Posttransplant bone disease

Abstract

Abstract Kidney transplantation reverses some of the disturbances of mineral and bone metabolism. However, the reversal or degree of improvement is often incomplete. The well-documented bone loss, especially in the early posttransplant period, contributes to an increased incidence of fractures in kidney transplant recipients. To better understand the mechanism of bone loss posttransplant, we need to take in consideration both bone quantity (density) and quality (bone microarchitecture, turnover rate). In addition to bone density, which is a measure of bone quantity, there are other invasive and noninvasive tools that provide information about the bone architecture and turnover and may be helpful in evaluating kidney transplant recipients at risk of fractures. There are several factors that contribute to the development of bone loss in the posttransplant period. Among these, the use of glucocorticoids, as part of the posttransplant immunosuppressive regimen, remains the single most important risk factor for bone loss post–kidney transplant. Interventions for evaluation and management of bone disease posttransplant are described and discussed. Some of these measures have been shown to increase bone density, but so far, none have demonstrated an ability to reduce the fracture incidence.