Metabolic Bone Disease in Renal Transplant Recipients

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Abstract

Renal transplantation is associated with several abnormalities of function and structure of the skeletal system. Some of these abnormalities result from incomplete resolution of abnormalities of bone and mineral metabolism due to chronic renal failure before transplantation. Hyperparathyroidism, accumulation of β2-microglobulin and aluminum, and diabetes mellitus type 1 may cause osseous disorders prior to transplantation which may persist to variable degrees after engraftment. Persistent hyperparathyroidism may accelerate bone loss and increase the risk for osteonecrosis, the most debilitating skeletal complication after transplantation. Although aluminum-associated osteomalacia generally resolves after transplantation, bone complications due to β2-microglobulin amyloidosis and diabetes mellitus type 1 often fall to improve. Alternatively, skeletal abnormalities may arise after transplantation, many of which are due to the the toxicities of the immunosuppressive medications. Treatment with glucocorticoids increases the risk for fractures by decreasing cancellous bone mass and synthesis of bone matrix, dampens linear growth in pediatric recipients, and contributes to the pathogenesis of osteonecrosis. Osteopenia, osteonecrosis, and short stature remain important complications in renal transplant patients. Therapy should minimize pretransplant bone disease and attenuate the abnormalities of bone and mineral metabolism after transplantation.

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