Suggested mechanisms for AK-induced nephropathy include mitochondrial damage with increased ROS production together with declines in renal antioxidant molecules (e.g., GSH/SOD/GPx1/CAT), thus promoting the formation of free radicals, lipid peroxides, and protein adducts that subsequently provoke renal cell damage [3, 4, 7, 9]. This evidence concerns the gene SOD1 and kidney disorder.