Recovery versus persistence of disordered mineral metabolism in kidney transplant recipients.

In patients with end-stage renal disease, successful renal transplantation improves the quality of life and increases survival, as compared with long-term dialysis treatment. Although it long has been believed that successful kidney transplantation to a large extent solves the problem of chronic kidney disease-mineral and bone disorders (CKD-MBD), increasing evidence indicates that it only changes the phenotype of CKD-MBD. Posttransplant CKD-MBD reflects the effects of immunosuppression, previous CKD-MBD persisting after transplantation, and de novo CKD-MBD. A major and often-underestimated problem after successful renal transplantation is persistent hyperparathyroidism. Besides contributing to posttransplant hypercalcemia and hypophosphatemia, persistent hyperparathyroidism may be involved in the pathogenesis of allograft dysfunction (nephrocalcinosis), progression of vascular calcification, and bone disease (uncoupling of bone formation and bone resorption and bone mineral density loss) in renal transplant recipients. Similar to nontransplanted patients, CKD-MBD has a detrimental impact on (cardiovascular) mortality and morbidity. Additional studies urgently are needed to get more insights into the pathophysiology of posttransplant CKD-MBD. These new insights will allow for a more targeted and causal therapeutic approach.