Bone disease is a very frequent complication after renal transplantation (RTx). The main features of transplant bone disease include the osteopenic-osteoporotic syndrome, often complicated by fractures, avascular osteonecrosis of bones, bone pain syndrome and growth retardation in the children. The bone loss is greater during the first 12 months after RTx and can reach the osteoporotic range in above 40% of patients, with a fracture rate of 2-3% per year. The story of bone disease over the long pre-uremic and uremic period is one of the main causal factors. After RTx, glucocorticoid therapy seems to play the major causal role. Much more disputed is the role of the other immunosuppressive drugs, of persistent secondary hyperparathyroidism, and age. Hypophosphatemia and some genetic factors could also affect bone loss after RTx. Diabetic patients are particularly prone to develop bone disease after RTx. The main prophylactic interventions consist in the optimal control of hyperparathyroidism during the pre-transplant period, prescribing parathyroidectomy for autonomous hyperparathyroidism, not-responding to medical therapy. After RTx, both bisphosphonate and vitamin D metabolites, variably associated with calcium supplementation, have been demonstrated to have some beneficial effect on bone loss, at least in the first year after RTx. However, there are no data about the possible efficacy of these treatments on fracture rate.
|Number of pages||12|
|Journal||Giornale italiano di nefrologia : organo ufficiale della Società italiana di nefrologia|
|Publication status||Published - Jul 2004|
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