Phosphate regulation and the FGF23 arm

Phosphate is co-regulated with calcium so the calcium×phosphate product stays below precipitation: the FGF23 lowering arm returns a phosphate load to setpoint. The phosphate set-point is the renal threshold TmP/GFR, here computed exactly (Walton–Bijvoet) and cross-checked to the adult reference range; FGF23 lowers it. Only γ-prediction of the absolute value stays open.

Phosphate is co-regulated with calcium so that the calcium×phosphate product stays below precipitation. FGF23 (the osteocyte arm) is the phosphate-lowering effector: a phosphate load raises FGF23, which drives phosphaturia and lowers phosphate.

The FGF23 lowering arm

A phosphate load raises FGF23 (the negative-feedback lowering arm), which increases renal phosphate excretion and returns phosphate to setpoint (final 1.000). The calcium×phosphate product stays below the precipitation threshold (maximum 1.399, normalized), protecting against vascular calcification and stones.

The renal threshold TmP/GFR (computed, not deferred)

The phosphate set-point IS the renal threshold TmP/GFR: plasma phosphate is held near it, and above it phosphate spills into urine. It is computed exactly from measurable inputs by the Walton–Bijvoet nomogram — an invented number is not needed:

stateTmP/GFR (mmol/L)in reference 0.80–1.35
high FGF23 (XLH-type)0.450no — low → hypophosphatemia
normal1.114yes
low FGF23 / PTH (hypoPTH-type)2.342no — high → hyperphosphatemia

FGF23 and PTH lower the threshold (the phosphaturic direction), reproduced as the monotone fall high-FGF23 < normal < low-FGF23. The residual open item is now precise [O]: γ sets loop stability (barrier b=γ²/4 → gain k), not the absolute value — so predicting the TmP/GFR number from γ alone stays open by design; the value is clinical [CAL] / exact-algebra [F], cross-checked to the adult reference range [L].