RT Journal Article
T1 Endothelial damage and vascular calcification in patients with chronic kidney disease
A1 Soriano, Sagrario
A1 Carmona, Andrés
A1 Triviño, Francisco
A1 Rodríguez, Mariano
A1 Álvarez Benito, Marina
A1 Martín Malo, Alejandro
A1 Álvarez Lara, María Antonia
A1 Ramírez, Rafael
A1 Aljama, Pedro
A1 Carracedo Añón, Julia María
AB Vascular calcification (VC) is a frequent complication of chronic kidney disease (CKD) and is a predictor of cardiovascular morbidity and mortality. In the present study, we investigated the potential involvement of endothelial microparticles (MPs) and endothelial progenitor cells (EPCs) in the generation of VC in CKD patients. The number of circulating EMPs is greater in patients with VC than without VC (307 ± 167 vs. 99 ± 75 EMPs/μl, P < 0.001). The percentage of EPCs is significantly lower in patient with VC than in patients without VC (0.14 ± 0.11% vs. 0.25 ± 0.18%, P = 0.002). The number of EPCs expressing osteocalcin (OCN) was higher in VC patients (349 ± 63 cells/100,000) than in non-VC patients (139 ± 75 cells/100,000, P < 0.01). In vitro, MPs obtained from CKD patients were able to induce OCN expression in EPCs from healthy donors; the increase in OCN expression was more accentuated if MPs were obtained from CKD patients with VC. MPs from CKD patients also induced OCN expression in vascular smooth muscle cells and fibroblasts. In CKD patients, the rise in endothelial MPs associated with a decrease in the number of EPCs, suggesting an imbalance in the processes of endothelial damage and repair in CKD patients, mainly those with VC. Our results suggest that EPCs, through OCN expression, may directly participate in the process of VC.
PB American Physiological Society
SN 1931-857X
YR 2014
FD 2014-10-22
LK https://hdl.handle.net/20.500.14352/131831
UL https://hdl.handle.net/20.500.14352/131831
LA eng
NO Soriano, S., Carmona, A., Triviño, F., Rodriguez, M., Alvarez-Benito, M., Martín-Malo, A., Alvarez-Lara, M.-A., Ramírez, R., Aljama, P., & Carracedo, J. (2014). Endothelial damage and vascular calcification in patients with chronic kidney disease. American Journal of Physiology - Renal Physiology, 307(11), 1302-1311. https://doi.org/10.1152/ajprenal.00114.2014
NO ACKNOWLEDGMENTS: The authors are grateful to M. J. Jimenez and R. Moyano for technical assistance. GRANTS: This work was supported by Fondo de Investigación Sanitaria, Instituto de Salud Carlos III Grants PI0900836, PI1000960, PI1101536, and PI1201489; RETICs Red Renal Grant RD0600160007; Junta de Andalucía Grants JA0797-2010, P08-CTS-3797, P010-CTS-6337, P11-CTS-7352; and Fundación Nefrológica. J. Carracedo was supported by a contract from Fundación de Investigaciones Biomédicas de Córdoba (Programa Nicolás Monardes).
NO Instituto de Salud Carlos III (España)
NO RETICs Red Renal (España)
NO Junta de Andalucía
NO Fundación Nefrológica (España
NO Fundación de Investigaciones Biomédicas de Córdoba (España)
DS Docta Complutense
RD 20 abr 2026