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Kidney Week

Abstract: SA-PO338

Patrolling Monocyte Subsets in Patients with CKD and Coronary Heart Disease

Session Information

Category: Hypertension and CVD

  • 1403 Hypertension and CVD: Mechanisms


  • Hueso, Miguel, Hospital de Bellvitge, l'Hospitalet de Llobregat, Spain
  • Casas Parra, Angela Isabel, Hospital de Bellvitge, l'Hospitalet de Llobregat, Spain
  • Mallén, Adrián, IDIBELL, Hospitalet de Llobregat, Spain
  • Guiteras, Jordi, IDIBELL, Hospitalet de Llobregat, Spain
  • Castaño, Esther, CCiTUB, L'Hospitalet, Barcelona, Spain
  • Barroso, Beatriz, CCiTUB, L'Hospitalet, Barcelona, Spain
  • Bolanos, Nuria, IDIBELL, Hospitalet de Llobregat, Spain
  • Blasco lucas, Arnau, Hospital de Bellvitge, l'Hospitalet de Llobregat, Spain
  • Sbraga, Fabrizio, Hospital de Bellvitge, l'Hospitalet de Llobregat, Spain
  • Navarro, Estanislao, IDIBELL, Hospitalet de Llobregat, Spain
  • Torras, Juan, Hospital de Bellvitge, l'Hospitalet de Llobregat, Spain

Chronic low-grade inflammation is prevalent in Chronic Kidney Disease (CKD) patients and plays a role in the development and progression of cardiovascular diseases. Monocytes are key factors in atherosclerosis progression and can be classified into subtypes based on their profiles of LPS co-receptor CD14 and FCgIII CD16 expression. The aim of this work is to analyze circulating monocytes subsets in CKD patients with atherosclerotic coronary artery lesions undergoing coronary Artery Bypass Surgery (CABG).


A prospective Case-Control study was conducted in CABG patients. Controls were patients with non-coronary lesions undergoing valve repair heart surgery. The expression of CD14+ and CD16+ antigens were analyzed by flow cytometry in peripheral blood mononuclear cells. A sample of perivascular adipose tissue and a punch from aorta were also obtained from patients included in the study.


A total of 72 CABG patients (56 males) from which 40 suffered CKD (stages 3 to 5) and 26 non-coronary heart surgery controls (17 males) from which 11 patient suffered CKD were included. Here, we show the flow cytometry analysis. The proportion of classical CD14+CD16- monocytes (78.5±11% in CABG vs 75.9±12.1% in controls; p=0.3), CD14++CD16+ (10.8±8% in CABG vs 12.9±9.7 in controls; p=0.2) and CD14+CD16++ (10.9±6.6 vs 11.1±5.2 %: p=0.9) was similar in CABG than in controls. CKD was associated with a depletion of the CD14+CD16++ subset (CD14+CD16-: 76.4±12.5% in patients without CKD; n=50, vs 78.6±10.1% in CKD, n=48; p=0.4; CD14++CD16+: 11.2±8.1% without CKD vs 11.7±8.8% in CKD; p=0.4; and CD14+CD16++:12.4±7.2 vs 9.7±4.5 %: p=0.026). The depletion of CD14+CD16++ monocytes showed a significant negative correlation with systolic arterial pressure (R=-0.374, p=0.0001).


CKD and systolic arterial pressure were associated with a depletion in CD14+CD16++ monocytes in peripheral blood of patients. Next, we plan to study the expression of adhesion molecules in the surface of the CD14+CD16++ monocytes to determine their ability to adhere to endothelial cells.


  • Government Support - Non-U.S.