Abstract
It seems well established that acute administration of vitamin D enhances renal reabsorption of sodium, phosphate and calcium in the dog and in the rat (1–5). These effects are thought to be the result of vitamin D action on the proximal tubule (1,2). Vitamin D deficiency secondary either to inadequate dietary intake or to intestinal malabsorption may be associated with the development of metabolic acidosis. This metabolic acidosis has been attributed to the secondary hyperparathyroidism of vitamin D deficiency (6,7). Pharmacological doses of parathyroid hormone depress renal bicarbonate reabsorption but not to a level low enough to result in metabolic acidosis (8,9). These studies have cast doubt on the role of parathyroid hormone per se in the generation of metabolic acidosis of hyperparathyroidism. The occurrance of metabolic acidosis in vitamin D deficiency (10) suggests that vitamin D may play a role in renal hydrogen ion secretion. Accordingly, we measured bicarbonate reabsorption before and after administration of 25 hydroxycholecalciferol (25 OHD) to dogs.
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References
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Siegfried, D., Kumar, R., Arruda, J., Kurtzman, N. (1977). Influence of Vitamin D on Bicarbonate Reabsorption. In: Massry, S.G., Ritz, E. (eds) Phosphate Metabolism. Advances in Experimental Medicine and Biology, vol 81. Springer, New York, NY. https://doi.org/10.1007/978-1-4613-4217-5_40
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DOI: https://doi.org/10.1007/978-1-4613-4217-5_40
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