TY - JOUR
T1 - A prospective cohort study of mineral metabolism after kidney transplantation
AU - Wolf, Myles
AU - Weir, Matthew R.
AU - Kopyt, Nelson
AU - Mannon, Roslyn B.
AU - Visger, Jon Von
AU - Deng, Hongjie
AU - Yue, Susan
AU - Vincenti, Flavio
N1 - Funding Information:
M.W.: Scientific advisor and clinical trial executive committee member for Amgen. M.R.W.: Scientific advisor and clinical trial executive committee member for Amgen Inc. N.K.: Clinical trial investigator for Amgen-sponsored studies. R.B.M.: Past (> 1 year) clinical trial investigator for Amgen-sponsored studies and consultant for Amgen. J.V.V.: Clinical trial advisory board member for Amgen Inc. H.D.: Employee and stockholder of Amgen. S.Y.: Employee and stockholder of Amgen Inc. F.V.: Research grants from Amgen Inc. The authors thank Holly Tomlin and Tim Peoples for medical writing and journal formatting assistance and Yumi Kubo for statistical analysis assistance (all employees and stockholders, Amgen, Inc).
Publisher Copyright:
© Copyright 2015 Wolters Kluwer Health, Inc. All rights reserved.
PY - 2016
Y1 - 2016
N2 - Background. Kidney transplantation corrects or improves many complications of chronic kidney disease, but its impact on disordered mineral metabolism is incompletely understood. Methods.We performed a multicenter, prospective, observational cohort study of 246 kidney transplant recipients in the United States to investigate the evolution of mineral metabolism from pretransplant through the first year after transplantation. Participants were enrolled into 2 strata defined by their pretransplant levels of parathyroid hormone (PTH), low PTH (>65 to ≤300 pg/mL; n = 112), and high PTH (>300 pg/mL; n = 134) and underwent repeated, longitudinal testing for mineral metabolites. Results. The prevalence of posttransplant, persistent hyperparathyroidism (PTH >65 pg/mL) was 89.5%, 86.8%, 83.1%, and 86.2%, at months 3, 6, 9, and 12, respectively, among participants who remained untreated with cinacalcet, vitamin D sterols, or parathyroidectomy. The results did not differ across the low and high PTH strata, and rates of persistent hyperparathyroidism remained higher than 40% when defined using a higher PTH threshold greater than 130 pg/mL. Rates of hypercalcemia peaked at 48% at week 8 in the high PTH stratum and then steadily decreased through month 12. Rates of hypophosphatemia (<2.5 mg/dL) peaked at week 2 and then progressively decreased through month 12. Levels of intact fibroblast growth factor 23 decreased rapidly during the first 3 months after transplantation in both PTH strata and remained less than 40 pg/mL thereafter. Conclusions. Persistent hyperparathyroidism is common after kidney transplantation. Further studies should determine if persistent hyperparathyroidism or its treatment influences long-Term posttransplantation clinical outcomes.
AB - Background. Kidney transplantation corrects or improves many complications of chronic kidney disease, but its impact on disordered mineral metabolism is incompletely understood. Methods.We performed a multicenter, prospective, observational cohort study of 246 kidney transplant recipients in the United States to investigate the evolution of mineral metabolism from pretransplant through the first year after transplantation. Participants were enrolled into 2 strata defined by their pretransplant levels of parathyroid hormone (PTH), low PTH (>65 to ≤300 pg/mL; n = 112), and high PTH (>300 pg/mL; n = 134) and underwent repeated, longitudinal testing for mineral metabolites. Results. The prevalence of posttransplant, persistent hyperparathyroidism (PTH >65 pg/mL) was 89.5%, 86.8%, 83.1%, and 86.2%, at months 3, 6, 9, and 12, respectively, among participants who remained untreated with cinacalcet, vitamin D sterols, or parathyroidectomy. The results did not differ across the low and high PTH strata, and rates of persistent hyperparathyroidism remained higher than 40% when defined using a higher PTH threshold greater than 130 pg/mL. Rates of hypercalcemia peaked at 48% at week 8 in the high PTH stratum and then steadily decreased through month 12. Rates of hypophosphatemia (<2.5 mg/dL) peaked at week 2 and then progressively decreased through month 12. Levels of intact fibroblast growth factor 23 decreased rapidly during the first 3 months after transplantation in both PTH strata and remained less than 40 pg/mL thereafter. Conclusions. Persistent hyperparathyroidism is common after kidney transplantation. Further studies should determine if persistent hyperparathyroidism or its treatment influences long-Term posttransplantation clinical outcomes.
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U2 - 10.1097/TP.0000000000000823
DO - 10.1097/TP.0000000000000823
M3 - Article
C2 - 26177089
AN - SCOPUS:84952360920
SN - 0041-1337
VL - 100
SP - 184
EP - 193
JO - Transplantation
JF - Transplantation
IS - 1
ER -