Related Subjects:
|PTH Physiology
|Calcium Physiology
|Magnesium Physiology
|Calcitonin
|Hypocalcaemia
|Hypercalcaemia
|Hypomagnesaemia
|Hypermagnesaemia
|Primary Hyperparathyroidism
|Familial hypocalciuric hypercalcaemia (FHH)
|Sarcoidosis
๐งช Secondary Hyperparathyroidism is driven by low calcium, high phosphate, and vitamin D deficiency โ often due to chronic kidney disease (CKD). This triggers a compensatory rise in PTH, which can eventually become autonomous (progressing to tertiary hyperparathyroidism).
๐ About
- Defined as a compensatory increase in PTH secretion in response to chronic hypocalcaemia and hyperphosphataemia.
- Most commonly associated with CKD, but also occurs in vitamin D deficiency and malabsorption syndromes.
- Chronic stimulation of parathyroid glands may cause nodular hyperplasia and, over time, autonomous function โ tertiary hyperparathyroidism.
๐ Causes
- ๐ณ Low Vitamin D intake/deficiency โ impaired calcium absorption.
- ๐ง Chronic Kidney Disease โ reduced calcium reabsorption, phosphate retention, โ 1ฮฑ-hydroxylase activity โ โ calcitriol (active vitamin D).
- Malabsorption syndromes (e.g. coeliac disease, IBD).
โ๏ธ Aetiology & Pathophysiology
- CKD is the primary driver of SHPT due to reduced excretion of phosphate and impaired vitamin D metabolism.
- Resulting hypocalcaemia stimulates parathyroid glands to increase PTH secretion ๐ฆด.
- With persistent stimulation, parathyroid glands undergo hyperplasia and may lose feedback control โ tertiary hyperparathyroidism.
๐ฉบ Clinical Features
- Often subtle, dominated by features of underlying CKD.
- Renal osteodystrophy โ bone pain, fractures, skeletal deformities.
- Vascular & soft tissue calcification โ increased cardiovascular morbidity and mortality ๐.
- Pruritus, muscle weakness, and extraskeletal calcification may develop.
๐ฌ Investigations
- ๐งช Biochemistry:
- โ Urea & Creatinine (reduced eGFR, CKD).
- โ or normal calcium.
- โ Phosphate (due to retention).
- โ 1,25(OH)โ Vitamin D.
- โ ALP (due to increased bone turnover).
- โ PTH (appropriate compensatory rise).
- ๐ฆด X-rays: subperiosteal erosions, osteitis fibrosa cystica, osteomalacia.
- Bone density scans may reveal osteopenia/osteoporosis.
๐ Management
- ๐ฝ๏ธ Diet: Low-phosphate diet + phosphate binders (e.g. calcium carbonate, sevelamer).
- โ๏ธ Vitamin D analogues: Alfacalcidol or calcitriol to suppress PTH and correct hypocalcaemia.
- ๐งช Cinacalcet: Calcimimetic agent used if PTH remains >85 pmol/L despite other measures.
- ๐ช Parathyroidectomy: For refractory cases or severe bone disease.
- Optimisation of CKD management (dialysis, transplant consideration).
๐ References