Diagnostic utility of FGF-23 in mineral bone disorder during chronic kidney disease

Authors

  • Luisa Albanese Unity of Clinical and Molecular Pathology, AOU, University of Campania “Luigi Vanvitelli”, Naples - Italy
  • Gemma Caliendo Unity of Clinical and Molecular Pathology, AOU, University of Campania “Luigi Vanvitelli”, Naples - Italy
  • Giovanna D'Elia Unity of Clinical and Molecular Pathology, AOU, University of Campania “Luigi Vanvitelli”, Naples - Italy
  • Luana Passariello Unity of Clinical and Molecular Pathology, AOU, University of Campania “Luigi Vanvitelli”, Naples - Italy
  • Anna Maria Molinari Unity of Clinical and Molecular Pathology, AOU, University of Campania “Luigi Vanvitelli”, Naples and Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, Naples - Italy
  • Claudio Napoli Department of Advanced Medical and Surgical Sciences (DAMSS), University of Campania “Luigi Vanvitelli”, Naples and Clinical Department of Internal Medicine and Specialistic Units, AOU, University of Campania “Luigi Vanvitelli”, Naples - Italy
  • Maria Teresa Vietri Unity of Clinical and Molecular Pathology, AOU, University of Campania “Luigi Vanvitelli”, Naples and Department of Precision Medicine, University of Campania “Luigi Vanvitelli”, Naples - Italy

DOI:

https://doi.org/10.33393/jcb.2022.2328

Keywords:

Bone density, CDK, FGF-23

Abstract

Our data confirm that intact fibroblast growth factor 23 (iFGF-23) concentration is increased in patients with chronic kidney disease (CKD) and that it increases with disease progression (stages I-V). Therefore, iFGF-23 could be considered an early biomarker in the course of chronic kidney disease-mineral bone disorder (CKD-MBD), which has several aspects that make it potentially useful in clinical practice. The availability of an automated method for iFGF-23 assay may represent an added value in the management of the patient with CKD-MBD already from the early stages of the disease, before the increase of the routinely used laboratory parameters, 1-84 parathyroid hormone (PTH) and 25-OH-vitamin D (25-OH-vitD), which occur in more advanced stages of the disease.

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References

Moe S, Drüeke T, Cunningham J, et al; Kidney Disease: Improving Global Outcomes (KDIGO). Definition, evaluation, and classification of renal osteodystrophy: a position statement from Kidney Disease: Improving Global Outcomes (KDIGO). Kidney Int. 2006;69(11):1945-1953. https://doi.org/10.1038/sj.ki.5000414 PMID:16641930

Hu MC, Shiizaki K, Kuro-o M, Moe OW. Fibroblast growth factor 23 and Klotho: physiology and pathophysiology of an endocrine network of mineral metabolism. Annu Rev Physiol. 2013;75(1):503-533. https://doi.org/10.1146/annurev-physiol-030212-183727 PMID:23398153

Ho BB, Bergwitz C. FGF23 signalling and physiology. J Mol Endocrinol. 2021;66(2):R23-R32. https://doi.org/10.1530/JME-20-0178 PMID:33338030

Shimada T, Urakawa I, Isakova T, et al. Circulating fibroblast growth factor 23 in patients with end-stage renal disease treated by peritoneal dialysis is intact and biologically active. J Clin Endocrinol Metab. 2010;95(2):578-585. https://doi.org/10.1210/jc.2009-1603 PMID:19965919

Angelin B, Larsson TE, Rudling M. Circulating fibroblast growth factors as metabolic regulators—a critical appraisal. Cell Metab. 2012;16(6):693-705. https://doi.org/10.1016/j.cmet.2012.11.001 PMID:23217254

Wolf M. Update on fibroblast growth factor 23 in chronic kidney disease. Kidney Int. 2012;82(7):737-747. https://doi.org/10.1038/ki.2012.176 PMID:22622492

Bergwitz C, Jüppner H. Regulation of phosphate homeostasis by PTH, vitamin D, and FGF23. Annu Rev Med. 2010;61(1):91-104. https://doi.org/10.1146/annurev.med.051308.111339PMID:20059333

Isakova T, Wahl P, Vargas GS, et al. Fibroblast growth factor 23 is elevated before parathyroid hormone and phosphate in chronic kidney disease. Kidney Int. 2011;79(12):1370-1378. https://doi.org/10.1038/ki.2011.47 PMID:21389978

Isakova T, Xie H, Yang W, et al; Chronic Renal Insufficiency Cohort (CRIC) Study Group. Fibroblast growth factor 23 and risks of mortality and end-stage renal disease in patients with chronic kidney disease. JAMA. 2011;305(23):2432-2439. https://doi.org/10.1001/jama.2011.826PMID:21673295

Takashi Y, Fukumoto S. FGF23 beyond Phosphotropic Hormone. Trends Endocrinol Metab. 2018;29(11):755-767. https://doi.org/10.1016/j.tem.2018.08.006 PMID:30217676

Shimizu Y, Fukumoto S, Fujita T. Evaluation of a new automated chemiluminescence immunoassay for FGF23. J Bone Miner Metab. 2012;30(2):217-221. https://doi.org/10.1007/s00774-011-0306-4 PMID:21898178

Souberbielle JC, Prié D, Piketty ML, et al. Evaluation of a New Fully Automated Assay for Plasma Intact FGF23. Calcif Tissue Int. 2017;101(5):510-518. https://doi.org/10.1007/s00223-017-0307-y PMID:28761972

Napoli C, Casamassimi A, Crudele V, Infante T, Abbondanza C. Kidney and heart interactions during cardiorenal syndrome: a molecular and clinical pathogenic framework. Future Cardiol. 2011;7(4):485-497. https://doi.org/10.2217/fca.11.24 PMID:21797745

Vasco M, Benincasa G, Fiorito C, et al. Clinical epigenetics and acute/chronic rejection in solid organ transplantation: an update. Transplant Rev (Orlando). 2021;35(2):100609. https://doi.org/10.1016/j.trre.2021.100609 PMID:33706201

Economidou D, Dovas S, Papagianni A, Pateinakis P, Memmos D. FGF-23 Levels before and after Renal transplantation. J Transplant. 2009;2009:379082. https://doi.org/10.1155/2009/379082PMID:20107581

Published

2022-01-08

How to Cite

Albanese, L., Caliendo, G., D’Elia, G., Passariello, L., Molinari, A. M., Napoli, C., & Vietri, M. T. (2022). Diagnostic utility of FGF-23 in mineral bone disorder during chronic kidney disease. Journal of Circulating Biomarkers, 11(1), 1–4. https://doi.org/10.33393/jcb.2022.2328

Issue

Section

Short communication
Received 2021-08-04
Accepted 2021-12-06
Published 2022-01-08

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