The impact of high-flux hemodialysis on clinical outcomes remains controversial. We have previously shown that in vivo transmigrated leukocytes from patients with low-flux bioincompatible hemodialysis have an impaired capacity to upregulate CD11b at the site of interstitial inflammation. In the present study, we investigated the in vivo capacity of transmigrated monocytes and granulocytes to express CD11b at the site of interstitial inflammation in 10 patients on biocompatible high-flux hemodiafiltration or high-flux hemodialysis and 12 healthy subjects, and the in vitro response to a bacteria-related peptide (N-formyl-methionyl-leucyl-phenylalanine (fMLP)). Leukocyte formation of hydrogen peroxide (H(2)O(2)) and leukocyte apoptosis were also studied. In patients, both monocytes and granulocytes had a preserved capacity to express CD11b following in vivo transmigration to sites of interstitial inflammation, compared with cells from healthy subjects. Furthermore, monocytes and granulocytes from patients showed a preserved ability to respond to challenge with fMLP in the extravascular milieu. The intracellular killing capacity of leukocytes (H(2)O(2) production) in the interstitium was similar as of cells from healthy subjects both before and after stimulation with fMLP. Following maximal receptor independent stimulation (phorbol 12-myristate 13-acetate), leukocytes from patients showed lower H(2)O(2) production at the site of intense inflammation, compared with cells from healthy subjects. Finally, leukocyte apoptosis in interstitial inflammation was similar in patients and healthy subjects. We conclude that in vivo transmigrated leukocytes from patients on biocompatible high-flux hemodiafiltration or high-flux hemodialysis have a preserved capacity to express CD11b at the site of interstitial inflammation. This may have important biological implications.