Evaluation and management of bone disease and fractures post transplant

Bone disease is common in recipients of kidney, liver, heart, and lung transplants and results in fractures in 20–40% of patients, a rate much higher than expected for age. Fractures occur because of the presence of bone disease as well as other factors such as neuropathy, poor balance, inactivity, and low body or muscle mass. Major contributors to bone disease include both preexisting bone disease and bone loss post transplant, which is greatest in the first 6–12 months when steroid doses are highest. Bone disease in kidney transplant recipients should be considered different from that which occurs in other solid organ transplant recipients for several reasons including the presence of renal osteodystrophy, which contributes to low bone mineral density in these patients; the location of fractures (more common in the legs and feet in these patients than in spine and hips as in other solid organ recipients); and the potential danger in using bisphosphonate therapy, which may cause more harm than good in kidney transplant recipients with low bone turnover.Evaluation in all patients should preferably occur in the pretransplant period or early post transplant and should include assessment of fracture risk as well as metabolic factors that can contribute to bone disease. Bone mineral density measurement is recommended in all patients even if its predictive value for fracture risk in the transplant population is unproven.Management of bone disease should be directed toward decreasing fracture risk as well as improving bone density. Pharmacologic and nonpharmacologic treatment strategies are discussed in this review. Although there have been many studies describing a beneficial effect of bisphosphonates and vitamin D analogues on bone density, none have been powered to detect a decrease in fracture rate.