Cadmium Induced Nephrotoxicity

Abstract

Cadmium (Cd) is an extremely hazardous and non-essential metal that has significantly damaged the environment due to human activities. It mostly affects the kidneys, liver, lungs, and bones, triggering serious health concerns for both humans and animals. Previous literature on Cd toxicity demonstrated that the kidney is a major target for Cd deposition. The primary site for cadmium accumulation in the kidneys within the nephrons is the proximal tubule that generates oxidative stress, which results in reactive oxygen species (ROS), which in turn causes mitochondrial malfunction, inflammation, fibrosis, and apoptotic cell death. Prolonged exposure to cadmium impairs renal processes such as tubular reabsorption and glomerular filtration, leading to proteinuria and glucosuria. Due to its lengthy biological half-life (20–30 years), cadmium also causes chronic toxicity. Biomarkers such as kidney injury molecule-1 (KIM-1) and low molecular weight proteins in urine are essential for the early diagnosis of cadmium nephrotoxicity. The studies on examination of the kidney tissues revealed that heavy metal exposure, specifically cadmium, was found to cause tubular degeneration, fibrosis, and vacuolation. This review article summarizes the cellular and molecular mechanisms of Cadmium, as well as its pharmacokinetics and exposure sources that results in nephrotoxicity