[Acquired resistance to acute renal failure in cisplatin-induced renal failure of rats].
Studies were performed to investigate whether prior cisplatin-induced acute renal failure affords resistance to a second challenge with cisplatin in Sprague-Dawley rats. Both the increase in serum creatinine and tubular damage following a challenge with cisplatin (5 mg/kg, i. p.) were significantly less in rats which had received cisplatin (3 mg/kg, i. p.) 14 days prior to the rechallenge compared with the previously untreated animals. Attenuation of nephrotoxicity was more obvious in the histological index than in the increase in serum creatinine, and increase in serum creatinine concentration did not correlate with tubular necrosis. There were fewer tubular cells that expressed proliferating cell nuclear antigen in previously treated kidneys, suggesting that the enhanced regeneration of tubular cells plays a minor role in the decrease of tubular damage in kidneys recovering from prior acute renal failure. These findings suggest that rats recovering from previous acute renal failure are resistant to a second insult with cisplatin and that the attenuation of nephrotoxicity is more prominent in histological damage than in functional disturbance.
Ming
C J
CJ
First Department of Medicine, Hamamatsu University School of Medicine, Japan.
Ohishi
K
K
Yonemura
K
K
Hishida
A
A
D058186:Acute Kidney Injury / Q000139:chemically induced* / Q000473:pathology; D000818:Animals; D002452:Cell Count; D002455:Cell Division; D002945:Cisplatin / Q000008:administration & dosage / Q000009:adverse effects*; D004351:Drug Resistance; D008297:Male; D018809:Proliferating Cell Nuclear Antigen / Q000032:analysis*; D051381:Rats; D017207:Rats, Sprague-Dawley
D018809:Proliferating Cell Nuclear Antigen; D002945:Cisplatin