Cytokine induction in patients undergoing regular online hemodiafiltrationtreatment

End-stage renal disease (ESRD) patients are known to suffer from chronic in flammation as the result of an ongoing subacute cytokine induction, which m ay contribute considerably to dialysis-related, long-term morbidity and mor tality. Preparation of infusate from cytokine-inducing dialysis fluid and i ts administration in large quantities as well as the use of high-flux membr anes bear the risk of aggravating the chronic inflammatory response among o nline hemodiafiltration (online HDF) patients. In order to assess the infla mmatory risk associated with online HDF, we compared the cytokine induction profile of ESRD patients receiving either online HDF or low-flux hemodialy sis (low-flux HD). Specifically, we measured spontaneous and lipopolysaccha ride (LPS)-stimulated tumor necrosis factor alpha (TNF alpha) and interleuk in-1 receptor antagonist (IL-1Ra) release during ex vivo incubation of whol e blood. Ultrapure dialysis fluid and polysulfone membranes were used for b oth treatment modalities. LPS-stimulated release of TNF alpha and IL-1Ra wa s elevated for both online HDF and low-flux HD patients compared to healthy individuals (TNF alpha: 2,336 +/- 346 and 2,192 +/- 398 versus 1,218 +/- 2 24 pg/10(6) white blood cells [WBC]; IL-1Ra: 2,410 +/- 284 and 2,326 +/- 18 6 versus 1,678 +/- 219 pg/10(6) WBC). Likewise, spontaneous production of T NF alpha, but not IL-1Ra, was higher in online HDF and low-flux HD patients than in normal controls (37 +/- 32 and 22 +/- 19 versus 0.8 +/- 0.3 pg TNF alpha/10(6) WBC). There was no difference in spontaneous and LPS-stimulate d cytokine release between both dialysis groups. In addition, intradialytic cytokine induction was not significant for either treatment modality as sp ontaneous and LPS-stimulated cytokine release were not increased postdialys is. These findings indicate that online HDF does not contribute to chronic leukocyte activation and, consequently, does not place ESRD patients at gre ater risk with respect to inflammatory morbidity and mortality.