Beneficial effect of thyroxin in the treatment of ischemic acute renal failure.

To evaluate the effect of thyroxin (T4) on recovery from ischemic acute renal failure, rats were treated with T4 (10 or 20 micrograms/100 g body wt.) or normal saline (NS) either immediately prior to, immediately after or 24 h after 45 min of renal ischemia. Animals given T4 prior to ischemia had no significant increase in Inulin clearance (Cin) (377 +/- 40 microliters/min per 100 g body wt.) as compared with saline-treated ischemic controls (306 +/- 54). In contrast, animals treated immediately after ischemia with either dose of T4 demonstrated significantly better kidney function (Cin 515 +/- 59 microliters/min per 100 g body wt., Uosm 842 +/- 88 mosmol/kg, FENa 0.52% +/- 0.12% and Cin 543 +/- 71, Uosm 939 +/- 103, FENa 0.48 +/- 0.12, for 10 and 20 micrograms/100 g body wt., respectively). Moreover, the improvement in renal function was sustained and Cin was significantly better at day 3 (748 +/- 70) and day 7 (990 +/- 75) compared with saline controls (560 +/- 30 and 732 +/- 45, respectively). Animals which received T4 24 h after ischemia showed significantly higher Cin when compared with ischemic controls. To assess the impact of T4 on recovery of renal ATP, 31P-NMR was used. T4-treated rats demonstrated 90% +/- 5% recovery of renal ATP by 120 min of reflow, whereas NS animals had only 64% +/- 1%. In addition, cellular morphology was better preserved in T4 animals. These data indicate that animals treated postischemically with T4 showed accelerated and sustained recovery from acute renal failure. This beneficial effect appears to be related to cellular mechanisms which are essential for the restoration of sublethally injured cells.