Calcium regulation: PTH, vitamin D and calcitonin !
- Regulation
- Exam priority: high
When blood calcium falls, the parathyroid releases PTH, which pulls it from bone, saves it in the kidney and activates vitamin D.
Updated 2026-11-01
Also called: Parathyroid hormone, Calcitriol, Calcium homeostasis
See it in 3D: Parathyroid glands · Thyroid gland · Kidneys
What it is
Ionized calcium is held in a narrow range because nerves, muscles and clotting depend on it. Parathyroid chief cells sense it with a calcium-sensing receptor (CaSR) and answer within seconds with PTH. PTH acts on bone and kidney, and through calcitriol on the gut as well. Calcitonin plays a minor role in adults.
How it works, step by step
- Ionized calcium falls and stops activating the chief cell's CaSR.
- Stored PTH is released within seconds; synthesis rises within hours and the gland grows over weeks.
- In bone PTH acts on osteoblasts: RANKL rises and osteoprotegerin falls, and osteoclasts release calcium and phosphate.
- In the kidney it raises distal tubule calcium reabsorption and blocks proximal phosphate cotransport (phosphaturia).
- It also stimulates proximal tubule 1α-hydroxylase: calcitriol rises.
- Calcitriol increases gut calcium absorption; calcium normalizes and brakes PTH (and calcitriol represses its own gene).
Hormone axes and feedback
Calcium regulation (PTH, calcitriol, calcitonin)Lesion None (normal)
Tap a box to see the hormone, or choose a lesion to see the lab pattern.
- Stimulates (+)
- Inhibits / negative feedback (−)
- Level ↑
- Level ↓
Equations
- Ca
- mg/dL
- albumin
- g/dL
It is an estimate; when in doubt, ionized calcium is measured.
Adult reference values (they vary by laboratory)
| Parameter | Value | Note |
|---|---|---|
| Total calcium | ≈8.5–10.5 mg/dL (2.1–2.6 mmol/L) | |
| Ionized calcium | ≈4.5–5.3 mg/dL (1.1–1.3 mmol/L) | |
| Intact PTH | ≈10–65 pg/mL | |
| 25-OH vitamin D | sufficiency ≥20–30 ng/mL | the cut-off varies by guideline |
| Phosphate | ≈2.5–4.5 mg/dL |
Approximate values for a healthy adult at rest; each laboratory sets its own ranges.
Lab patterns
| Disorder | Ca²⁺ | PO₄³⁻ | PTH |
|---|---|---|---|
| Primary hyperparathyroidism | ↑ | ↓ | ↑ |
| Hypercalcemia of malignancy (PTHrP) | ↑ | ↓ | ↓ |
| Hypoparathyroidism (e.g., after thyroidectomy) | ↓ | ↑ | ↓ |
| Vitamin D deficiency | ↓ or normal | ↓ | ↑ |
| Secondary hyperparathyroidism of chronic kidney disease | ↓ or normal | ↑ | ↑ |
Clinical notes
- Hypocalcemia: perioral tingling, carpopedal spasm, Chvostek and Trousseau signs, long QT.
- Hypercalcemia: kidney stones, bone pain, constipation, polyuria, confusion and short QT.
- Chronic kidney disease retains phosphate and loses 1α-hydroxylase: low calcitriol and high PTH.
- Vitamin D deficiency: rickets in children and osteomalacia in adults; less common in the tropics, but it appears with little sun exposure.
Test yourself
Think of the answer, then tap the question to see it.
Why does primary hyperparathyroidism come with low phosphate?
PTH inhibits proximal tubule sodium–phosphate cotransport; the kidney wastes phosphate and its level falls, even though PTH also releases it from bone.
Why can anxious hyperventilation cause tingling and carpopedal spasm?
Respiratory alkalosis frees more negative charges on albumin, which binds more calcium; ionized calcium falls although total calcium is normal.
Why doesn't hypocalcemia in a patient with hypomagnesemia correct with calcium alone?
Magnesium is needed to secrete PTH and for PTH to act on its tissues; until it is replaced, the parathyroid cannot respond.
Why does chronic kidney disease raise PTH?
The failing kidney retains phosphate and makes little calcitriol; calcium absorption falls, ionized calcium tends to drop, and high phosphate and FGF-23 stimulate the parathyroid.
Hypercalcemia with suppressed PTH: which group of causes does it suggest?
Non-parathyroid causes: PTHrP-secreting tumors, bone metastases, calcitriol-making granulomas or vitamin D excess; the parathyroid responds normally by shutting off.
See it in 3D
The structures of Durgical's 3D anatomy where it happens.
Related topics
- Bone remodeling
- Phosphate and FGF-23
- Hormones: types, receptors and feedback
- Metabolic alkalosis and its compensation
Related conditions
- Hypocalcaemia
- Hypercalcaemia
- Primary hyperparathyroidism
- Rickets and osteomalacia
- Chronic kidney disease
In Biochemistry
Educational physiology content; not a diagnostic or treatment guide and no substitute for a health professional's advice. Values are approximate references. No doses are given.
Sources: 17.5 The Parathyroid Glands (OpenStax (Rice University), 2022); Parathyroid Hormone (PTH) Test: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2024); Primary Hyperparathyroidism (StatPearls (NCBI Bookshelf), 2024); Vitamin D Test: MedlinePlus Medical Test (MedlinePlus, US National Library of Medicine, 2024); Hall JE. Guyton and Hall Textbook of Medical Physiology, 13th ed. (ch. 80). Reference book used to check facts; its text and figures are not reproduced (Elsevier, 2016).
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Representative model, for educational purposes only.