Secondary hyperparathyroidism
Effect · PTH up Ca low or normal
A correct response by normal glands to a persistent hypocalcaemic stimulus, usually vitamin D deficiency or chronic kidney disease. PTH is high while calcium is low or low-normal; the serum phosphate tells you which cause you are looking at.
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
- Secondary hyperparathyroidism
Detail
- Vitamin D deficiency pattern
- 25(OH)D low, calcium low-normal, phosphate LOW, PTH high, alkaline phosphatase high
- Chronic kidney disease pattern
- Phosphate HIGH, calcitriol low, calcium low or normal, PTH high, FGF23 high
- Other causes
- Malabsorption, chronic hypocalcaemia of any cause, hyperphosphataemia, and drugs that accelerate vitamin D catabolism
- Management
- Correct the stimulus: cholecalciferol for deficiency; dietary phosphate restriction, phosphate binders, active vitamin D analogues and calcimimetics in chronic kidney disease
When it goes wrong
A high PTH reported with a normal or low serum calcium
Secondary, not primary: measure 25(OH)D, creatinine and phosphate before ever considering the parathyroid glands
Vitamin D deficiency treated with calcium supplements alone
PTH stays high and the skeleton keeps demineralising; the vitamin D itself must be replaced
Practise this structure
1 question in the bank tagged Parathyroid.