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Phosphaturia and the phosphate arm

Effect · PTH and FGF23 both

PTH and FGF23 both dump phosphate into the urine. That is what stops the calcium-phosphate product rising when bone resorption releases the two ions together, and it explains why PTH excess lowers phosphate while renal failure, where phosphaturia is no longer possible, raises it.

Traced from the start

  1. Fall in ionised calciumRise in ionised calcium
  2. Calcium-sensing receptor on parathyroid chief cells
  3. Phosphate load and hyperphosphataemia
  4. Osteocyte phosphate sensing
  5. Parathyroid hormoneFibroblast growth factor 23
  6. Renal proximal tubule: phosphate handling
  7. Phosphaturia and the phosphate arm

Detail

PTH excess
Serum phosphate falls and urinary phosphate rises; calcitriol is high because PTH also drives the 1-alpha-hydroxylase
FGF23 excess
Serum phosphate falls but calcitriol is low or inappropriately normal, because FGF23 suppresses the same enzyme PTH stimulates: the discriminator between the two
Why it matters
The calcium x phosphate product; when phosphate cannot be excreted, calcium phosphate precipitates in vessels and soft tissue

When it goes wrong

Primary hyperparathyroidism

High calcium with a low phosphate, a raised or inappropriately normal PTH, hypercalciuria and a mild hyperchloraemic metabolic acidosis

Chronic kidney disease

Phosphate cannot be excreted despite maximal FGF23 and PTH: hyperphosphataemia, vascular and valvular calcification and calciphylaxis; managed with dietary restriction and phosphate binders

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