Metabolism and secretion of retinol transport complex in acute renal failure.

Tissue uptake and distribution of retinol from circulatory vitamin A transport complex was studied in order to determine the origin of the increased serum retinol in rats with short-term acute renal failure. In rats with acute renal failure, serum retinol increased 37-70% within 2 h after surgery. After an injection of donor plasma containing 1.8 muCi of [3H]retinol in retinol transport complex, in rats with renal failure the ability to clear radioactivity was decreased 36% by 0.5 h and 57% by 2 h, as compared to sham-operated rats. The uptake and distribution of radioactivity by nonrenal tissues was similar in rats with acute renal failure and with intact kidneys. The lack of renal function did not alter hepatic cycling of [3H]retinol from the circulation and thus could not account for the increased serum retinol in renal failure. When hepatic release of retinol-retinol binding protein was blocked by colchicine, the up-regulation of serum retinol, normally observed in rats with acute renal failure, was abolished. Our studies provide strong evidence that kidney has an important role in maintaining serum retinol homeostasis by influencing the release of retinol-retinol binding protein from liver into circulation. Peripheral tissue uptake of circulatory retinol and hepatic cycling of nonutilized retinol are not directly influenced by the kidney.