In:
American Journal of Nephrology, S. Karger AG, Vol. 31, No. 3 ( 2010), p. 230-238
Kurzfassung:
〈 i 〉 Background/Aims: 〈 /i 〉 Fibroblast growth factor 23 (FGF23) has been shown to suppress parathyroid hormone (PTH) secretion. α-Klotho has been demonstrated to function as a fibroblast growth factor receptor (FGFR) cofactor for FGF23. Thus, both α-Klotho and FGFR may play roles in PTH synthesis and/or secretion. Functions of α-Klotho and FGFR in secondary hyperparathyroidism (SHPT) remain to be studied. The present studies explore the role of α-Klotho and FGFR in SHPT. 〈 i 〉 Methods: 〈 /i 〉 Hyperplastic parathyroid glands (n = 44) were obtained from patients with SHPT. 〈 i 〉 Results: 〈 /i 〉 Immunohistochemical study showed that both α-Klotho and FGFR1c expression in hyperplastic glands was significantly decreased compared with that in normal glands (Klotho p 〈 0.01, and FGFR1c p 〈 0.05). A significant positive correlation was observed between α-Klotho and FGFR1c (r 〈 sup 〉 2 〈 /sup 〉 = 0.375, p 〈 0.01) indicating a cooperative system. Both α-Klotho (r 〈 sup 〉 2 〈 /sup 〉 = 0.235, p 〈 0.05) and FGFR1c (r 〈 sup 〉 2 〈 /sup 〉 = 0.181, p 〈 0.05) correlated positively with the calcium-sensing receptor (CaR), which plays an important role in the development of SHPT. In addition, expression of α-Klotho correlated negatively with parathyroid cell proliferation, as confirmed by Ki67 staining (r 〈 sup 〉 2 〈 /sup 〉 = 0.148, p 〈 0.05). 〈 i 〉 Conclusion: 〈 /i 〉 Decreased expression of α-Klotho and FGFR1c in parallel with CaR expression and parathyroid cell growth may be involved in the pathogenesis of SHPT.
Materialart:
Online-Ressource
ISSN:
0250-8095
,
1421-9670
Sprache:
Englisch
Verlag:
S. Karger AG
Publikationsdatum:
2010
ZDB Id:
1468523-1
