Mineral and Bone Disease After Kidney Transplantation: Risk of Fracture, Graft Dysfunction and Mortality - a Review

The mineral and bone disease of chronic kidney disease (CKD-MBD) is a combination of three components: abnormalities in calcium, phosphorus, PTH, fibroblast growth factor 23 (FGF23) and vitamin D metabolism; abnormalities of bone metabolism, mineralization, volume, growth and strength; and vascular and other soft tissue calcification. During the natural course of kidney disease, there is an increase in FGF23 levels, inhibition of calcitriol production, secondary hyperparathyroidism, hypocalcemia and hyperphosphatemia. These changes have consequences on the cardiovascular and bone systems. Regarding cardiovascular disease, left ventricular hypertrophy is highlighted, associated with an increase in FGF23 and vascular calcification, directly related to hyperphosphatemia. The main types of bone disease are cystic fibrous osteitis (high turnover) and adynamic bone disease (low turnover), both of which are associated with a high risk of fracture in this population. Successful kidney transplantation (KT) does not fully correct the mineral, bone and cardiovascular abnormalities generated by CKD-MBD. In the first months after transplantation, PTH and FGF23 levels remain elevated in most patients. There is an increase in the production of calcitriol by the graft. These are the main alterations responsible for a mineral phenotype that resembles primary hyperparathyroidism, with hypercalcemia, hypophosphatemia and elevated PTH levels. Cardiovascular disease does not revert after KT and the transplant patient has a higher cardiovascular risk than the general population. In relation to bone disease, in addition to the pre-existing bone alteration, specific factors of the post-KT period add damage to the bone, especially the use of corticosteroids. The main types of bone disease in renal transplant patients are bone fracture, renal osteodystrophy, osteoporosis and osteonecrosis. CKD-MBD is a complex disease that affects patients with CKD, increasing their morbidity and mortality. KT does not fully reverse the disease and still adds other specific risk factors that make its approach challenging. This review sought to show the association between the bone mineral disease of chronic kidney disease and the risk of fractures, vascular and other tissue calcifications, graft dysfunction and kidney transplant patient mortality.