Phosphorous Depletion and Vitamin D Metabolism
In man, phosphate deprivation (or depletion) is reportedly attended by decreased renal tubular reabsorption of sodium, magnesium, bicarbonate, uric acid and glucose, red cell dysfunction with decreased concentrations of 2,3-DPG and ATP, platelet abnormalities with thrombocytopenia, impairment of clot retraction, shortened survival time and decreased ATP levels, decreased leucocytic ATP concentrations with suppressed phagocytic, chemotactic and bacterocidal activities, central nervous system dysfunction characterized by varying degrees of numbness, dysarthria, paresthesiaes, convulsive diatheses, and coma, rhabdomyolysis and myalgia, abnormal hepatic cellular function, hypercalciuria, occasional hypercalcemia, augmentation of the intestinal absorption of calcium, hypophosphatemia and elevations in circulating 1,25(OH)2D in women (1–5). These latter alterations in calcium metabolism when documented in phosphate deprived laboratory animals (predominantly rats), have been attended by increased bone resorption (6,7) and stimulated renal 1-hydroxylase activity with more rapid conversion of 25OHD3 to 1,25(OH)2D3 (8–10). Stimulated 1-hydroxy-lase activity has also been documented in vitro using renal tubular mitochondrial preparations from hypophosphatemic chicks (11).
KeywordsCalcium Balance Intestinal Calcium Absorption Idiopathic Hypercalciuria Phosphate Depletion Phosphate Deprivation
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