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Elevated fibroblast growth factor 23 levels as a cause of early post-renal transplantation hypophosphatemia.
Transplant Proc. 2012 Apr; 44(3):657-60.TP

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)(2)VitD) 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)(2)VitD 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 (r(2) = 0.406; P = .011); PTH was not independently associated with Pi (r(2) = 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.

Authors+Show Affiliations

Department of Internal Medicine, Keimyung University School of Medicine, and Keimyung University Kidney Institute, Daegu, Korea. hansy@dsmc.or.krNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

22483462

Citation

Han, S Y., et al. "Elevated Fibroblast Growth Factor 23 Levels as a Cause of Early Post-renal Transplantation Hypophosphatemia." Transplantation Proceedings, vol. 44, no. 3, 2012, pp. 657-60.
Han SY, Hwang EA, Park SB, et al. Elevated fibroblast growth factor 23 levels as a cause of early post-renal transplantation hypophosphatemia. Transplant Proc. 2012;44(3):657-60.
Han, S. Y., Hwang, E. A., Park, S. B., Kim, H. C., & Kim, H. T. (2012). Elevated fibroblast growth factor 23 levels as a cause of early post-renal transplantation hypophosphatemia. Transplantation Proceedings, 44(3), 657-60. https://doi.org/10.1016/j.transproceed.2011.11.046
Han SY, et al. Elevated Fibroblast Growth Factor 23 Levels as a Cause of Early Post-renal Transplantation Hypophosphatemia. Transplant Proc. 2012;44(3):657-60. PubMed PMID: 22483462.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Elevated fibroblast growth factor 23 levels as a cause of early post-renal transplantation hypophosphatemia. AU - Han,S Y, AU - Hwang,E A, AU - Park,S B, AU - Kim,H C, AU - Kim,H T, PY - 2012/4/10/entrez PY - 2012/4/10/pubmed PY - 2012/7/31/medline SP - 657 EP - 60 JF - Transplantation proceedings JO - Transplant Proc VL - 44 IS - 3 N2 - 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)(2)VitD) 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)(2)VitD 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 (r(2) = 0.406; P = .011); PTH was not independently associated with Pi (r(2) = 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. SN - 1873-2623 UR - https://www.unboundmedicine.com/medline/citation/22483462/Elevated_fibroblast_growth_factor_23_levels_as_a_cause_of_early_post_renal_transplantation_hypophosphatemia_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0041-1345(11)01643-5 DB - PRIME DP - Unbound Medicine ER -