Secondary hyperparathyroidism and hypoparathyroidism
- Mechanism
When calcium stays low, the parathyroids grow to compensate. When they are lost, or the body ignores PTH, calcium falls.
What it is
Secondary hyperparathyroidism is a compensatory response to chronic hypocalcaemia, most often from chronic kidney disease, and sometimes from vitamin D deficiency or malabsorption. All four glands become hyperplastic, and after years one or more may become autonomous (tertiary). Hypoparathyroidism is the opposite: too little PTH, most often after neck surgery. In pseudohypoparathyroidism PTH is high but the tissues cannot respond because of GNAS defects.
Step by step
- Failing kidneys retain phosphate and make less calcitriol.
- Phosphate binds calcium, calcitriol deficiency lowers gut absorption, FGF23 rises: serum calcium falls.
- Low calcium and high phosphate stimulate all parathyroid glands to grow and secrete.
- High PTH resorbs bone (osteitis fibrosa) and calcium phosphate deposits in vessels and soft tissue.
- After years, a nodule within the hyperplastic glands may become autonomous: tertiary hyperparathyroidism.
Parathyroid disorders by calcium and PTH
| Disorder | Calcium | Phosphate | PTH | Main cause |
|---|---|---|---|---|
| Primary hyperparathyroidism | High | Low | High | Adenoma |
| Secondary hyperparathyroidism | Low or normal | High in CKD, low in vitamin D deficiency | High | CKD, vitamin D deficiency |
| Tertiary hyperparathyroidism | High | Variable | Very high | Long-standing CKD |
| Hypoparathyroidism | Low | High | Low | Neck surgery, autoimmunity, 22q11.2 deletion |
| Pseudohypoparathyroidism | Low | High | High | GNAS loss, end-organ resistance |
Clinical notes
- Hypocalcaemia: tetany, perioral numbness, Chvostek and Trousseau signs, prolonged QT, seizures, basal ganglia calcification, cataracts.
- Calciphylaxis: painful necrotic skin lesions from calcified small vessels in dialysis patients.
- Magnesium deficiency both reduces PTH secretion and causes PTH resistance.
Test yourself
Think of the answer, then tap the question to see it.
Why do the parathyroid glands become hyperplastic in chronic kidney disease?
Phosphate retention, low calcitriol and low calcium all stimulate PTH secretion and gland growth.
What is tertiary hyperparathyroidism?
Autonomous PTH secretion with hypercalcaemia after long-standing secondary hyperparathyroidism, often persisting after kidney transplant.
Why does the parent of origin matter in GNAS loss?
GNAS is imprinted in some tissues: maternal loss causes hormone resistance plus Albright osteodystrophy; paternal loss gives the physical features only.
Elsewhere in DurgiPedia
- Calcium regulation: PTH, vitamin D and calcitonin
- Vitamin D (calcitriol)
- Genomic imprinting: Prader–Willi and Angelman
- Trisomies 21, 18 and 13, and the 22q11.2 deletion
Connections
Educational content on the mechanisms of disease; not a diagnostic or treatment guide and no substitute for a health professional's advice. No doses are given.
Sources: Hyperparathyroidism: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025); Hypoparathyroidism: MedlinePlus Medical Encyclopedia (MedlinePlus, US National Library of Medicine, 2025).
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Representative model, for educational purposes only.