Abstract: SA-PO878

Immune Cell Subsets Related to Vascular Calcification in Hemodialysis Patients

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

  • Rodriguez-Carrio, Javier, Hospital Universitario Central de Asturias, Instituto Reina Sofía de Investigación, REDinREN del ISCIII, Oviedo, Spain
  • Seijo, Mariana, Hospital Universitario Central de Asturias, Instituto Reina Sofía de Investigación, REDinREN del ISCIII, Oviedo, Spain
  • Ulloa, Catalina, Hospital Universitario Central de Asturias, Oviedo, Spain
  • Carrillo-Lopez, Natalia, Hospital Universitario Central de Asturias, Instituto Reina Sofía de Investigación, REDinREN del ISCIII, Oviedo, Spain
  • Rodriguez, Minerva, Hospital Universitario Central de Asturias, Oviedo, Spain
  • Suarez, Ana, University of Oviedo, Oviedo, Spain
  • Cannata-Andia, Jorge B., Hospital Universitario Central de Asturias, Instituto Reina Sofía de Investigación, REDinREN del ISCIII, Oviedo, Spain
  • Dusso, Adriana S., Hospital Universitario Central de Asturias, Instituto Reina Sofía de Investigación, REDinREN del ISCIII, Oviedo, Spain
Background

In CKD patients, inflammation contributes to the disproportionally high incidence of vascular calcification (VC) through immune mechanisms that remain incompletely understood. This study aims to characterize different immune cell subsets related to VC in the context of CKD.

Methods

A group of individuals with normal renal function (n=5) and non-diabetic hemodialysis (HD) patients (n=17), matched by CKD etiology, age and gender but with either none, moderate or severe arterial calcification (Kauppila and Lumbar Spine indexes) were studied for inflammatory and aging markers (flow cytometry) and biochemical parameters of bone and mineral homeostasis.

Results

HD patients exhibited an increased frequency of the senescent CD4+CD28nullT-cell subset (p=0.030), which were associated with the degree of VC and negatively correlated with 25-hydroxyvitamin D levels (r=-0.594, p=0.025). Angiogenic T cells (CD3+CD31+CD184+), related to vascular homeostasis, were decreased in HD patients (p=0.024), regardless of their degree of VC. The frequency of regulatory T cells (Treg, CD4+CD25highCD127low/negFOXP3+) did not differ between HD patients and healthy controls, although they were slightly reduced in patients without VC (p=0.022) compared to those with VC (moderate and severe groups). However, the analysis of cytokine expression may point to a non-regulatory phenotype of Treg in the latter. Additionally, ACE expression was higher in monocytes from HD patients (p=0.020) compared to healthy counterparts. This increase was restricted to intermediate monocytes (CD14+CD16+), strongly increased in patients (p<0.001), and was found even in patients without VC. ACE expression on intermediate monocytes was negatively associated with vitamin D (r=-0.499, p=0.060) and positively with PTH (r=0.578, p=0.030). Finally, a higher percentage of low-density granulocytes (CD14lowCD15+) was observed in CKD (p<0.001).

Conclusion

Several immune cell subsets related to inflammation, immunosenescence and vascular homeostasis are altered in CKD, even in the early stages of VC. Impaired vitamin D levels may be associated with this abnormal immune profile. This study paves the ground for the identification of early biomarkers to identify patients at higher risk of developing VC.

Funding

  • Government Support - Non-U.S.