Rhabdomyolysis (RM) can be induced by severe muscles injury, strenuous exercise, intrinsic metabolic of muscle cells, and the toxic effects of chemical, physical, or biological agents. Myoglobin induced tubular obstruction, renal vasoconstriction, inflammation and apoptosis play a key role in rhabdomyolysis-associated kidney damage. Lipid peroxidation of renal tubular epithelial cells mediated by myoglobin is closely related to glutamate metabolism, whichinduce renal proximal tubular ferroptosis through a variety of signal molecules. Ferroptosis plays a key role in myoglobin induced acute renal injury (AKI). Desferrioxamine is an iron chelator that inhibits lipid peroxidation by reducing myoglobin-derived acute kidney injury. However, it is limited in clinical practice because of its hydrophilic properties and direct nephrotoxic effects.. Deferoxamine conjugated to adamantyl derivatives, which obtains lipophilic capacity. Baicalein, a kind of traditional Chinese medicine, can enhance cellular anti-ferroptosis capacity, which may be a potential therapeutic agent for ferroptosis-associated tissue injury. Myoglobin can be removed by high cut off hemofiltration (HCO), which has become the preferred treatment mode of renal replacement of RM-induced AKI.