Abstract: SA-PO871
Fibroblast Growth Factor-23 and Vascular Calcification in Human Atherosclerosis
Session Information
- Vascular Calcification
November 04, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Mineral Disease
- 1205 Vascular Calcification
Authors
- Navarro-Gonzalez, Juan F., Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain
- Donate, Javier, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain
- Martín-Núñez, Ernesto, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain
- Ferri, Carla M., Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain
- López-Castillo, Angel, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain
- Delgado-Molinos, Alejandro, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain
- Pérez-Delgado, Nayra, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain
- Hernández-Carballo, Carolina, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain
- Castro López-Tarruella, Victoria, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain
- Mora, Carmen, Hospital Universitario Nuestra Señora de Candelaria, Santa Cruz de Tenerife, Spain
Background
Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone implicated in disorders of serum phosphorus concentration and vitamin D, as well as in cardiovascular disease. Vascular calcification (VC) is a significant component of vascular disease and atherosclerosis in chronic kidney disease, with important clinical and outcome implications. However, the role of FGF23 in VC remains controversial. In this study we investigate the relationship between FGF23 and VC in patients with clinical atherosclerotic disease.
Methods
Eighty-six patients (mean age, 69.7±10.3 years; 76% males) undergoing an elective open vascular surgery procedure affecting different vascular territories (carotid, aorta, femoral) were included in this study. Serum intact and C-terminal FGF-23 were measured by ELISA. A rabbit polyclonal anti-FGF-23 antibody (1:250 dilution) was used for immunohistochemistry. Transcripts encoding for FGF-23, RunX-2 and GAPDH (housekeeping gene) were measured by TaqMan real-time quantitative PCR.
Results
VC was present in 35 patients (41%). Serum concentrations of FGF-23, both the intact form and the C-terminal, were significantly higher in patients with VC: 24.2 (12-44) vs. 16.8 (10-26) pg/mL; and 36 (27-93) vs. 31.7 (19-52) RU/mL, respectively (P<0.01). We also determined the expression levels of FGF-23 and RunX-2 genes in vascular samples. Expression levels of both genes were significantly higher in samples with VC (P<0.05). Correlation analysis showed a significant association between vascular expression levels of FGF-23 and RunX-2 (r = 0.74, P<0.01). Finally, FGF-23 immunoreactivity was present in 90% of artery samples obtained from subjects with VC, but only in 56% of samples recovered from patients without VC (P<0.05). In all the samples with positive immunoreactivity for FGF-23, the signal for this factor was detected both intra- and extra-cellularly.
Conclusion
In conclusion, FGF-23 is related to VC in patients with clinical atherosclerosis. These findings suggest that transformation of vascular smooth muscle cells (the main cell type involved in VC process in the renal patient) towards an osteogenic phenotype is associated with the capability of these cells to produce FGF-23.
Funding
- Government Support - Non-U.S.