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Assessment of Vascular Function in Patients With Chronic Kidney Disease
08:50

Assessment of Vascular Function in Patients With Chronic Kidney Disease

Published on: June 16, 2014

15.4K

Endothelial damage and vascular calcification in patients with chronic kidney disease

Sagrario Soriano1, Andrés Carmona1, Francisco Triviño2

  • 1Instituto Maimónides de Investigación Biomédica de Córdoba, Reina Sofía University Hospital, University of Córdoba, Córdoba, Spain; Nephrology Unit, Reina Sofía University Hospital, Córdoba, Spain; RETICs Red Renal (Instituto de Salud Carlos III), Madrid, Spain; and.

American Journal of Physiology. Renal Physiology
|October 24, 2014
PubMed

Insights

Vascular calcification in chronic kidney disease is linked to more endothelial microparticles and fewer endothelial progenitor cells. These microparticles may drive calcification by increasing osteocalcin expression in progenitor cells.

Area of Science:

  • Nephrology
  • Cardiovascular Medicine
  • Cell Biology

Background:

  • Vascular calcification (VC) is a significant complication in chronic kidney disease (CKD), increasing cardiovascular risks.
  • Endothelial microparticles (MPs) and endothelial progenitor cells (EPCs) are implicated in vascular health and disease.

Purpose of the Study:

  • To investigate the role of endothelial MPs and EPCs in the development of VC in CKD patients.
  • To explore the mechanisms by which MPs and EPCs influence VC, particularly osteocalcin (OCN) expression.

Main Methods:

  • Quantified circulating endothelial MPs and EPCs in CKD patients with and without VC.
  • Assessed OCN expression in EPCs from CKD patients.
  • Conducted in vitro experiments using MPs from CKD patients to induce OCN expression in healthy EPCs, vascular smooth muscle cells, and fibroblasts.

Main Results:

  • CKD patients with VC had significantly higher levels of circulating endothelial MPs and lower percentages of EPCs compared to those without VC.
  • EPCs expressing OCN were more numerous in CKD patients with VC.
  • MPs from CKD patients induced OCN expression in healthy EPCs, vascular smooth muscle cells, and fibroblasts, with a more pronounced effect from MPs of VC patients.

Conclusions:

  • An imbalance between endothelial damage (increased MPs) and repair (decreased EPCs) contributes to VC in CKD.
  • EPCs, via OCN expression, may directly participate in the pathogenesis of vascular calcification in CKD patients.

Keywords:
chronic kidney diseaseendothelial damageendothelial microparticlesendothelial progenitors cellsvascular calcification

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