Bone disease: Renal Osteodystrophy
The term 'renal osteodystrophy' embraces the various forms of bone disease which may develop alone or in combination in chronic renal failure - hyperparathyroid bone disease, osteomalacia, osteoporosis and osteosclerosis. Covert renal osteodystrophy is present in many patients with moderate renal impairment and in almost all of those with end-stage renal failure.
Decreased renal production of the 1α-hydroxylase enzyme results in reduced conversion of 25-(OH) 2 D 3 to the more metabolically active 1,25-(OH) 2 D 3 . Receptors for this exist on the parathyroid glands, failure of occupancy of which leads to increased release of parathyroid hormone. 1,25-Dihydroxycholecalciferol deficiency also results in gut calcium malabsorption.
Phosphate retention owing to reduced excretion by the kidneys also indirectly (and probably directly) results in an increase in PTH secretion and release. PTH promotes reabsorption of calcium from bone and increased proximal renal tubular reabsorption of calcium, and this opposes the tendency to develop hypocalcaemia induced by 1,25-(OH) 2 D 3 deficiency and phosphate retention.
This 'secondary' hyperparathyroidism leads to increased osteoclastic activity, cyst formation and bone marrow fibrosis (osteitis fibrosa cystica).
Radiologically, digital subperiosteal erosions and 'pepperpot skull' are seen. Long-standing secondary hyperparathyroidism ultimately leads to hyperplasia of the glands with autonomous or 'tertiary' hyperparathyroidism in which hypercalcaemia is present.
Serum alkaline phosphatase concentration is raised in both secondary and tertiary hyperparathyroidism. Long-standing parathyroid hormone excess is also thought to cause increased bone density (osteosclerosis) seen particularly in the spine where alternating bands of sclerotic and porotic bone give rise to a characteristic 'rugger jersey' appearance.
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