A correlation between decreased parathyroid α-Klotho and fibroblast growth factor receptor 1 expression with pathological category and parathyroid gland volume in dialysis patients
PURPOSE OF REVIEW The aim of this article is to describe the intriguing action of fibroblast growth factor 23 on the parathyroid. RECENT FINDINGS Fibroblast growth factor 23 inhibits renal phosphate reabsorption and calcitriol production. It is the principal phosphaturic factor in a bone-kidney axis coordinating systemic phosphate homeostasis and bone mineralization. Fibroblast growth factor 23 acts at its target tissues by binding to the Klotho-FGFR1c complex and it has recently been confirmed that the fibroblast growth factor 23 receptor is present not only in renal tissue but also in the parathyroid. Fibroblast growth factor 23 leads to a decrease in parathyroid hormone mRNA and serum parathyroid hormone levels by the mitogen-activated protein kinase pathway both in vivo and in vitro. SUMMARY Fibroblast growth factor 23 is secreted by osteocytes and acts through its receptor the heterodimer of Klotho-FGFR1c in the kidney and parathyroid. In the kidney it leads to phosphaturia and decreased calcitriol synthesis, and in the parathyroid it activates the mitogen-activated protein kinase pathway to decrease parathyroid hormone gene expression and secretion. The decreased parathyroid hormone levels would then also contribute to a decrease in calcitriol synthesis. A bone-kidney-parathyroid hormonal network is now apparent which regulates phosphate, calcium and calcitriol homeostasis. Fibroblast growth factor 23 is the major factor regulating phosphate, and parathyroid hormone the major factor for calcium and calcitriol balances between these factors.