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Role of protein adsorption on haemodialysis-induced complement activation and neutrophil defects

P Neveceral1, M Markert, J P Wauters

  • 1Division of Nephrology, University Hospital, Lausanne, Switzerland.

Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association
|January 1, 1995
PubMed

The present clinical study investigated the role of protein adsorption on complement activation and neutrophil functions during in vivo haemodialysis. The parameters were measured simultaneously at the arterial and venous sites of a cuprophan (CU) dialyser with or without pretreatment with human albumin, human immunoglobulins or human total plasma proteins (PLP). Leukocyte count, complement activation (C3a des arg), oxygen radical production and chemotaxis were measured at time zero and 15 min at the arterial and venous sites of the dialyser. Leukopenia observed at both sites was prevented only with PLP treatment. Complement activation was maximal at the venous site, but was not prevented by any of the treatments. Neutrophil oxygen radical production and chemotaxis were significantly decreased only at the venous site and restored to normal with any of the three treatments. Complement activation was maximal at the venous site, but was not prevented by any of the treatments. Protein adsorption on the dialyser membrane seems to modulate the bioincompatibility parameters in a different way. Depending on the functions tested, the protein fractions have different protecting effects, indicating the multifactorial mechanism implicated in the CU haemodialysis-induced leukopenia, complement activation and neutrophil defect.

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