Skeletal Complications after Renal Transplantation

Bone is a complex tissue that not only protects vital organs and contributes to locomotion, but also serves as a mineral reservoir, containing 99% of the body's total calcium, 85% of its phosphorus, and 66% of its magnesium.Bone formation and resorption are regulated at the local level and controlled by systemic factors such as parathyroid hormone (PTH), vitamin D, sex hormones, calcitonin (CT), prostaglandins, and growth factors.The status of bone reflects the patient's age, sex, and body weight.Aging, altered locomotion, or underlying diseases such as metabolic or hormonal abnormalities can put skeleton's structural integrity at risk.Additional metabolic derangements may be produced by therapies that may interfere with bone metabolism.Patients on dialysis may have skeletal abnormalities such as osteitis fibrosa, aluminum osteopathy, or ß 2 microglobulin-related amyloidosis, which are often present simultaneously.A successful renal transplant represents the best therapy for uremic bone disease.The restoration of renal function corrects most of the causes of renal osteodystrophy, including inadequate synthesis of calcitriol, insufficient intestinal calcium absorption, increased secretion of PTH, hyperphosphatemia, hyperaluminemia, and reduced ß 2 microglobulin excretion.Nevertheless some metabolic-skeletal abnormalities persist after transplantation as a consequence of graft dysfunction, while new bone disease may be triggered by anti-rejection agents that interfere with bone metabolism.