Pneumology - Original Articles
June 5, 2025

Evaluation of fibroblast growth factor 23 as a marker of severity in stable chronic obstructive pulmonary disease

Publisher's note
All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.
78
Views
29
Downloads

Authors

Chronic obstructive pulmonary disease (COPD), a multi-component disease, is one of the leading causes of morbidity and mortality globally. Considering the drawbacks of current severity markers of COPD, there is a need to find newer alternatives that are easily accessible and provide insight into the underlying pathophysiology of the disease. This study evaluated fibroblast growth factor 23 (FGF23), a pro-inflammatory hormone, as a severity marker for COPD. A total of 54 stable COPD patients were recruited as per the inclusion and exclusion criteria. All participants were subjected to spirometry and body plethysmography with diffusion capacity of lungs for carbon monoxide (DLCO) evaluation. Plasma FGF23 levels were measured for all participants. This study aimed to evaluate FGF23 as a severity indicator of COPD, along with its association with serum phosphate levels, static lung volumes, and DLCO. The mean age of the study population (n=54) was 59±11 years. The majority of study participants had moderate COPD (50%), followed by severe (27.8%), mild (20.4%), and very severe (1.9%). The mean plasma FGF23 value observed was 115±169 pg/mL. A significant negative correlation was observed between FGF23 levels and forced expiratory volume in 1 second (FEV1) (% predicted), demonstrating the diagnostic role of FGF23. The phosphaturic action of FGF23 was validated by a strong negative correlation observed between serum phosphate and plasma FGF23 levels. Receiver-operating characteristic curve analysis of FGF23 showed that cut-off levels of 73.71 pg/mL can be used to distinguish mild to moderate COPD from severe to very severe, with a sensitivity and specificity of 62.5% and 68.4%, respectively. FGF23 levels were found to be significantly increased in individuals with poor lung function and compromised lung volumes. FGF23 levels were negatively correlated with FEV1 (% predicted) and can be used as a potential severity marker. Hence, plasma FGF23 levels showed a promising role as a severity marker of COPD.

Altmetrics

Downloads

Download data is not yet available.

Citations

Global Initiative for Chronic Obstructive Lung Disease. Global strategy for the diagnosis, management and prevention of COPD 2024. Available from: http://www.goldcopd.org/.
López‐Campos JL, Tan W, Soriano JB. Global burden of COPD. Respirology 2016;21:14-23. DOI: https://doi.org/10.1111/resp.12660
Hoesein FA, Zanen P, Lammers JW. Lower limit of normal or FEV1/FVC< 0.70 in diagnosing COPD: an evidence-based review. Respir Med 2011;105:907-15. DOI: https://doi.org/10.1016/j.rmed.2011.01.008
Kakavas S, Kotsiou OS, Perlikos F et al. Pulmonary function testing in COPD: looking beyond the curtain of FEV1. NPJ Prim Care Respir Med 2021;31:23. DOI: https://doi.org/10.1038/s41533-021-00236-w
Tilert T, Dillon C, Paulose-Ram R et al. Estimating the US prevalence of chronic obstructive pulmonary disease using pre-and post-bronchodilator spirometry: the National Health and Nutrition Examination Survey (NHANES) 2007–2010. Respir Res 2013;14:103. DOI: https://doi.org/10.1186/1465-9921-14-103
Kuro-O M. The FGF23 and Klotho system beyond mineral metabolism. Clin Exp Nephrol 2017:64-9. DOI: https://doi.org/10.1007/s10157-016-1357-6
Gulati S, Wells JM, Urdaneta GP et al. Fibroblast growth factor 23 is associated with a frequent exacerbator phenotype in COPD: a cross-sectional pilot study. Int J Mol Sci 2019;20:2292. DOI: https://doi.org/10.3390/ijms20092292
Aryal S, Diaz-Guzman E, Mannino DM. COPD and gender differences: an update. Transl Res 2013;162:208-18. DOI: https://doi.org/10.1016/j.trsl.2013.04.003
Laniado-Laborín R. Smoking and chronic obstructive pulmonary disease (COPD). Parallel epidemics of the 21st century. Int J Environ Res Public Health 2009;6:209-24. DOI: https://doi.org/10.3390/ijerph6010209
Salvi SS, Barnes PJ. Chronic obstructive pulmonary disease in non-smokers. Lancet 2009;374:733-43. DOI: https://doi.org/10.1016/S0140-6736(09)61303-9
Díaz AA, Pinto-Plata V, Hernández C et al. Emphysema and DLCO predict a clinically important difference for 6MWD decline in COPD. Respir Med 2015;109:882-9. DOI: https://doi.org/10.1016/j.rmed.2015.04.009
Hanudel MR, Laster M, Salusky IB. Non-renal-related mechanisms of FGF23 pathophysiology. Curr Osteoporos Rep 2018;16:724-9. DOI: https://doi.org/10.1007/s11914-018-0492-2
Faul C, Amaral AP, Oskouei B et al. FGF23 induces left ventricular hypertrophy. J Clin Invest 2011;121:4393-408. DOI: https://doi.org/10.1172/JCI46122
Seiler S, Heine GH, Fliser D. Clinical relevance of FGF-23 in chronic kidney disease. Kidney Int Suppl 2009;76:S34-42. DOI: https://doi.org/10.1038/ki.2009.405
Musgrove J, Wolf M. Regulation and effects of FGF23 in chronic kidney disease. Annu Rev Physiol 2020;82:365-90. DOI: https://doi.org/10.1146/annurev-physiol-021119-034650
Lu X, Hu MC. Klotho/FGF23 axis in chronic kidney disease and cardiovascular disease. Kidney Dis 2017;3:15-23. DOI: https://doi.org/10.1159/000452880
Stöhr R, Schuh A, Heine GH, Brandenburg V. FGF23 in cardiovascular disease: innocent bystander or active mediator? Front Endocrinol 2018;9:351. DOI: https://doi.org/10.3389/fendo.2018.00351
Lutfi MF. The physiological basis and clinical significance of lung volume measurements. Multidiscip Respir Med 2017;12:1-2. DOI: https://doi.org/10.1186/s40248-017-0084-5
Yetkin O, Gunen H. Inspiratory capacity and forced expiratory volume in the first second in exacerbation of chronic obstructive pulmonary disease. Clin Respir J 2008;2:36-40. DOI: https://doi.org/10.1111/j.1752-699X.2007.00040.x
Kraen M, Frantz S, Nihlén U, et al. Fibroblast growth factor 23 is an independent marker of COPD and is associated with impairment of pulmonary function and diffusing capacity. Respir Med 2021;182:106404 DOI: https://doi.org/10.1016/j.rmed.2021.106404
Kitaguchi Y, Fujimoto K, Kubo K, Honda T. Characteristics of COPD phenotypes classified according to the findings of HRCT. Respir Med 2006;100:1742-52. DOI: https://doi.org/10.1016/j.rmed.2006.02.003
Gravelyn TR, Brophy N, Siegert C, Peters-Golden M. Hypophosphatemia-associated respiratory muscle weakness in a general inpatient population. Am J Med 1988;84:870-6. DOI: https://doi.org/10.1016/0002-9343(88)90065-4

Ethics Approval

the study protocol was reviewed and approved by the Institutional Ethics Committee, GMCH (Government Medical College and Hospital, Sector 32, Chandigarh, India) with document approval number GMCH/IEC/774R/2022/189.

How to Cite



“Evaluation of Fibroblast Growth Factor 23 As a Marker of Severity in Stable Chronic Obstructive Pulmonary Disease”. 2025. Monaldi Archives for Chest Disease, June. https://doi.org/10.4081/monaldi.2025.3271.