Tertiary hyperparathyroidism
Effect · Ca up PTH up
Long-standing secondary hyperparathyroidism in which nodular chief-cell hyperplasia becomes autonomous, so PTH stays high even once the stimulus is removed. It belongs to years of dialysis, and classically declares itself after a successful renal transplant.
Traced from the start
- Fall in ionised calciumRise in ionised calcium
- Calcium-sensing receptor on parathyroid chief cells
- Phosphate load and hyperphosphataemia
- Osteocyte phosphate sensing
- Cholecalciferol from skin and diet
- Hepatic 25-hydroxylation
- Parathyroid hormoneFibroblast growth factor 2325-hydroxyvitamin D (calcifediol)
- Renal proximal tubule: 1-alpha-hydroxylaseRenal proximal tubule: phosphate handling
- Tertiary hyperparathyroidism
Detail
- Biochemistry
- Calcium HIGH, which is what separates it from secondary hyperparathyroidism; PTH high; phosphate variable, often high on dialysis and low after transplantation
- Setting
- Years of dialysis-dependent chronic kidney disease; commonly recognised as persistent hypercalcaemia months after a successful renal transplant
- Mechanism
- Prolonged stimulation produces nodular hyperplasia with reduced calcium-sensing receptor and vitamin D receptor expression, so the gland no longer listens to calcium
- Treatment
- Cinacalcet, or subtotal (three and a half gland) parathyroidectomy, with or without forearm autotransplantation
When it goes wrong
Persistent hypercalcaemia with a high PTH months after a successful renal transplant
Tertiary hyperparathyroidism; it drives graft dysfunction, bone disease and stones, so parathyroidectomy is considered
Practise this structure
1 question in the bank tagged Parathyroid.