Phosphate metabolism disorders

Abstract

Serum phosphate levels are tightly regulated by vitamin D, parathyroid hormone (PTH), and fibroblast growth factor-23 (FGF-23). In particular PTH and FGF-23 decrease renal phosphate reabsorption by proximal tubular epithelial cells via phosphate transporters NPT2a and c. Disturbances of hormone regulation or carrier function may cause hypo- or hyperphosphatemia. In addition, phosphate shifts between the intracellular and extracellular space or decreased or increased gastrointestinal phosphate uptake may cause these disturbances. Severe hypophosphatemia causes energy depletion of cells with consecutive symptoms. Hypophosphatemia is treated by oral phosphate supplementation. Intravenous phosphate therapy should be restricted to symptomatic cases. Severe hyperphosphatemia may occur with massive cytolysis or ingestion of excessive amounts of phosphate. Complications include hypocalcemia and renal failure due to acute phosphate nephropathy. If necessary, severe hyperphosphatemia needs to be treated by hemodialysis. Recent evidence suggests that high normal phosphate levels may be associated with increased cardiovascular risk.