Fosfathomeostase

Fosfathomeostase refers to the physiological regulation of phosphate levels in the body to support essential processes such as energy metabolism, nucleic acid synthesis, signaling, and bone mineralization. Phosphate circulates in the blood, is taken up from the diet in the intestine, stored largely in bone, and excreted by the kidneys. Maintaining appropriate plasma phosphate is important for cellular function and acid-base balance.

The regulation of phosphate involves three main compartments: the gut, bone, and kidney. Intestinal absorption occurs via sodium-dependent phosphate transporters, while renal reabsorption takes place mainly in the proximal tubule through sodium-phosphate cotransporters. Bone serves as a large reservoir that can release or store phosphate in response to metabolic needs. Hormonal signals coordinate these tissues to keep serum phosphate within a narrow range.

Key regulators include parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), and vitamin D metabolites. PTH promotes renal phosphate excretion, decreasing reabsorption, and increases calcium reabsorption. FGF23 lowers serum phosphate by reducing renal phosphate reabsorption and by inhibiting 1,25-dihydroxyvitamin D synthesis. Active vitamin D (1,25(OH)2D) enhances intestinal phosphate absorption, contributing to the overall balance. Kidney function is a major determinant of phosphate levels, so disturbances in renal handling can disrupt fosfathomeostase.

Clinical relevance centers on hyperphosphatemia and hypophosphatemia. Elevated phosphate commonly occurs in chronic kidney disease and can contribute to vascular calcification and bone disorders. Low phosphate can arise in malnutrition, refeeding syndrome, or certain genetic disorders. Management typically targets dietary phosphate intake, renal handling, and hormonal regulation.