Posttransplantation bone disease is a complex disorder, which may lead to reduction of bone strength and quality. It should be managed properly for reducing the risk of fractures and ideal management mineral metabolism. Otherwise, it could result in increasing the risk of mortality and morbidity with decreasing graft lifespan along with poor quality of life.              Persistent hyperparathyroidism has been reported up to 25% of renal transplant recipients 1 year after transplantion despite normalization of renal function, though PTH levels usually decline rapidly during the first 3–6 months after transplantation along with a reduction in functional parathyroid gland mass. Normally, polyclonal parathyroid hyperplasia will slowly regress after kidney transplantation, because of the recovery of renal function and correction of metabolic and endocrine disturbances. But, when the parathyroid glands go to the stage of tumoral growth, so that the response of parathyroid secretion and proliferation to physiologic regulatory mechanisms is reduced or lost, metabolic derrangement, so–called tertiary hyperparathyroidism can be persistent, and it is manifested with hypercalcemia, hypophosphatemia, high bone turnover with excessive bone resorption, and rapidly progressive soft tissue calcifications, including nephrocalcinosis. Hypercalcemia develops more easily post-transplant, probably because the skeletal resistance to the action of PTH decreases or even disappears with the correction of the uremic syndrome. This metabolic abnormality has been known as a risk factor for graft function and mortality. So, close monitoring of mineral metabolism parameters and bone strength and constructive therapeutic approaches including both medical and surgical treatment should be considered.