Ferroptosis, a newly identified form of programmed cell death, is characterized by iron-dependent lipid peroxidation and oxidative stress. It has been implicated in various kidney diseases, including acute kidney injury (AKI), chronic kidney disease (CKD), polycystic kidney disease (PKD), diabetic nephropathy (DN), lupus nephritis (LN), and clear cell renal cell carcinoma (ccRCC). Ferroptosis is regulated by multiple pathways, including iron metabolism, cysteine metabolism, glutathione peroxidase 4 (GPX4) inactivation, polyunsaturated fatty acid (PUFA) synthesis, and the Nrf2 and p53 signaling pathways. In AKI, ferroptosis is associated with tubular cell death and oxidative stress, while in CKD, it contributes to renal fibrosis. In PKD, ferroptosis promotes cyst growth, and in DN, it is linked to oxidative stress and lipid accumulation. Ferroptosis also plays a role in the progression of ccRCC and LN, with iron accumulation and oxidative stress being key factors. Therapeutic approaches targeting ferroptosis include ferroptosis inhibitors such as ferrostatin-1 and small-molecule inhibitors like vitamin E and rosiglitazone. Natural compounds and traditional Chinese medicine have also shown potential in modulating ferroptosis. Understanding the role of ferroptosis in kidney diseases could lead to new therapeutic strategies for their prevention and treatment.Ferroptosis, a newly identified form of programmed cell death, is characterized by iron-dependent lipid peroxidation and oxidative stress. It has been implicated in various kidney diseases, including acute kidney injury (AKI), chronic kidney disease (CKD), polycystic kidney disease (PKD), diabetic nephropathy (DN), lupus nephritis (LN), and clear cell renal cell carcinoma (ccRCC). Ferroptosis is regulated by multiple pathways, including iron metabolism, cysteine metabolism, glutathione peroxidase 4 (GPX4) inactivation, polyunsaturated fatty acid (PUFA) synthesis, and the Nrf2 and p53 signaling pathways. In AKI, ferroptosis is associated with tubular cell death and oxidative stress, while in CKD, it contributes to renal fibrosis. In PKD, ferroptosis promotes cyst growth, and in DN, it is linked to oxidative stress and lipid accumulation. Ferroptosis also plays a role in the progression of ccRCC and LN, with iron accumulation and oxidative stress being key factors. Therapeutic approaches targeting ferroptosis include ferroptosis inhibitors such as ferrostatin-1 and small-molecule inhibitors like vitamin E and rosiglitazone. Natural compounds and traditional Chinese medicine have also shown potential in modulating ferroptosis. Understanding the role of ferroptosis in kidney diseases could lead to new therapeutic strategies for their prevention and treatment.