reduction in the concentration of phosphate in the blood serum, thus disrupting the body's energy metabolism and impairing the delivery of oxygen through the bloodstream to the tissues. Hypophosphatemia usually occurs in conjunction with other metabolic disturbances that affect the normal equilibrium between the blood circulation, the intestinal absorption of nutrients, the loss of phosphate through the kidneys, and the storage of phosphate in the bones and red blood cells. Defects in any one of these areas or, more often, in a combination of areas will reduce phosphate levels in the blood. Acute hypophosphatemia causes such neurological symptoms as weakness, tingling, depressed reflexes, tremors, and confusion. Chronic hypophosphatemia, in which a prolonged deficiency depletes the body's normal phosphate stores, causes generalized debility, weakness, and anorexia. Treatment in either case involves correction of the underlying metabolic disturbance and phosphate supplements to replenish the body's stores of that nutrient.

Familial hypophosphatemia is a sex-linked inherited disorder that is a principal cause of rickets (q.v.) in the developed nations. Familial hypophosphatemia is caused by a metabolic defect that leads to the loss of phosphate through the kidneys. The resulting low concentration of phosphate in the blood results in the reduced deposition in the bones of calcium phosphate, which is the substance responsible for the rigidity of bone. The result, in children, is the curved and stunted bones that are the chief symptoms of rickets.