title: Haemodialysis activates phospholipase A2 enzyme.
abstract: BACKGROUND
  Clinical and experimental evidence suggest that haemodialysis (HD) procedure is an inflammatory process. For the production of proinflammatory lipid mediators in many inflammatory reactions, the release of arachidonic acid by phospholipase A2 (PLA2) enzyme is a prerequisite. Therefore, the purpose of the present investigation was to establish whether the activity of PLA2 increases during HD and whether the increase depends on the type of dialyser used.
  
  
  METHODS
  We performed dialysis in eight chronic HD patients. Blood samples entering and leaving the dialyser were obtained before and at 15, 60, 120 and 180 min after the dialysis was started, on one occasion using a cuprophane and on another occasion a cellulose triacetate dialyser. PLA2 activity was assessed in crude plasma and in plasma extract.
  
  
  RESULTS
  PLA2 activity in plasma extract exhibited similar biochemical properties to that of inflammatory human synovial fluid PLA2 enzyme which is of group II PLA2. PLA2 activity in crude plasma represents a type of PLA2 other than the synovial type. In HD patients, baseline PLA2 activities in a crude plasma and plasma extract were significantly increased when compared to normal subjects. An increase in PLA2 activity was observed in crude plasma with a peak appearing at 15 min when the patients were dialysed with cuprophane and cellulose triacetate membranes. This increase was observed in both arterial and venous blood samples and was more pronounced when the patients were dialysed with cuprophane than with cellulose triacetate membranes. When PLA2 was assessed in plasma extract, the activity increased only with cuprophane but not with cellulose triacetate membranes.
  
  
  CONCLUSIONS
  PLA2 activity in plasma is increased in HD patients and increases during the dialysis procedure to a greater extent with a less biocompatible membrane. Continuous activation of PLA2 might be relevant for long-term deleterious consequences of HD.
authors.affiliation: Department of Medicine, Inselspital, University of Berne, Switzerland.
authors.forename: B S
authors.initials: BS
authors.lastname: Vishwanath
authors.forename: C A
authors.initials: CA
authors.lastname: Fux
authors.forename: D E
authors.initials: DE
authors.lastname: Uehlinger
authors.forename: B M
authors.initials: BM
authors.lastname: Frey
authors.forename: R C
authors.initials: RC
authors.lastname: Franson
authors.forename: F J
authors.initials: FJ
authors.lastname: Frey
mesh_terms: D000328:Adult; D000368:Aged; D016718:Arachidonic Acid / Q000378:metabolism; D001672:Biocompatible Materials; D015415:Biomarkers / Q000097:blood; D002482:Cellulose / Q000031:analogs & derivatives; D004789:Enzyme Activation; D005260:Female; D006801:Humans; D006863:Hydrogen-Ion Concentration; D007249:Inflammation / Q000097:blood / Q000201:enzymology* / Q000209:etiology; D008297:Male; D008567:Membranes, Artificial; D008875:Middle Aged; D010741:Phospholipases A / Q000097:blood*; D054467:Phospholipases A2; D006435:Renal Dialysis / Q000009:adverse effects* / Q000295:instrumentation
chemical_list: D001672:Biocompatible Materials; D015415:Biomarkers; D008567:Membranes, Artificial; D016718:Arachidonic Acid; D002482:Cellulose; C024671:cellulose triacetate; D010741:Phospholipases A; D054467:Phospholipases A2