Figure 5.

Adrenocorticotropic hormone (ACTH) gel therapy attenuates acute kidney injury in tumor necrosis factor (TNF)–injured rats via, at least in part, a steroid-independent mechanism. Rats were pretreated with saline or ACTH gel subcutaneously at indicated doses 60 min before intravenous bolus injection of recombinant rat TNF (2 mg/kg wt). Rats were killed 8 h later and plasma and kidney specimens were collected. (a) Plasma corticosterone levels were determined by enzyme-linked immunosorbent assay and suggested that the steroidogenic response to ACTH above a dose of 5 IU/kg reaches a plateau; *P<0.05 versus other groups (n=5); ^&not significant. (b) Severity of tubulointerstitial injury was scored as stated in Figure 3 and revealed that the renoprotective effect of ACTH continues to increase with even higher doses than 5 IU/kg, suggesting that steroid-independent mechanisms also contribute to kidney protection; *P<0.05 versus other groups (n=5); ^#P<0.05.