular accumulation associated with different pathological conditions including acute kidney injury (AKI). However, the mechanism involved in this process still poorly known. In this context, there is a strict correlation between development of tubule-interstitial injury and tubular reabsorption of proteins in renal cortex.