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±80×10 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 γ 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.