Paediatric Imaging

Renal osteodystrophy

a general term used to describe the bony changes associated with chronic renal disease, usually seen in late childhood. Chronic renal tubular dysfunction (e.g. vitamin D-resistant rickets, Fanconis syndrome and renal tubular acidosis result in urinary loss of calcium or phosphate causing deficient mineralization of growing bones and rickets. Chronic renal glomerular dysfunction, e.g. chronic glomerulonephritis inhibits phosphate excretion and resorption of calcium resulting in a high serum phosphate and low serum calcium which stimulates excretion of parathyroid hormone causing secondary hyperparathyroidism. Glomerular defects may also complicate end-stage renal tubular disease, causing radiographic features of both rickets and secondary hyperparathyroidism in these children.

The radiographic changes of rickets associated with renal osteodystrophy are similar to rickets from other causes. The rapidity of bone changes is dependent on age, being much more rapid in young infants than in older children. The changes are most marked at the ends of rapidly growing long bones with apparent physeal widening (representing a widened zone of provisional calcification), metaphyseal flaring, cupping and irregularity. There is frequently coxa vara and slipped capital femoral epiphysis (SCFE). However, the radiographic features of secondary hyperparathyroidism may predominate: these include focal areas of subperiosteal bone resorption and osteopenia. Common sites of involvement include the radial aspect of the phalanges, distal radius, distal clavicle, symphysis pubis, sacroiliac joints and lateral aspect of the femoral neck. At these sites the cortical margins become indistinct and there is rarefaction and subperiosteal resorption of bone (Fig.1). In some patients there may be generalized increase in bone density with indistinct trabecular architecture. Osteosclerosis of the vertebral end plates may cause a "rugger jersey" spine. Ectopic calcification may occur including subcutaneous, vascular and periarticular calcifications. Renal osteodystrophy is also associated with slipped epiphyses particularly the capital femoral epiphysis. This is much more common than in other forms of rickets and probably reflects the chronicity of the disorder and metaphyseal resorption due to the more marked secondary hyperparathyroidism in renal osteodystrophy than other forms of rickets. In severe long-standing cases brown tumour may develop, these are rounded lucencies with indistinct margins seen particularly within the pelvis or long bones (Fig.2), they may thin and expand the cortex and are prone to pathological fractures. Blood tests show low serum calcium, increased phosphate and ALP, markedly increased PTH and markedly reduced 25 and 1,25 dihydroxyvitamin D. Management involves management of the primary renal disease by dialysis or renal transplantation. Occasionally parathyroidectomy is required to control the hyperparathyroidism.

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Fig.2

Knee radiograph demonstrating a Brown tumour in the proximal right fibular metaphysis. In addition, there is increased bone density secondary to renal osteodystrophy.
Renal osteodystrophy, Fig.1
Renal osteodystrophy, Fig.2