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 g/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 (C_in) (377±40 l/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 (C_in 515±59 l/min per 100 g body wt., U_osm 842±88 mosmol/kg, FE_Na 0.52%±0.12% and C_in 543±71, U_osm 939±103, FE_Na 0.48±0.12, for 10 and 20 g/100 g body wt., respectively). Moreover, the improvement in renal function was sustained and C_in 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 C_in 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.