Major clinical sequelae usually occur only in severe hypophosphatemia. Hypophosphatemia is caused by the intracellular shift of phosphate from serum into cells, increased urinary excretion of phosphate, or decreased intestinal absorption of phosphate. Hypophosphatemia may be transient, reflecting intracellular shift with minimal clinical consequences. The disease also may reflect a deeper state of total body phosphate depletion with significant sequelae. Intracellular shift Respiratory alkalosis moves phosphate into cells by activating phosphofructokinase, which stimulates intracellular glycolysis.
Glycolysis leads to phosphate consumption as phosphorylated glucose precursors are produced.
Since respiratory alkalosis is one of the most common causes of hypophosphatemia, discovery of hypophosphatemia should prompt a search for the serious causes of hyperventilation. Administering carbohydrate lowers serum phosphate by stimulating the release of insulin, which moves phosphate and glucose into cells. Catecholamines and beta-receptor agonists also stimulate phosphate uptake into cells. In most cases of intracellular phosphate shift, serum phosphate normalizes once the precipitating cause is removed. Increased urinary excretion Since parathyroid hormone stimulates the kidneys to excrete phosphate, hypophosphatemia is a common sequela of primary and secondary hyperparathyroidism.