Vitamin D (calcitriol) !

Vitamin D is made in sunlit skin and activated in the liver and kidney; it raises calcium and phosphate to mineralise bone.

Updated 2026-11-01

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Key facts

Activated in three places: skin (7-dehydrocholesterol + UVB light → cholecalciferol), liver (25-hydroxylase → calcidiol) and kidney (1α-hydroxylase → calcitriol).
Calcidiol (25-OH-D) is the form measured to judge stores; calcitriol is the active form.
Renal 1α-hydroxylase (CYP27B1) is stimulated by PTH and low phosphate and inhibited by FGF23.
Deficiency: rickets in children and osteomalacia in adults. Excess: hypercalcaemia.

Skin: UVB light opens a ring of 7-dehydrocholesterol (previtamin D3), which rearranges with body heat into cholecalciferol. Dark skin, sunscreen and little sun exposure reduce this synthesis.
Diet: oily fish, egg yolk and fortified foods (D3); mushrooms exposed to light (D2).
Liver: 25-hydroxylase (mainly CYP2R1) makes 25-hydroxycholecalciferol (calcidiol), with little regulation; it circulates bound to vitamin D-binding protein.
Kidney (proximal tubule): 1α-hydroxylase makes 1,25-dihydroxycholecalciferol (calcitriol). Any surplus is inactivated by 24-hydroxylase.
Action: calcitriol binds the nuclear receptor VDR. In the gut it increases calcium (calbindin) and phosphate absorption; in bone, together with PTH, it mobilises mineral; in the kidney it saves calcium.
Deficiency: little sunlight, malabsorption, liver or kidney disease; low calcium raises PTH (secondary hyperparathyroidism), which wastes phosphate in urine, and bone fails to mineralise.
Excess (almost always from supplements, or from granulomas that make calcitriol, as in sarcoidosis): hypercalcaemia, thirst, polyuria, kidney stones.
Lab: serum 25-OH-D, calcium, phosphate, alkaline phosphatase and PTH. Calcitriol is measured only in special cases (kidney disease, granulomas, genetic rickets).

Also called: Cholecalciferol (D3), Ergocalciferol (D2), Calcidiol (25-OH-D), Calcitriol (1,25-(OH)₂-D)
Formula: C₂₇H₄₄O₃
PubChem: CID 5280453

A secosteroid: a steroid with ring B opened. The hydroxyls at positions 1, 3 and 25 are what the VDR receptor recognises.
D3 (cholecalciferol) is the human and animal form; D2 (ergocalciferol) is the plant and fungal form, with an extra double bond and methyl in the side chain.

In chronic kidney disease 1α-hydroxylation fails: hypocalcaemia, secondary hyperparathyroidism and renal osteodystrophy follow; already-activated analogues are used.
Sarcoidosis, tuberculosis and some lymphomas have macrophages with their own 1α-hydroxylase and can cause hypercalcaemia.
Vitamin D-dependent rickets type 1 (CYP27B1 failure) and type 2 (VDR receptor failure) are rare genetic causes.

Think of the answer, then tap the question to see it.

Which form of vitamin D is measured to assess stores, and why?

25-hydroxyvitamin D (calcidiol): it has a long half-life and its liver production depends on supply, not on hormonal control.

Which enzyme makes calcitriol and where is it?

1α-hydroxylase (CYP27B1) in the renal proximal tubule; PTH and low phosphate stimulate it.

Why does chronic kidney disease cause hypocalcaemia?

The damaged kidney cannot 1α-hydroxylate: calcitriol falls, gut calcium absorption drops and PTH rises.

Why can sarcoidosis cause hypercalcaemia?

Granuloma macrophages have a 1α-hydroxylase that ignores PTH and overproduce calcitriol.

Molecules are shown in their neutral form, as the databases deposit them; in the cell the acids and phosphates are ionised.

Educational information, not medical advice. For any symptom, see a health professional.

Sources: Calcitriol (CID 5280453) (PubChem, NCBI, 2026) · Public domain; Vitamin D: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2026); Vitamin D Test: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2026); CYP27B1 gene: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); CYP2R1 gene: MedlinePlus Genetics (MedlinePlus, US National Library of Medicine, 2026); Textbook of Biochemistry for Medical Students, 6th ed. (Jaypee Brothers Medical Publishers (Vasudevan DM, Sreekumari S, Vaidyanathan K), 2011).

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Representative model, for educational purposes only.