title: Microinflammation and endothelial damage in hemodialysis.
abstract: BACKGROUND
  Chronic kidney disease (CKD) stage 4-5 patients have increased cardiovascular morbidity and mortality rates compared with the general population. Chronic inflammation has been proposed as a cardiovascular risk factor. We have previously demonstrated that the majority of CKD patients show a microinflammatory state with an increased percentage of CD14+/CD16+ monocytes in peripheral blood, even in patients who do not show clinical evidence of inflammatory disease. However, the role played by these microinflammatory cells on the endothelial damage that precede the development of cardiovascular disease has not been investigated.
  
  
  METHODS
  To study the effect of microinflammation on endothelial cell injury we have developed an experimental co-culture model in which isolated CD14+/CD16+ cells were seeded in 24-well tissue-culture plates. Human umbilical vein endothelial cells were placed on the top of the culture well in a insert that permitted intercellular soluble network communication. To stimulate the release of proinflammatory products, monocytes were activated with substimulating doses of bacterial DNA. Endothelial injury was characterized measuring intracellular reactive oxygen species activity and cell apoptosis.
  
  
  RESULTS
  Only CD14+/CD16+ cells released proinflammatory cytokines when they were stimulated by bacterial DNA. In the culture wells in which inflammatory cytokines were detected, endothelial cells showed an increased reactive oxygen species activity and features of apoptosis.
  
  
  CONCLUSIONS
  Our results support the hypothesis that independently of uremia, in CKD stage 4-5 patients microinflammation mediated by CD14+/CD16+ cells induces endothelial damage and thus may contribute to the increased risk of atherosclerosis and cardiovascular disease that has been reported in this population.
authors.affiliation: Department of Nephroplogy and Research Unit, University Hospital Reina Sofia, Cordoba, Spain.
authors.forename: Ana
authors.initials: A
authors.lastname: Merino
authors.forename: Sonia
authors.initials: S
authors.lastname: Nogueras
authors.forename: Paula
authors.initials: P
authors.lastname: Buendía
authors.forename: Raquel
authors.initials: R
authors.lastname: Ojeda
authors.forename: Julia
authors.initials: J
authors.lastname: Carracedo
authors.forename: Rafael
authors.initials: R
authors.lastname: Ramirez-Chamond
authors.forename: Alejandro
authors.initials: A
authors.lastname: Martin-Malo
authors.forename: Pedro
authors.initials: P
authors.lastname: Aljama
mesh_terms: D050197:Atherosclerosis / Q000209:etiology; D002318:Cardiovascular Diseases / Q000209:etiology; D002908:Chronic Disease; D042783:Endothelial Cells / Q000502:physiology*; D006801:Humans; D007249:Inflammation / Q000150:complications*; D007674:Kidney Diseases / Q000150:complications; D018950:Lipopolysaccharide Receptors / Q000032:analysis; D009000:Monocytes / Q000502:physiology; D017452:Receptors, IgG / Q000032:analysis; D006435:Renal Dialysis
chemical_list: D018950:Lipopolysaccharide Receptors; D017452:Receptors, IgG