A prospective cohort study of mineral metabolism after kidney transplantation

Kidney transplantationis the preferred treatment for end-stage renal disease (ESRD) because it reverses many complications of chronic kidney disease (CKD), improves recipients' quality of life, and prolongs survival.1 Advances in immune suppression, which vastly enhanced short-term allograft outcomes, have enabled the transplant community to focus more attention on managing the nonimmune aspects of the posttransplant period to optimize recipients' long-term health. Disordered mineral metabolism is a common complication of CKD that begins early in the course of disease and progressively worsens as patients approach ESRD.2 In its most severe form, disordered mineral metabolism in ESRD is characterized by hyperphosphatemia, hypocalcemia, deficiencies of 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D, and markedly elevated levels of parathyroid hormone (PTH) and fibroblast growth factor 23(FGF23).3-8 Individually and in aggregate, these alterations are associated with increased risks of cardiovascular disease, fracture, and death.8-12 Although restoring normal kidney function by transplanting a healthy kidney might be expected to fully reverse disordered mineral metabolism due to ESRD, most existing data suggest that transplantation only partially corrects certain alterations.13-18 Furthermore, presence of a healthy allograft that can respond to the hormonal effects of lingering elevations in PTH and FGF23 levels can precipitate de novo alterations in mineral metabolism, including hypercalcemia and hypophosphatemia.19,20 Posttransplant hypercalcemia and hypophosphatemiapresent clinicians with management challenges because they may jeopardize graft function and bone healthand exacerbate fracture and cardiovascular risk.20-22 The postkidney transplant period should be considered a unique phase in the natural history of disordered mineral metabolism associated with CKD that requires dedicated investigation.14 Few studies have systematically studied mineral metabolism in the posttransplant period. Among those that did, most previous studies were small, single-center, brief, and failed to measure a comprehensive panel of mineral metabolites.23-28 As a result, the frequency of hypercalcemia, hypophosphatemia, and persistent hyperparathyroidism during the first year after kidney transplantationremain incompletely characterized. We conducted the current prospective, observational study to examine the evolution of persistent hyperparathyroidism and associated alterations in mineral metabolism during the first year after kidney transplantation.