Mild hypophosphatemia is not usually associated with clinical symptoms. In severe hypophosphatemia, pts may have muscle weakness, numbness, paresthesia, and confusion. Rhabdomyolysis may develop during rapidly progressive hypophosphatemia. Respiratory insufficiency can result from diaphragm muscle weakness.

The causes of hypophosphatemia include decreased intestinal absorption (vitamin D deficiency, phosphorus-binding antacids, malabsorption); urinary losses (hyperparathyroidism, hyperglycemic states, X-linked hypophosphatemic rickets, oncogenic osteomalacia, alcoholism, or certain toxins); and shifts of phosphorus from extracellular to intracellular compartments (administration of insulin in diabetic ketoacidosis or by hyperalimentation or refeeding in a malnourished pt). In syndromes of severe primary renal phosphate wasting (X-linked hypophosphatemic rickets, autosomal dominant hypophosphatemic rickets, oncogenic osteomalacia), the phosphatonin hormone FGF23 (fibroblast growth factor 23) plays a key pathogenetic role.

Mild hypophosphatemia can be replaced orally with milk, carbonated beverages, or Neutra-Phos or K-Phos (up to 2 g/d in divided doses). For severe hypophosphatemia (0.75 mmol/L; [<2.0 mg/dL]), IV phosphate may be administered at initial doses of 0.2–0.8 mmol/kg of elemental phosphorus over 6 h. The total body phosphate depletion cannot be predicted from the serum phosphate level; careful monitoring of therapy is therefore required. Hypocalcemia should be corrected first, and the dose reduced 50% in hypercalcemia. Serum calcium and phosphate levels should be measured every 6–12 h; a serum calcium × phosphate product of >50 must be avoided.