This chapter summarizes the major aspects of the pathogenesis, clinical manifestations, histologic features, and therapeutic interventions currently used in the management of CKD-MBD. The clinical and histologic features of bone diseases after successful kidney transplantation are also described. The kidney plays a major role in bone and mineral homeostasis by regulating calcium, phosphorus, parathyroid hormone (PTH), fibroblast growth factor-23 (FGF-23) and calcitriol (1,25 dihydroxyvitamin D, 1,25(OH)2D) metabolism. Disordered regulation of mineral metabolism occurs early in the course of chronic kidney disease (CKD) and results in alterations in bone modeling and remodeling. A growing body of evidence demonstrates that cardiovascular calcifications accompany CKD, that cardiovascular disease is the leading cause of mortality in patients with CKD, and that therapy designed to treat the skeletal consequences of CKD affect the progression of vascular pathology. This has led to a reclassification of the mineral, skeletal, and vascular complications associated with progressive kidney disease, resulting in alterations that are now termed "CKD Mineral and Bone Disorder" ("CKD-MBD"). The CKD-MBD is defined as a systemic disorder of mineral and bone metabolism due to CKD that is manifested by either one or a combination of abnormalities of calcium, phosphorus, PTH, or vitamin D metabolism.