Does the downregulation of the FGF23 signaling pathway in hyperplastic parathyroid glands contribute to refractory secondary hyperparathyroidism in CKD patients?

Abstract

Compared to normal tissue, hyperplastic parathyroid glands of patients with chronic kidney disease on dialysis express lower levels of FGFR1 and Klotho proteins. Similar findings are reported in uremic rats with advanced chronic kidney disease. Moreover, in these animals, FGF23 administration fails to reduce PTH serum levels in vivo and to transmit downstream signals in parathyroid cells ex vivo. These findings may explain, at least partly, the concomitant elevation of both FGF23 and PTH serum levels in chronic kidney disease secondary hyperparathyroidism.