We studied 50 chronic dialysis patients with end-stage renal disease.
Mean platelet count was within normal limits. An inverse linear correl
ation was observed between pre-dialysis platelet count and serum creat
inine (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=0.0
001). Post-dialysis triglyceride decreased (1.67+/-1.27 mmol/L, pre; 1
.23+/-0.96, post; p=0.0001). Tissue factor pathway inhibitor (TFPI) an
tigen plasma level was higher in uremic patients than in controls (114
+/-42 ng/ml vs. 64+/-2, p= 0.0001). TFPI increased 2.3 times following
dialysis and such an increase was directly correlated with post-dialy
sis plasma heparin concentration (r=0.571, p=0.0002) and inversely cor
related with postdialysis triglyceride variation (r=0.407, p=0.005). S
ix of fifty patients (12%) had anti-heparin/platelet factor 4 antibodi
es (Hab), 3 IgG, and 3 IgM. Female sex and the use of cuprophane membr
anes 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 manif
estations. Serum albumin and gamma globulin decreased following dialys
is 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 tha
n Hab are involved in the development of heparin-induced thrombocytope
nia. Besides a blunted immunological response, increased levels of TFP
I, the use of anti-aggregating drugs, and the observed behavior of ser
um proteins might play a role in this regard. (C) 1998 Elsevier Scienc
e Ltd.