title: Platelet count, anti-heparin/platelet factor 4 antibodies and tissue factor pathway inhibitor plasma antigen level in chronic dialysis.
abstract: We studied 50 chronic dialysis patients with end-stage renal disease. Mean platelet count was within normal limits. An inverse linear correlation was observed between pre-dialysis platelet count and serum creatinine (r=0.304, p=0.038). Dialysis caused a decrease in platelet count (216+/-80x10(9)/L, pre; 198+/-68, post; p=0.0001), and the higher the pre-dialysis platelet count, the greater the decrease (r=0.623, p=0.0001). Post-dialysis triglyceride decreased (1.67+/-1.27 mmol/L, pre; 1.23+/-0.96, post; p=0.0001). Tissue factor pathway inhibitor (TFPI) antigen plasma level was higher in uremic patients than in controls (114+/-42 ng/ml vs. 64+/-12, p=0.0001). TFPI increased 2.3 times following dialysis and such an increase was directly correlated with post-dialysis plasma heparin concentration (r=0.571, p=0.0002) and inversely correlated with post-dialysis triglyceride variation (r=0.407, p=0.005). Six of fifty patients (12%) had anti-heparin/platelet factor 4 antibodies (Hab), 3 IgG, and 3 IgM. Female sex and the use of cuprophane membranes were more frequent among Hab-positive patients (p=0.0001), while a lower percentage of them were on anti-aggregating drugs as compared to Hab-negative patients (p=0.002). Only one Hab-positive patient was slightly thrombocytopenic and none showed bleeding or thrombotic manifestations. Serum albumin and y globulin decreased following dialysis in Hab-positive patients, while the opposite was seen in those Hab-negative (-2.47+/-1.72 g/L, vs. 0.21+/-1.77, p=0.001 and -0.48+/-0.60 g/L vs. 0.64+/-0.97, p=0.007, respectively). In vivo factors other than Hab are involved in the development of heparin-induced thrombocytopenia. Besides a blunted immunological response, increased levels of TFPI, the use of anti-aggregating drugs, and the observed behavior of serum proteins might play a role in this regard.
authors.affiliation: 2nd Department of Medicine, Padua University Hospital, Padova, Italy.
authors.forename: G
authors.initials: G
authors.lastname: Luzzatto
authors.forename: M
authors.initials: M
authors.lastname: Bertoli
authors.forename: G
authors.initials: G
authors.lastname: Cella
authors.forename: F
authors.initials: F
authors.lastname: Fabris
authors.forename: B
authors.initials: B
authors.lastname: Zaia
authors.forename: A
authors.initials: A
authors.lastname: Girolami
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D000925:Anticoagulants / Q000008:administration & dosage / Q000276:immunology*; D005260:Female; D006493:Heparin / Q000008:administration & dosage / Q000276:immunology*; D006801:Humans; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000276:immunology / Q000628:therapy; D008074:Lipoproteins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D010976:Platelet Count; D010978:Platelet Factor 4 / Q000276:immunology*; D006435:Renal Dialysis / Q000009:adverse effects*
chemical_list: D000925:Anticoagulants; D008074:Lipoproteins; C051928:lipoprotein-associated coagulation inhibitor; D010978:Platelet Factor 4; D006493:Heparin