Complement activation (plasma levels of the anaphylatoxins C3a and C5a), the aggregation of polymorphonuclear neutrophils (PMN) on 12-O-tetradecanoyl-4 beta-phorbol-13-acetate (TPA) 2.5 microM, A23187 5 microM, arachidonic acid 0.1 mM and TPA-induced thromboxane A2 production by PMN were examined in 10 uraemic patients at times 0, 15 and 240 min after the onset of haemodialysis with Cuprophan (CU) and polyacrylonitrile (PAN) membranes. The rise in plasma C3a and C5a was intense during haemodialysis with CU, but mild with PAN. PMN aggregation in uraemic patients was lower (as compared to normal controls) independently of the agonist used. At 15 min of haemodialysis with CU, PMN aggregation increased and decreased at 240 min, while during haemodialysis on PAN no significant changes in PMN aggregation were noticed. TPA-induced TxA2 synthesis by PMN was decreased in uraemic patients. It was normalized after haemodialysis with PAN, but not with CU. Apparently the mechanisms underlying PMN aggregation and TxA2 synthesis during haemodialysis may not be entirely dependent on complement activation. Evidently, dialysable plasma factors may be responsible for the abnormal PMN function in uraemic patients. Thus, removal of these factors by haemodialysis with an appropriate membrane may improve the PMN functions.