In accordance with this hypothesis, it has been reported that oxidative stress plays a crucial role in the pathogenesis of RM-AKI by validating the increase in the renal concentration of 8-OHdG (8-hydroxy-2’-deoxyguanosine), an indicator of lipid peroxidation [21,22] and malondialdehyde (MDA), an indicator of oxidative stress, and a decrease in the renal levels of superoxide dismutase (SOD), an antioxidant enzyme [23–25]. Here, SOD1 is linked to acute kidney injury.