Related Subjects:
|PTH Physiology
|Calcium Physiology
|Magnesium Physiology
|Calcitonin
|Hypocalcaemia
|Hypercalcaemia
|Hypomagnesaemia
|Hypermagnesaemia
|Primary Hyperparathyroidism
|Familial hypocalciuric hypercalcaemia (FHH)
|Sarcoidosis
๐ About
- Tertiary hyperparathyroidism develops after prolonged secondary hyperparathyroidism ๐ (usually from chronic kidney disease, CKD).
- Due to parathyroid hyperplasia becoming autonomous โ PTH secretion continues even after correction of hypocalcaemia.
- Biochemically characterised by hypercalcaemia โฌ๏ธ (unlike secondary HPT, which is usually normo- or hypocalcaemic).
๐ฉบ Clinical Features
- Occurs in the context of advanced CKD or post-renal transplant.
- Features of hypercalcaemia: "stones, bones, abdominal groans, and psychiatric moans" ๐ชจ๐ฆด๐.
- Bone disease (renal osteodystrophy), pruritus, muscle weakness.
- Vascular and soft-tissue calcification โ cardiovascular risk ๐.
๐ฌ Investigations
- CKD markers: โฌ๏ธ Urea and Creatinine.
- Biochemical profile:
- โฌ๏ธ Calcium
- โฌ๏ธ Phosphate
- โฌ๏ธ Alkaline phosphatase (ALP)
- โฌ๏ธ PTH (markedly elevated)
- โฌ๏ธ 1,25(OH)โ Vitamin D (impaired renal activation)
- Imaging: Sestamibi parathyroid scan (for localisation if considering surgery).
- DEXA scanning may show low bone density.
โ๏ธ Management
- ๐ฏ Definitive therapy โ Parathyroidectomy (subtotal or total with autotransplantation).
- ๐ Cinacalcet (calcimimetic) useful for patients unsuitable for surgery or awaiting transplant.
- Vitamin D analogues (e.g. alfacalcidol, calcitriol) may help suppress PTH.
- Phosphate binders and dietary phosphate restriction to control โฌ๏ธ phosphate.
- Conservative management may be considered in frail/elderly patients if hypercalcaemia is controlled medically.
๐ References