Define Hyperparathyroidism & Renal Osteodystrophy. Describe its clinical features and complications.

Definition & Physiology

Parathyroid hormone (PTH) raises the serum calcium by mobilising it from bone (stimulating osteoclasts), increasing renal calcium reabsorption and phosphate excretion, and activating vitamin D. Hyperparathyroidism — excess PTH — therefore causes bone resorption and characteristic skeletal and biochemical changes. It is classified as primary, secondary or tertiary.

Skeletal Manifestations

Excess PTH drives osteoclastic bone resorption, producing osteitis fibrosa cystica: subperiosteal bone resorption (classically along the radial borders of the phalanges), a ‘salt-and-pepper’ skull, generalised osteopenia, and brown tumours (localised osteoclastic ‘tumours’ — lytic lesions that can mimic a neoplasm and cause pathological fracture).

Renal Osteodystrophy

Renal osteodystrophy is the complex bone disease of chronic kidney disease. Failing kidneys retain phosphate and cannot activate vitamin D, causing hypocalcaemia that drives secondary hyperparathyroidism. The resulting bone disease is a mixture of osteitis fibrosa (from high PTH), osteomalacia (defective mineralisation) and osteoporosis — part of the wider ‘CKD–mineral and bone disorder’ with vascular calcification.

Investigations & Management

• Biochemistry defines the type (calcium, phosphate, PTH, vitamin D, renal function, alkaline phosphatase)
• imaging shows subperiosteal resorption and brown tumours
• localisation studies (ultrasound, sestamibi) find a parathyroid adenoma.
• Primary hyperparathyroidism is treated by parathyroidectomy (or monitoring if mild).
• Secondary/renal disease is managed medically — phosphate binders, active vitamin D analogues and calcimimetics, with control of the CKD
• refractory (tertiary) disease may need parathyroidectomy.

Clinical Features of Hypercalcaemia

• When primary hyperparathyroidism raises the serum calcium, the patient may develop the features summarised as ‘stones, bones, abdominal groans and psychic moans’: renal stones and nephrocalcinosis and polyuria
• bone pain and the changes of osteitis fibrosa
• abdominal symptoms including constipation, peptic ulceration and pancreatitis
• neuropsychiatric features such as fatigue, depression, poor concentration and, when severe, confusion. Many cases today, however, are detected incidentally through a raised calcium on routine testing before symptoms appear.

Complications

The complications of hyperparathyroidism reflect both the high calcium and the bone disease: renal stones, nephrocalcinosis and progressive renal impairment; pathological fractures through brown tumours and osteitis fibrosa; peptic ulceration and pancreatitis; and, in severe hypercalcaemia, a hypercalcaemic crisis with dehydration, confusion and cardiac arrhythmia. In renal osteodystrophy the wider CKD–mineral and bone disorder brings vascular and soft-tissue calcification that contributes to the high cardiovascular mortality of chronic kidney disease, so control of phosphate and PTH is important well beyond the skeleton.

Subperiosteal erosion of the radial side of middle phalanges is classic.

• PTH raises calcium (bone resorption, renal Ca reabsorption, vit D activation, phosphate excretion).
• Primary (adenoma; ↑Ca ↑PTH), secondary (CKD/vit-D deficiency; ↓/normal Ca ↑PTH), tertiary (autonomous).
• Bone: osteitis fibrosa cystica — subperiosteal resorption, salt-and-pepper skull, brown tumours.
• ‘Stones, bones, groans, moans’ in primary disease.
• Primary → parathyroidectomy; renal → phosphate binders, vitamin D analogues, calcimimetics.