Atherosclerosis and the subsequent cardiovascular diseases are the most important causes of morbidity and mortality in patients with chronic kidney disease (CKD). CKD atherosclerosis is closely associated with the inflammatory status which is chronically present in these patients. Hemodiafiltration (HDF) is a highly effective dialysis modality expanding the spectrum of removed uremic toxins from small to middle-sized molecular solutes. In addition, the online (OL) HDF using high fluid substitution allows a greater clearance of large uremic toxins. We have shown that OL-HDF markedly reduces the number of CD14+CD16+ monocyte-derived dendritic cells and their proinflammatory potential in CKD patients without clinical evidence of inflammatory disease. Moreover, we have also reported that OL-HDF improved endothelial dysfunction with a decrease in the number of endothelial microparticles (EMP) in peripheral blood and an increase in the percentage of endothelial progenitor cells (EPC) as compared with high-flux hemodialysis (HF-HD). The results obtained showed in both studies a reduction of CD14+CD16+ dendritic cells, EMP and ECP in comparison with HF-HD. These data strongly suggest that the microinflammation status observed in CKD patients is associated with endothelial damage and that amelioration of the chronic microinflammation using high convective transport appears to reduce endothelial damage and promote endothelial repair. Future studies will have to assess the mechanisms of these immunological changes and their relevance in the reported improved survival of patients treated with OL-HDF.