In the treatment of solid tumors, one of the most common chemotherapeutic agents is cisplatin. The binding of cisplatin to DNA causes the death of neoplasms, while nephrotoxicity is the main downside of this therapy. In a rat model of cisplatin nephrotoxicity, damage even part of the proximal tubule (PK) occurs. Epithelial-mesenchymal transition (EMT) manifests itself through unique molecular and morphological changes, wherein cells undergo alterations in protein expression, lose polarity, differentiation, and epithelial barrier function. Previously observed cytoskeletal changes in actin and tubulin in PK epithelial cells, along with a change in the expression of intermediate protein vimentin, would indicate whether EMT occurs in cisplatin nephrotoxicity. Archival nephrotoxicity model samples were used after a single treatment with cisplatin (i.p. at a dose of 5 mg/kg) in male Wistar rats. The most pronounced toxicity effect occurs on the 5th day after treatment, during which the time course of EMT was also monitored. Vimentin distribution was observed through immunofluorescence on tissue sections. The presence of vimentin was monitored in the homogenates of kidney tissue by western blot analysis, while changes in the expression of messenger RNA were monitored using endpoint RT-PCR technique. The appearance of vimentin expression was observed over time (day 3) in tissue sections, and a change in the presence of proteins in tissue homogenates was found on day 5. The nephrotoxicity of cisplatin has not yet been fully elucidated, and our results indicate an involvement of EMT that can explain the loss of kidney function, pointing to defense mechanisms against secondary tumors and nephrotoxicity in patients treated with cisplatin.