Effect of different dialysis modalities on microinflammatory status and endothelial damage.
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.
Merino
Ana
A
Unidad de Investigación, Servicio de Nefrología, Hospital Universitario Reina Sofía, Córdoba, Spain.
Portolés
José
J
Selgas
Rafael
R
Ojeda
Raquel
R
Buendia
Paula
P
Ocaña
Javier
J
Bajo
M Auxiliadora
MA
del Peso
Gloria
G
Carracedo
Julia
J
Ramírez
Rafael
R
Martín-Malo
Alejandro
A
Aljama
Pedro
P
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
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