Abstract
The effect of acute renal failure on plasma vitamin A concentration was examined to clarify the role of kidney in vitamin A homeostasis. Male Sprague-Dawley rats with sufficient vitamin A stores were nephrectomized or sham-operated. Three hours after surgery plasma retinol concentration of nephrectomized rats had increased to 5.30±0.42 nmol/mL as compared to 2.88±0.32 nmol/mL observed in sham-operated controls; this elevated retinol level was maintained for at least 24h. A time course study of the response to short-term nephrectomy was performed in rats whose body stores of vitamin A were replaced by radiolabeled vitamin A. As early as 1 h after nephrectomy plasma retinol increased by 35% compared to sham-operated controls. Chromatography of plasma proteins on Sephadex G-100 revealed that most of the labeled retinoids were associated with the fraction characteristic of retinol binding protein (RBP)-transthyretin complex in both nephrectomized and control rats; the retinoid in this protein was identified to be retinol. Very little retinoid and protein were associated with the elution area characteristic of holo-and apo-RBP. Our observations in the short-term nephrectomized rats differ from those in chronic renal failure patients, who are reported to have increased holo-and apo-RBP. In rats with low liver stores of vitamin A, there was no increase in plasma retinol concentration after nephrectomy. Our studies suggest a direct involvement of kidney in vitamin A homeostasis by regulating retinol release from liver and by regulating excretion and reutilization of vitamin A.
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