The fate of bone after renal transplantation

Post-transplantation bone disease is a multifactorial, complex condition. It derives in a significant part from pre-existing renal osteodystrophy, but it is aggravated by factors emerging after renal transplantation. Among the latter factors, the key pathophysiological contributor to bone disease is immunosuppressive agent application (especially glucocorticoids (GC)). Post-transplantation bone disease is detectable even years after renal transplantation in the vast majority of patients, and potentially it never resolves completely. Due to post-transplantation bone disease, a rapid reduction of bone mineral density (BMD) develops that can exceed 10% in the first 12 months. Subsequently, the bone loss slows down or even a secondary increase occurs. Post-transplantation bone disease results in a significantly elevated fracture risk, which largely contributes to the increased morbidity in transplant patients. Currently, vitamin D metabolites and bisphosphonates are the most extensively tested therapeutic agents against this accelerated bone loss. Both substances have proven effective. However, it is yet unproven that they reduce the fracture risk. In patients with adynamic bone disease, bisphosphonate usage cannot be recommended, since this group of drugs could oversuppress bone metabolism.