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Decreased Parathyroid Klotho Expression Is Associated with Persistent Hyperparathyroidism after Kidney Transplantation

Y. Hong, M. Lee, J. Kim, H. Whang, G. Ahn, Y. Cho, B. Chung, B. Choi, C. Park, Y. Kim, S. Lim, Y. Chang, C. Yang

Department of Internal Medicine, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, Korea
Department of Internal Medicine, Daejeon St. Mary's Hospital, The Catholic University of Korea, Daejeon, Korea
Transplantation Research Center, Seoul St. Mary's Hospital, The Catholic University of Korea, Seoul, Korea

Meeting: 2013 American Transplant Congress

Abstract number: A575

Background. Although successful kidney transplantation usually corrects hyperparathyroidism, the condition will persist in some patients. The present study was designed to determine whether Klotho or fibroblast growth factor 23 (FGF23), the key regulator of parathyroid hormone, is involved in persistent hyperparathyroidism in kidney transplant recipients (KTRs).

Method. Nineteen hyperplastic parathyroid glands were obtained from end-stage renal disease (ESRD) patients and kidney transplant recipients (KTRs), and six normal parathyroid glands were used as normal controls (NC). We compared the expression of Klotho, FGFR1, and Calcium sensing receptor (CaSR) in the KTRs and ESRD patients. The expression of Klotho, FGFR1, CaSR and Vitamin D receptor (VDR) was evaluated by immunohistochemistry, and quantified as the number of positive cells per unit area.

Results. The Klotho, FGFR1, and CaSR expression in parathyroid glands of the PSKT group and the ESRD group were significantly decreased compared to the normal control. In the ESRD group, the Klotho expression and number of PCNA-positive cells in the parathyroid gland were significantly decreased in parathyroid adenoma as compared to parathyroid hyperplasia. The expression of FGFR1 and CaSR in the parathyroid glands was significantly increased in the PSKT group compared with the ESRD group. There was no significant difference in Klotho expression between the PSKT and ESRD patients.

Conclusions. Persistent hyperparathyroidism after kidney transplantation is associated with incomplete recovery of Klotho and FGFR1 expression in hyperplastic parathyroid tissues. The incomplete recovery of Klotho and FGFR1 does not seem related to renal function but does seem related to FGF23 resistance in the parathyroid gland of PSKT patients.

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To cite this abstract in AMA style:

Hong Y, Lee M, Kim J, Whang H, Ahn G, Cho Y, Chung B, Choi B, Park C, Kim Y, Lim S, Chang Y, Yang C. Decreased Parathyroid Klotho Expression Is Associated with Persistent Hyperparathyroidism after Kidney Transplantation [abstract]. Am J Transplant. 2013; 13 (suppl 5). https://atcmeetingabstracts.com/abstract/decreased-parathyroid-klotho-expression-is-associated-with-persistent-hyperparathyroidism-after-kidney-transplantation/. Accessed May 14, 2025.

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