• Ana Merino, José Portolés, Rafael Selgas, Raquel Ojeda, Paula Buendia, Javier Ocaña, M Auxiliadora Bajo, Gloria del Peso, Julia Carracedo, Rafael Ramírez, Alejandro Martín-Malo, and Pedro Aljama.
• Unidad de Investigación, Servicio de Nefrología, Hospital Universitario Reina Sofía, Córdoba, Spain.
• Clin J Am Soc Nephrol. 2010 Feb 1; 5 (2): 227-34.

Background And ObjectivesWe studied the relationship between microinflammation and endothelial damage in chronic kidney disease (CKD) patients on different dialysis modalities.Design, Setting, Participants, & MeasurementsFour 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 ResultsCKD-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.ConclusionsThere 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.

44 keywords...

hide…