Metabolic bone disease after renal transplantation.

PURPOSE OF THE REVIEW: Posttransplantation mineral and bone disorder (MBD) is an important issue in the care of children after kidney transplantation (KTx) resulting in increased comorbidity, for example, bone pain, fractures, growth failure, and vascular calcifications. It is distinctly different from common forms of osteoporosis and mainly due to preexisting renal osteodystrophy at the time of KTx, glucocorticoid treatment, and reduced graft function. The purpose of this review is to give an overview of the pathogenesis and treatment of posttransplant MBD in children.

RECENT FINDINGS: Recent studies underline the impact of elevated levels of the phosphaturic hormone fibroblast growth factor-23 on posttransplant MBD. Glucocorticoid treatment results in impairment of bone strength, increased fracture risk, and lack of significant catch up, whereas steroid-sparing protocols allow for a normal adult height in the majority of patients. Whether the latter also improves bone strength remains to be elucidated.

SUMMARY: Therapeutic efforts to reduce MBD after KTx should focus on steroid-sparing immunosuppressive protocols, adequate treatment of alterations of calcium, phosphate and vitamin D metabolism, maintenance of regular physical activity, and preservation of transplant function. Preemptive KTx, that is with no prior dialysis, can prevent progressive vascular calcifications.