Effect of changing from a cellulose acetate to a polysulphone dialysis membrane on protein oxidation and inflammation markers.
BACKGROUND
In vitro, synthetic dialysis membranes induce less activation of blood components to produce pro-inflammatory cytokines and reactive oxygen species compared with cellulose acetate membranes. However, the long-term effect of switching from a cellulose-based dialysis membrane to a synthetic membrane on protein oxidation and systemic inflammation in hemodialysis patients is not well defined.


METHODS
Nineteen patients receiving hemodialysis were followed prospectively after changing from a low-flux cellulose acetate membrane to a low-flux polysulphone membrane for 11-17 months (n = 15) and then returning to the cellulose acetate membrane for 1 month (n = 13). Plasma markers of protein oxidation, cell activation and systemic inflammation and concentrations of soluble cell adhesion molecules were measured at baseline and at the end of each intervention period.


RESULTS
Plasma levels of protein thiols (18%), IL-6 (34%), VCAM-1 (33%), ICAM-1 (21%) and beta2-microglobulin (21%) increased significantly and dityrosine fluorescence (-36%), protein lipofuscin-like fluorophores (-18%) and TNF-alpha (-20%) decreased significantly in the patients after they switched to the polysulphone membrane. After reverting to the cellulose acetate membrane for 1 month, plasma levels of protein thiols and IL-6 returned to baseline while levels of other variables were not significantly different from values at the end of the polysulphone dialysis period. There was substantial intra-individual variation between 2 baseline measurements of plasma cytokines.


CONCLUSIONS
Switching from a cellulose acetate membrane to a low-flux polysulphone dialysis membrane for a year or more may decrease the level of protein oxidation suggesting a decrease in oxidant stress and greater biocompatibility of the polysulphone membrane. The effect of this change in dialysis membrane on systemic inflammation is uncertain due to increases in some but not other inflammation-sensitive molecules.
Walker
R J
RJ
Department of Medical and Surgical Sciences, Dunedin School of Medicine, University of Otago, Dunedin, New Zealand. rob.walker@stonebow.otago.ac.nz
Sutherland
W H F
WH
De Jong
S A
SA
D001798:Blood Proteins / Q000378:metabolism*; D002482:Cellulose / Q000031:analogs & derivatives*; D016207:Cytokines / Q000097:blood*; D005260:Female; D006437:Hemodialysis, Home / Q000295:instrumentation; D006801:Humans; D007249:Inflammation; D007688:Kidneys, Artificial; D008297:Male; D008567:Membranes, Artificial; D008875:Middle Aged; D010084:Oxidation-Reduction; D011108:Polymers; D011446:Prospective Studies; D013450:Sulfones
D001798:Blood Proteins; D016207:Cytokines; D008567:Membranes, Artificial; D011108:Polymers; D013450:Sulfones; C017662:polysulfone P 1700; C005062:acetylcellulose; D002482:Cellulose