Bone Mineral Disease After Kidney Transplantation

Chronic kidney disease-mineral bone disorder (CKD-MBD) after transplantation is a mix of pre-existing disorders and new alterations. The final consequences are reflected fundamentally as abnormal mineral metabolism (hypercalcemia, hypophosphatemia) alterations [high or low turnover disease (as fibrous osteitis adynamic disease), an eventual compromise mineralization, decrease density fractures]. major cause post-transplantation hypercalcemia the persistence severe secondary hyperparathyroidism, treatment options include calcimimetics parathyroidectomy. On turn, hypophosphatemia caused by both high blood levels PTH and/or FGF23, with its correction being very difficult to achieve. most frequent morphology alteration disease, while high-turnover osteopathy decreases in frequency transplantation. Although pathogenic mechanisms these abnormalities have not been fully clarified, available evidence suggests that there number factors play important role, such immunosuppressive treatment, persistently PTH, vitamin D deficiency hypophosphatemia. Fracture risk four-fold higher transplanted patients compared general population. relevant for fracture transplant population diabetes mellitus, female sex, advanced age (especially > 65 years), dialysis vintage, phosphate levels, osteoporosis, pre-transplant stress doses prolonged steroids therapy. Treatment alternatives CKD-MBD minimization corticosteroids, use calcium supplements, antiresorptives (bisphosphonates Denosumab) osteoformers (synthetic parathyroid hormone). As lead increased morbidity mortality, presence changes has be prevented (if possible), minimized, diagnosed, treated soon possible.