The prevalence of anti-HCV(+) in HD has decreased markedly over the last decade in the participating units from most European countries. This decrease should reduce further the risk of nosocomial and occupational HCV infection in HD and ultimately contribute to improved long-term prognosis of HD patients and kidney graft recipients.

In order to test the existence of a possible oxidative damage during hemodialysis, plasma conjugated dienes (CD), plasma and red blood cell (RBC) thiobarbituric acid (TBA) reactants were investigated in 25 patients receiving regular dialysis treatment (RDT). The RBC TBA reactant concentration was significantly increased in RDT patients in comparison with healthy subjects. The extracellular antioxidant systems were evaluated by the assay of plasma antioxidant activity, plasma tocopherol, urate, transferrin, haptoglobin and ceruloplasmin levels. Except urate and transferrin, none of these parameters were different between the two groups. On the other hand, in RDT patients, RBC superoxide dismutase (SOD) and glutathione peroxidase (GPX) activities were significantly lower than in healthy subjects. There was an inverse correlation between decreased RBC GPX and RBC TBA reactant concentration. These results show in RDT patients the existence of an oxidizing stress, mainly intracellular, which could be due, in part, to a decrease in SOD and GPX activities.

We investigated expression of several antigens on neutrophils and monocytes, involved in cell adhesion, from patients hemodialyzed with cellulosic and polyacrylonitrile membranes. Among the antigens tested only the expression of CD15s and CD11b was significantly increased on neutrophils and monocytes in patients dialyzed with cellulosic membranes. No changes occurred with polyacrylonitrile membranes. Leukocyte counts from patients dialyzed with cuprophane membranes decreased at the same time as expression of cellular CD15s increased, resulting in a significant negative correlation at all time points tested. No correlation was found between the drop of monocytes and their expression of CD11b. When CD15s expression increased on neutrophils and monocytes, we observed a concomitant increase of CD62P, a specific selectin of activated platelets. When whole blood cells were incubated with complement activated serum both antigens increased but not when cells were incubated with hrC5a. We also observed that CD61, a platelet phenotypic antigen, was present on leukocytes incubated with complement activated serum. At the time when platelet-leukocyte coaggregates decreased, CD62P expression remained stable on leukocytes, suggesting that both neutrophils and monocytes are able to trap either CD62P shed by activated platelets or soluble CD62P present in normal human serum. The present study documents a major role of P-selectin (CD62P)/sialyl-Lewis x (CD15s) interaction in the transient leukocyte margination during hemodialysis.

The generation of compounds such as interleukin 1 (IL-1), tumor necrosis factor alpha (TNFα), and the possible encounter of circulating cells with endotoxin (LPS) have been demonstrated during hemodialysis. All these factors are able to induce the production of IL-6 by human monocytes. Anaphylatoxins can be generated following complement activation by cellulosic membrane dialysis. C5a is known to potentiate the LPS-induced production of IL-1 and TNFα, and we established that recombinant human C5a was able to act synergistically with LPS in the induction of IL-6 by human monocytes. We investigated whether IL-6 could be detected in the serum of long-term hemodialyzed and uremic patients. Using the very sensitive 7TD1 cell line bioassay, we demonstrated that circulating IL-6 activity was present in the serum of all 14 tested patients, whereas it was occasionally present in normal sera. The presence of serum IL-6 was confirmed using an anti-IL-6 antibody and a specific ELISA (109 ± 36 pg/ml). Most patients had a reproducible level of IL-6 activity throughout a period of 10 days. The dialysis session did not significantly modify these levels and patients had similar serum IL-6 activity at the start, during or the at end of the dialysis session. The different parameters of the dialysis session (i.e. standard or filtrated dialyzates, complement-activating or nonactivating membranes) did not significantly influence the levels of IL-6. Elevated levels of IL-6 were also observed in uremic patients compared to normal donors, although significantly lower than in hemodialyzed patients (p = 0.001). Since IL-6 is a hepatocyte-stimulating mediator, we searched for a correlation with C-reactive protein (CRP). Although 4/14 hemodialyzed patients and 5/9 uremic patients had high CRP values, there was no correlation with IL-6 levels. Whether or not the hemodialysis itself or the pathology is responsible of the elevated level of IL-6 is discussed.

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