title: Effect of different dialysis modalities on microinflammatory status and endothelial damage.
abstract: OBJECTIVE
  We studied the relationship between microinflammation and endothelial damage in chronic kidney disease (CKD) patients on different dialysis modalities.
  
  
  METHODS
  Four groups of CKD stage 5 patients were studied: 1) 14 nondialysis CKD patients (CKD-NonD); 2) 15 hemodialysis patients (HD); 3) 12 peritoneal dialysis patients with residual renal function >1 ml/min (PD-RRF >1); and 4) 13 peritoneal dialysis patients with residual renal function <or=1 ml/min (PD-RRF <or=1). Ten healthy subjects served as controls. CD14(+)CD16(+) cells and apoptotic endothelial microparticles (EMPs) were measured by flow cytometry. Serum vascular endothelial growth factor (VEGF) was measured by ELISA.
  
  
  RESULTS
  CKD-NonD and HD patients had a higher percentage of CD14(+)CD16(+) monocytes than PD groups and controls. CD14(+)CD16(+) was similar in the PD groups, regardless of their RRF, and controls. The four uremic groups displayed a marked increase in apoptotic EMPs and VEGF compared with controls. Apoptotic EMPs and VEGF were significantly higher in HD patients than in CKD-NonD and both PD groups. However, there were no significant differences between CKD-NonD and the two PD groups. There was a correlation between CD14(+)CD16(+) and endothelial damage in CKD-NonD and HD patients, but not in PD and controls.
  
  
  CONCLUSIONS
  There was an increase in CD14(+)CD16(+) only in CKD-NonD and HD patients. In these patients, there was a relationship between increased CD14(+)CD16(+) and endothelial damage. These results strongly suggest that other factors unrelated to the microinflammatory status mediated by CD14(+)CD16(+) are promoting the endothelial damage in PD, regardless of their RRF.
authors.affiliation: Unidad de Investigación, Servicio de Nefrología, Hospital Universitario Reina Sofía, Córdoba, Spain.
authors.forename: Ana
authors.initials: A
authors.lastname: Merino
authors.forename: José
authors.initials: J
authors.lastname: Portolés
authors.forename: Rafael
authors.initials: R
authors.lastname: Selgas
authors.forename: Raquel
authors.initials: R
authors.lastname: Ojeda
authors.forename: Paula
authors.initials: P
authors.lastname: Buendia
authors.forename: Javier
authors.initials: J
authors.lastname: Ocaña
authors.forename: M Auxiliadora
authors.initials: MA
authors.lastname: Bajo
authors.forename: Gloria
authors.initials: G
authors.lastname: del Peso
authors.forename: Julia
authors.initials: J
authors.lastname: Carracedo
authors.forename: Rafael
authors.initials: R
authors.lastname: Ramírez
authors.forename: Alejandro
authors.initials: A
authors.lastname: Martín-Malo
authors.forename: Pedro
authors.initials: P
authors.lastname: Aljama
mesh_terms: D000328:Adult; D000368:Aged; D017209:Apoptosis; D015415:Biomarkers / Q000097:blood; D055252:Cell-Derived Microparticles / Q000276:immunology / Q000473:pathology*; D002908:Chronic Disease; D004730:Endothelium, Vascular / Q000276:immunology / Q000473:pathology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005434:Flow Cytometry; D058851:GPI-Linked Proteins; D006801:Humans; D007249:Inflammation / Q000276:immunology* / Q000473:pathology; D018836:Inflammation Mediators / Q000097:blood*; D007674:Kidney Diseases / Q000276:immunology / Q000473:pathology / Q000628:therapy*; D018950:Lipopolysaccharide Receptors / Q000097:blood; D008297:Male; D008875:Middle Aged; D009000:Monocytes / Q000276:immunology*; D010530:Peritoneal Dialysis / Q000009:adverse effects; D017452:Receptors, IgG / Q000097:blood; D006435:Renal Dialysis / Q000009:adverse effects; D012307:Risk Factors; D042461:Vascular Endothelial Growth Factor A / Q000097:blood
chemical_list: D015415:Biomarkers; C428200:FCGR3B protein, human; D058851:GPI-Linked Proteins; D018836:Inflammation Mediators; D018950:Lipopolysaccharide Receptors; D017452:Receptors, IgG; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A