ACCELERATED RECOVERY FROM TOXIC ACUTE-RENAL-FAILURE WITH THYROXINE - STIMULATION OF RENAL PHOSPHOLIPID BIOSYNTHESIS

Thyroxine (T4) seems to accelerate recovery from various forms of acut e renal failure. The mechanisms of this effect are still debated. We d ecided to evaluate if thyroxine enhances the recovery of HgCl2 renal f ailure through an increment in the mitotic activity or through an incr ease in membrane phospholipid biosynthesis of the regenerating tubular cells. Male Wistar rats were allocated to four groups: one group rece ived 0.4 mg/100 g BW HgCl2 SC and saline IP (HgCl2 group); the second received the toxin and 24 and 48 h after it, T4 15 mu g/100 g BW IP (H gCl2 + T4 group); a third group received saline SC and T4 IP (T4 group ), and the last group received saline SC and IP (control group). On th e third day GFR was evaluated by 24-h creatinine clearance and afterwa rd rats were sacrificed and the kidneys removed. Some of them were stu died histologically, evaluating the severity of the tubular lesion usi ng a semiquantitative score (0-4) and the mitotic index (N mitotic fig ures per 10 high-power fields). Itt the other kidneys we studied phosp holipid synthesis through the incorporation of 32 P into the different renal phospholipids of the several kidney regions. The T4-treated gro up had a better recovery of GFR after the toxin (HgCl2 + T4: 0.44 +/- .09 vs. HgCl2: 0.23 +/- .06, p <.05). Both HgCl2-treated groups had si milar lesional scores and mitotic indexes. Phospholipid synthesis, eva luated as the % change of 32 P incorporation to phosphatidylcholine co mpared to control rats, showed a 21% decrease in incorporation in the HgCl2 group and a 95% increase in the HgCl2 + T4 group in the outer me dulla. We conclude that T4 accelerates the recover of HgCl2 through an increase in membrane phospholipid biosynthesis, and not through an in crease in the replication of tubular cells.