Kuntziger H, Altman J J
Rev Prat. 1989 Apr 13;39(11):949-53.
Disorders of phosphate metabolism are caused by a disrupted balance between intestinal absorption and renal excretion or by an altered distribution between intra- and extracellular pools. Hyperphosphatemia per se does not have any clinical effects except for ectopic calfifications. The most frequent cause is chronic renal disease. Other causes - increased tubular reabsorption as seen for instance un hypoparathyroïdism; increased intertinal absorption as seen with vitamin D excess; redistribution to the extracellular pool, as seen with the tumor lysis syndrome, are uncommon; and no one cause is outstanding in frequency. Hypophosphatemia is frequent caused by a redistribution of phosphate to the cellular pool, associated for instance with respiratory alkalosis or infusion of glucose and fructose. Hyperphosphaturia as a cause of hypophosphatemia is seen in primary and secondary hyperparathyroïdism as well as in familial hypophosphatemic rickets. Decreased intake of phosphate may be secondary to intravenous hyperalimentation, chronic ingestion of phosphate-binding antacids or vitamin D deficiency. Hypophosphatemia does not appear to produce any harmful effects. However acute hypophosphatemia, if it occurs in the presence of preexisting cellular injury and phosphate depletion, as in chronic alcoholic patients for instance, has been implicated as a cause of severe clinical syndromes. Chronic hypophosphatemia in children may induce rickets, and osteomalacia in adults.
