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Parathyroid cell resistance to fibroblast growth factor 23 in secondary hyperparathyroidism of chronic kidney disease

H Galitzer1, I Z Ben-Dov, Justin Silver

  • 1Department of Nephrology, Hadassah Hebrew University Medical Center, Jerusalem, Israel.

Kidney International
|December 18, 2009
PubMed

Insights

In chronic kidney disease, elevated fibroblast growth factor 23 (FGF23) fails to lower parathyroid hormone due to reduced Klotho-FGFR1c receptors in parathyroid glands, causing FGF23 resistance.

Area of Science:

  • Endocrinology
  • Nephrology
  • Molecular Biology

Background:

  • Fibroblast growth factor 23 (FGF23) normally suppresses parathyroid hormone (PTH) via Klotho-FGFR1c.
  • PTH levels paradoxically increase in chronic kidney disease (CKD) despite high FGF23.
  • The mechanism of FGF23 resistance in CKD parathyroid glands is unclear.

Purpose of the Study:

  • To investigate the factors contributing to parathyroid gland resistance to FGF23 in a rat model of CKD.
  • To determine the role of Klotho-FGFR1c receptor expression in FGF23 resistance in CKD.

Main Methods:

  • Dietary adenine-induced CKD model in rats.
  • Quantitative immunohistochemistry and RT-PCR on laser-captured parathyroid gland sections.
  • In vitro parathyroid gland organ culture with recombinant FGF23 stimulation.

Main Results:

  • Klotho and FGFR1 protein and mRNA levels were significantly decreased in parathyroid glands of CKD rats.
  • Recombinant FGF23 did not suppress PTH or activate MAPK signaling in advanced CKD rat parathyroid glands.
  • FGF23 reduced PTH secretion and mRNA in vitro in control and early CKD, but not advanced CKD, parathyroid glands.

Conclusions:

  • Downregulation of the Klotho-FGFR1c receptor complex in parathyroid glands leads to FGF23 resistance in established CKD.
  • This parathyroid FGF23 resistance is evident both in vivo and in vitro.
  • Therapeutic strategies targeting FGF23 signaling in CKD may need to address receptor complex restoration.

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