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Therapeutic management of post-kidney transplant hyperparathyroidism

Authors


  • Conflict of interest: The authors have declared association with the following organizations: Dr. Copley is currently employed by Bristol-Myers Squibb Company. His clinical research with cinacalcet and initial contributions to this manuscript were accomplished when he was with the Cleveland Clinic Florida. At that time, he served as an advisor and speaker for Abbott Laboratories, Novartis Pharmaceuticals, Merck, and AstraZeneca. Dr. Wüthrich has served as an advisor and speaker for Amgen, Astellas, Novartis, Roche, Vifor, and Wyeth.

Corresponding author:John B. Copley, MD, FASN, FACP, Department of Nephrology and Hypertension, Cleveland Clinic Florida, 2950 Cleveland Clinic Boulevard, Weston, FL 33331, USA.
Tel.: 609 897 2964; fax: 484 865 4355;
e-mail: brian.copley@bms.com

Abstract

Copley JB, Wüthrich RP. Therapeutic management of post-kidney transplant hyperparathyroidism.
Clin Transplant 2011: 25: 24–39. © 2010 John Wiley & Sons A/S.

Abstract:  Left uncontrolled, persistent post-kidney transplant hyperparathyroidism (HPT) may lead to or exacerbate pre-existing bone and cardiovascular disease. Parathyroidectomy has long been the primary treatment option for long-term uncontrolled HPT in post-kidney transplant patients. However, patients with contraindications for surgery and parathyroidectomy-associated complications, including graft loss, highlight the need for other approaches. Conventional medical therapies have limited impact on serum calcium (Ca) and parathyroid hormone (PTH) levels. Bisphosphonates and calcitonin, used to spare bone loss, and phosphorus supplementation, to correct hypophosphatemia, do not directly regulate PTH or Ca. Although vitamin D supplementation can reduce PTH, it is often contraindicated because of hypercalcemia. Studies of the calcimimetic cinacalcet in patients with post-kidney transplant HPT suggest that it can rapidly reduce serum PTH and Ca concentrations while increasing serum phosphorus concentrations toward the normal range. Although the clearest application for cinacalcet is the non-surgical treatment of hypercalcemic patients with persistent HPT, current indications for other transplant patients are as yet uncertain. Further studies are needed to determine the utility of cinacalcet in patients with spontaneous resolution of HPT or low bone turnover. This review discusses the pathophysiology of post-kidney transplant HPT, associated complications, and current options for clinical management.

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