Acute Nephrotoxicity of Cisplatin: Molecular mechanisms Authors

Nephrotoxic drugs are responsible for approximately 20% of the episodes of acute kidney injury (AKI) in hospital and outpatient settings. Among elderly individuals, the incidence of drug-induced nephrotoxicity can be as high as 66%. Cisplatin (cis-diamminedichloroplatinum II CDDP) is an oncologic medication included in most chemotherapy regimens for solid or hematologic tumors. Cisplatin’s antineoplastic properties were accidentally discovered by biophysicist Barnett Rosenberg, but nephrotoxicity was found to be a significant limiting factor for up to The nephrotoxic drugs have been responsible for about 20% of AKI episodes in inpatients and outpatients. The cisplatin nephrotoxicity is a major limiting factors in 20% of patients who have received the drug, triggering injuries in renal tubular epithelialcells. Cisplatin toxicity is determined by the target tissue and cells accumulation besides the interaction with various subcellular structures and macromolecules. Cisplatin accumulates and interferes with the functioning of different organelles such as mitochondria, lysosomes, endoplasmic reticulum, nuclei and cell membranes, causing inflammation and cell death. This review aims to define the pathophysiology and biochemistry of the cisplatin nephrotoxicity, reviewing the main molecular mechanisms that lead to tubular cisplatin toxicity. AbstrAct