Elevated Fibroblast Growth Factor 23 Levels As a Cause of Early Post–Renal Transplantation Hypophosphatemia

Authors
S.Y. HanE.A. HwangS.B. ParkH.C. KimH.T. Kim
Department
Dept. of Internal Medicine (내과학); Dept. of Surgery (외과학)
Issue Date
2012
Citation
Transplantation Proceedings, Vol.44(3) : 657-660, 2012
ISSN
0041-1345
Abstract
Background Hypophosphatemia is a common complication after renal transplantation. Hyperparathyroidism has long been thought to be the cause, but hypophosphatemia can persist after high parathyroid hormone (PTH) levels normalize. Furthermore, calcitriol levels remain inappropriately low after transplantation, suggesting that mechanisms other than PTH contribute. Fibroblast growth factor 23 (FGF-23) induces phosphaturia, inhibits calcitriol synthesis, and accumulates in chronic kidney disease. We performed prospective study to investigate if FGF-23 early after renal transplantation contributes to hypophosphatemia. Methods We measured FGF-23 levels before and at 1, 2, 4, and 12 weeks after transplantation in 20 renal transplant recipients. Serum creatinine, calcium (Ca), phosphate (Pi), intact PTH (PTH), and 1,25-dihydroxy vitamin D (1,25(OH)2VitD) were measured at the same time. Results FGF-23 levels decreased by 97% at 4 weeks after renal transplantation (PRT) (7,471 ± 11,746 vs 225 ± 295 pg/mL; P < .05) but were still above normal. PTH and Pi levels also decreased significantly after renal transplantation, and Ca and 1,25(OH)2VitD slightly increased. PRT hypophosphatemia of <2.5 mg/dL developed in 15 (75%) and 12 (60%) patients at 4 weeks and 12 weeks respectively. Compared with nonhypophosphatemic patients, the levels of FGF-23 of hypophosphatemic patients were higher (303 ± 311 vs 10 ± 6.9 pg/mL; P = .02) at 4 weeks PRT. FGF-23 levels were inversely correlated with Pi (r2 = 0.406; P = .011); PTH was not independently associated with Pi (r2 = 0.132; P = .151). Conclusions FGF-23 levels decrease dramatically after renal transplantation. During the early PRT period, Pi rapidly decreased, suggesting that FGF-23 is cleared by the kidney, but residual FGF-23 may contribute to the PRT hypophosphatemia. FGF-23, but not PTH levels, was independently associated with PRT hypophosphatemia.
URI
http://kumel.medlib.dsmc.or.kr/handle/2015.oak/34717
Appears in Collections:
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Internal Medicine (내과학)
1. Journal Papers (연구논문) > 1. School of Medicine (의과대학) > Dept. of Surgery (외과학)
Keimyung Author(s)
한승엽; 황은아; 박성배; 김현철; 김형태
Full Text
https://www.sciencedirect.com/science/article/pii/S0041134511016435?via%3Dihub
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