الفهرس 
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Abstract
Bacterial infection and septicemia account for appro-ximately one fifth of the deaths in populations with endstage renal disease, and are a major cause of morbidity and hospitalization. Several factors may contribute to this defective host defense against infection. Phagocytosis by poiymorphonuclear cells plays a critical role by ingestion of bacteria and their subsequent destruction by bactericidal mechanisms (Mailloux et al., 1991).
The defects in host defense mechanisms that explain the enhanced susceptibility to infection of uremic patients concern the function of polymorphonuclear neutrophils (Haag-Weber and 1-Ion, 1994).
Descaiups - Latscha et al. (1991) reported that phagocytosis of Polymorphonuclear Leukocytes (PMN) were depressed in patients on chronic hernodialysis.
Hemodialysis with new cellulose - based membranes, especially cuprophan, caused marked complement activation via the alternative pathway and formation of C3a and C5a peaked in
INTRODUCTION AND AIM OP TIlE WORK 2
the first 15 minutes of dialysis and decreased thereafter, approaching base line levels by the end of dialysis (Jacobs et al., 1989).
Arnadori et al. (1983) reported that early hernodialysis is accompanied by a profound, transient leulcopenia and complement activation can play a pivotal role in pathogenesis of hernodialysis - induced leulcopenia through the release of chemotactic factors as C5a, C567 and perhaps 3a
HIM OF THE WOAK
1] To study the effect of the hemodialysis session on phagocytic function of polymorphonuclear leukocyte and its effect on complement activation.
2] To study the relationship between the changes in phagocytic function of polymorphonuclear leukocyte and the changes in complement (C5 a) activation during hernodialysis session.