These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Decreased parathyroid Klotho expression is associated with persistent hyperparathyroidism after kidney transplantation.
    Author: Hong YA, Choi DE, Lim SW, Yang CW, Chang YK.
    Journal: Transplant Proc; 2013 Oct; 45(8):2957-62. PubMed ID: 24157012.
    Abstract:
    Although successful kidney transplantation usually corrects hyperparathyroidism, the condition persists in some patients. The present study was designed to determine whether Klotho or fibroblast growth factor 23, the key regulator of parathyroid hormone, is involved in persistent hyperparathyroidism in kidney transplant recipients (KTRs). Nineteen hyperplastic parathyroid glands were obtained from end-stage renal disease (ESRD) patients and KTRs; 6 normal parathyroid glands were used as controls. We compared the expression of Klotho, fibroblast growth factor receptor 1 (FGFR1) and calcium-sensing receptor (CaSR) in the KTRs and ESRD patients. Expressions of Klotho, FGFR1, CaSR and vitamin D receptor, as evaluated by immunohistochemistry, were quantified as the number of positive cells per unit area. The Klotho, FGFR1 and CaSR expressions in parathyroid glands of the post-kidney transplantation (PSKT) and the ESRD groups were significantly decreased compared with normal controls. In the ESRD group, Klotho expression and number of proliferating cell nuclear antigen-positive cells in the parathyroid gland were significantly decreased in parathyroid adenomas as compared with parathyroid hyperplasia. The expression of FGFR1 and CaSR in the parathyroid glands was significantly increased in the PSKT compared with the ESRD group. There was no significant difference in Klotho expression between the PSKT and ESRD groups. Incomplete recovery of Klotho levels in the parathyroid gland may play a role in the pathogenesis of tertiary hyperparathyroidism after kidney transplantation.
    [Abstract] [Full Text] [Related] [New Search]