Backgrounds. Cisplatin (CP) still is a novel choice for solid tumor therapy, but it is accompanied with the side effect of nephrotoxicity. Hydration may reduce the risk of CP-induced nephrotoxicity, while the issue is still challenging. In this study, five types of hydration protocols including saline, mannitol, dextrose saline, saline plus furosemide, and saline plus mannitol were examined in both sexes of rats during CP therapy. Methods. Seventy-six male and female Wistar rats in 14 groups of experiments were subjected to CP therapy, and five types of hydration protocols were implemented, and the induced nephrotoxicity was evaluated via biochemical markers, kidney function parameters, and pathology investigation. Results. Male and female rats had different responses to hydration protocol types. The higher mortality rate was seen in female rats that received mannitol or dextrose hydration types. In addition, the serum levels of blood urea nitrogen (BUN) and creatinine (Cr) and sodium excretion fraction (ENa%) increased and the clearance of Cr (ClCr) decreased significantly ( P < 0.05 ) in female rats hydrated with saline plus furosemide or mannitol plus saline-treated groups. The worsened condition in male rats is observed in the mannitol hydration group with a significant decrease of ClCr and significant increase of serum BUN and Cr and ENa% ( P < 0.05 ). The higher kidney tissue damage score (KTDS) in the mentioned groups verified the findings. Conclusion. Hydration with mannitol or dextrose promotes the risk of nephrotoxicity during CP therapy with more intensity on the female.

Background: The major side effect of cisplatin (CP) therapy in patients with cancer is nephrotoxicity, which limits the treatment. In two protocols of CP treatments, we tested 3 weeks of hormone therapy against CP induced nephrotoxicity in bilateral orchiectomized (OR) and ovariectomized (OV) rats. Methods: A total of 101 OR and OV rats were subjected to receive 3 weeks of testosterone (Ts, 10 mg/kg/week) and estradiol (Es, 250 µg/kg/week), respectively, followed by two protocols of CP therapies; continuous (divided) doses (3 mg/kg/day for period of 5 days) as protocol 1 and single dose (7.5 mg/kg) as protocol 2. The measurements were performed by the end of the 4th week. Results: CP increased the serum levels of blood urea nitrogen (BUN) and creatinine (Cr) in both OR and OV rats, which were related to the protocols of CP treatments. Es (not Ts) in protocol 2 attenuated the serum levels of BUN and Cr. Ts significantly increased body weight loss in protocol 1 compared with control group (P < 0.05). Es did not attenuate kidney tissue damage score (KTDS) in protocol 1 treated animal, but KTDS was decreased by Es in protocol 2 treated Rats. Hormone replacement therapy did not alter Cr clearance compared with control group. Conclusions: It seems that hormone therapy could not protect the kidney against CP induced nephrotoxicity.