One-Year Immunological Evaluation of Chronic Hemodialysis in End-Stage Renal Disease Patients

Abstract

Background: Much research has been devoted to the determination of acute leukocyte activation as well as acute cytokines production during and after blood hemodialysis membrane interaction. In contrast, few studies deal with chronic immunological evaluation of T-cell activation markers in hemodialysis. Methods: We evaluated different immune parameters using a modified cellulose low-flux hemophan vs. synthetic high-flux polyamide membrane during 1 year in 35 stable chronic hemodialysis patients. Leukocyte counts, lymphocyte subpopulations, T-cell activation markers (CD69, CD25, HLA-DR, CD54, CD62L, CD45RO, CD11a, CD28), complement-activation products (C3a) and serum elastase were measured at 0, 3, 6 and 12 months in the two patient groups and compared to 13 healthy control subjects. Results: Over dialysis time, all patients showed a significant level elevation of CD69/CD3 (p < 0.005) and CD25/ CD3 (p < 0.005) phenotypes. In contrast, HLA-DR and CD45RO remained unchanged suggesting a truncated pattern of activation. T lymphocyte subset analysis showed in both hemodialyzed groups a significant decrease in the expression of CD54 (ICAM-1) when compared to controls (p < 0.005). C3a and elastase measurements showed a significant upward trend with dialysis time in both hemodialyzed groups. Conclusion: Although the immunological changes seen in chronic hemodialyzed patients must be interpreted in conjunction with their basal uremic states and the membrane permeability properties, our study suggests that 1-year immunological evaluation of hemodialysis membranes biocompatibility is associated with changes in the pattern of chronic T-cell activation, which is in part related to the use of a particular membrane type. Moreover, some key molecules (CD54) are affected in patients with end-stage renal disease undergoing hemodialysis.

Evidence for Anti-Inflammatory Effects of Exercise in CKD

“…[54][55][56][57][58] Likewise, T lymphocytes from CKD patients show increased expression of early activation markers and heightened apoptotic turnover. [43][44][45][46][47][48][59][60][61] Of note, data from our control patients indicates a progressive state of monocyte activation over the study period. Thus, it seems that the apparent exerciseinduced downregulation of the immune response might be a small price to pay for the anti-inflammatory effects.…”

Alloantigen-stimulated induction and release of CD30 in patients with end-stage renal failure

“…0.450) as suggested by Süsal et al [18], none of the HC but as many as 43% of the ESRF patients showed a high sCD30 serum content. It is reasonable to suggest that a higher serum content of the T cell activation marker sCD30 in ESRF patients might be explained by chronic inflammation and persistent activation of circulating T cells, which are typical phenomena in patients with uremia [30][31][32][33]. This would be in agreement with previous observations in patients with HIV infection or autoimmunity, where in vitro and in vivo findings suggested that acute and chronic inflammatory/ infectious processes stimulate sCD30 secretion, and that high levels of sCD30 in serum and synovial fluid appear to be a reflection of preactivated CD30-committed T cells recruited to inflammatory sites [34,35].…”

CD4+/FOXP3+ Regulatory T Cells in End-Stage Kidney Disease: Molecular Pathways Trough Cell-Cycle Arrest and Apoptosis

“…Thus, in uremic patients, oxLDL seem to play a specific role in the frequencies and phenotypes of CD4 + /CD25 + /CD127¯ Tregs, which distinctly discriminates between nTreg and effector cell subsets [15]. Indeed, in these patients, oxLDL inhibit CD25 expression at the cell surface, whereas the expression of CD3 and CD4 (constitutively expressed on T cells), CD69 (early activation antigen) and HLA-DR (late activation antigen) is unchanged [9,15,41]. Thus oxLDL do not alter the steps of the signalling pathways triggering CD69 and HLADR expression, but mild oxidation of LDL is sufficient to dramatically disturb CD25 expression as demonstrated in a recent study [15].…”

“…Previous findings suggested that in patients with ESKD, a significantly high percentage of activated T cells ultimately did not proliferate but became apoptotic [41,42]. Circulating T cells from HD patients show clear signs of biological activation, likely caused by the combined action of activated complement components, blood-dialyzer interaction, and such dialysate contaminants as endotoxins.…”