Accelerated Recovery from Toxic Acute Renal Failure with Thyroxin: Stimulation of Renal Phospholipid Biosynthesis

Abstract

Thyroxine (T4) seems to accelerate recovery from various forms of acute renal failure. The mechanisms of this effect are still debated. We decided to evaluate if thyroxine enhances the recovery of HgCl₂ renal failure through an increment in the mitotic activity or through an increase in membrane phospholipid biosynthesis of the regenerating tubular cells. Male Wistar rats were allocated to four groups: one group received 0.4 mg/100g BW HgCl₂ SC and saline IP (HgCl₂ group); the second received the toxin and 24 and 48 h after it, T4 15 µg/100g BW IP (HgCl₂ +T4 Diuretics in Acute Renal Failure group); a third group received saline SC and T4 IP (T4 group), and the last group received saline SC and IP (control group). On the third day GFR was evaluated by 24-h creatinine clearance and afterward rats were sacrificed and the kidneys removed. Some of them were studied histologically, evaluating the severity of the tubular lesion using a semiquantitative score (0–4) and the mitotic index (N mitotic figures per 10 high-power fields). In the other kidneys we studied phospholipid synthesis through the incorporation of 32 P into the different renal phospholipids of the several kidney regions. The T4-treated group 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 similar lesional scores and mitotic indexes. Phospholipid synthesis, evaluated as the % change of 32 P incorporation to phosphatidylcholine compared 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 medulla. We conclude that T4 accelerates the recover of HgCl₂ through an increase in membrane phospholipid biosynthesis, and not through an increase in the replication of tubular cells.