Bone disease is common after renal transplantation. The main syndromes are bone loss with a consequent fracture rate of 3% per year, osteonecrosis of the hip, and bone pain. The causes of disease include preexisting uremic osteodystrophy (hyperparathyroidism, aluminum osteomalacia, β2-associated amyloidosis, and diabetic osteopathy), postoperative glucocorticoid therapy, poor renal function, and ongoing hyperparathyroidism, as the result of either autonomous transformation of the parathyroid gland or ongoing physiologic stimuli. Cyclosporine A treatment, hyperphosphaturia, and a pathogenic vitamin D allele have also been implicated. Bone loss is particularly pronounced during the first year after operation, amounting to up to 9% of bone mass. The clinical and biochemical picture is consistent with a high turnover bone disease, but histomorphometric studies do not completely support this. Principal prophylactic options include preoperative osteodystrophy prophylaxis; postoperative calcium, vitamin D, or calcitriol therapy; estrogen therapy for postmenopausal women; and parathyroidectomy for medically intractable hyperparathyroidism. Recently, prophylactic biphosphonate treatment has shown promise, but the exact indications for treatment remain to be determined.