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Background: Improved life expectancy of children with chronic renal failure (CRF) has increased the number of patients with renal osteodystrophy and has brought to light novel and severe forms of the disease. These factors have contributed to the need to evaluate new, noninvasive imaging modalities for the detection of bone involvement., Objectives: To evaluate the potential of MRI in the detection of the bone changes of renal osteodystrophy as compared to conventional X-rays., Materials and Methods: Fourteen children with CRF were examined with a 0.5-T MR unit using TI-weighted and STIR sequences and conventional radiographs. The following features were reviewed in a nonblinded study: skeletal deformities, thickening of cortical bone, trabecular pattern, intraosseous soft-tissue masses, osteonecrosis, extraskeletal calcifications and bone marrow signal changes., Results: MRI adequately demonstrated skeletal deformities, cortical thickening and irregular trabecular pattern. It showed osteonecrosis and intraosseous soft-tissue masses more conspicuously than X-ray. In addition, it revealed diffuse nonspecific signal changes in the bone marrow., Conclusion: MRI is a potentially useful tool for evaluating the bone changes of renal osteodystrophy.

One of the most important complication of patients with chronic renal failure is osteodystrophy. This causes skeletal deformities, growth failure, bone pain and decreased physical activity. Osteodystrophy is more frequent among children than uraemic adults. In fact, 50-80% of children with chronic renal failure may occur in metabolic bone disease and the incidence tends to be higher in those children who have been in uraemic state for a long time before starting chronic haemodialysis. Osteodystrophy is a result of: 1) lesions of rickets; 2) lesions of osteitis fibrosa: 3) osteosclerosis. In contrast to adult, metastatic calcifications are virtually never observed in uraemic children. Hyperphosphoraemia, that is secondary to the reduction of G.F.R., may be the principal responsible of hyperparathyroidism that is the main cause of osteodystrophy. Hyperparathyroidism is also maintained and increased by deficit of 1,25(OH)2D3 which is responsible for lesions of rickets. Haemodialysis may markedly improve osteitis fibrosa and it is efficacious in reversing the mineral defect. Dialysate calcium concentration should be maintained at approximately 3,5 mEq/l. In this case we can raise serum calcium. On the contrary dialysate has to be lacking in phosphorus to correct hyperphosphoraemia. It must be noted that we have to prepare a dialysate with deionized water lacking in aluminum to avoid encephalopathy compliance.