Fosfathomeostasen

Fosfathomeostasen, or phosphate homeostasis, is the physiological regulation of phosphate balance in body fluids and tissues to support energy metabolism, signaling, and bone mineralization. Most phosphate is stored in bone as hydroxyapatite, while a smaller fraction circulates in serum; normal fasting serum phosphate in adults is typically about 0.8–1.5 mmol/L (2.5–4.5 mg/dL).

Diet provides phosphate, which is absorbed mainly in the small intestine. Calcitriol (active vitamin D) promotes intestinal phosphate absorption and is modulated by dietary load and hormonal signals. In the kidney, proximal tubule reabsorption of phosphate occurs via sodium-phosphate cotransporters NaPi-IIa and NaPi-IIc. Reabsorption is inhibited by parathyroid hormone (PTH) and fibroblast growth factor 23 (FGF23), increasing urinary excretion. FGF23 also suppresses 1α-hydroxylase, lowering calcitriol production and further reducing intestinal phosphate absorption.

Bone serves as a reservoir, releasing phosphate during resorption and storing it during formation, under the regulatory influence of PTH, FGF23, and calcitriol. The system maintains phosphate within a narrow range to enable ATP production, nucleic acid synthesis, and cellular signaling, while supporting proper bone mineralization.

Clinical relevance: disturbances can cause hypophosphatemia or hyperphosphatemia. Hypophosphatemia can impair energy metabolism and bone health; hyperphosphatemia is associated with vascular calcification, especially in chronic kidney disease. Disorders include X-linked hypophosphatemic rickets and tumor-induced osteomalacia. Management may involve dietary adjustments, phosphate supplementation or binders, and modulation of vitamin D and FGF23 signaling where appropriate.