Cisplatin-induced acute kidney injury model in rats : a biochemical and histopathological study

Background. Cisplatin has been used to induce an animal model of toxin-induced acute kidney injury (AKI). Cisplatin-induced AKI is characterized by lack of correlation between functional parameters and the degree of kidney injury. The aim of the present study is to explain such lack of correlation by evaluating the extent of apoptosis in cisplatin-induced AKI in comparison to the pathological finding by light microscope.
Methods. A single intraperitoneal injection of cisplatin was used to induce AKI in rats. Animals received either saline, cisplatin (5 mg/kg), or cisplatin (7.5 mg/kg). Surviving animals were sacrificed 5 and 10 days after drug injection. Survival rate, serum creatinine, blood urea nitrogen (BUN), body weight, apoptosis, and renal tissue damage were determined.
Results. In rats sacrificed at the 5th day, serum creatinine and BUN were elevated but did not show any significant differences between the two cisplatin-injected groups. Mortality was significantly higher in the 7.5-mg group. Renal tissue damage in the 5 mg-group was limited to the layer of the outer strip of the outer medulla while in the 7.5-mg group, damage involved all the layers of the kidney. Apoptosis in the 5 mg-group involved all the kidney layers.
Conclusion. In a rat model of cisplatin-induced AKI, tubular cell apoptosis might extend beyond the pathological finding by light microscope. This unrecognized renal tissue affection might partially explain the lack of correlation between kidney function parameters and the degree of renal tissue damage in this model.