title: Acute nephrotoxicity of cisplatin: molecular mechanisms.
abstract: 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 epithelial cells. 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.
authors.forename: Luis Alberto Batista
authors.initials: LA
authors.lastname: Peres
authors.forename: Ademar Dantas
authors.initials: AD
authors.lastname: da Cunha
mesh_terms: D058186:Acute Kidney Injury / Q000139:chemically induced*; D000970:Antineoplastic Agents / Q000009:adverse effects* / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects; D002945:Cisplatin / Q000009:adverse effects* / Q000378:metabolism; D006801:Humans; D020928:Mitogen-Activated Protein Kinases / Q000187:drug effects / Q000502:physiology; D018384:Oxidative Stress
chemical_list: D000970:Antineoplastic Agents; D020928:Mitogen-Activated Protein Kinases; D002945:Cisplatin