Platelet hyperaggregability in the nephrotic syndrome which is not dependent on arachidonic acid metabolism or on plasma albumin concentration.

Abstract

In 20 patients with nephrotic syndrome we confirm previous findings of in vitro platelet hyperaggregability to arachidonic acid, and describe similar hyperaggregability to ristocetin. As previously reported also, the addition of albumin to nephrotic platelet-rich plasmas corrected platelet hyperaggregability to arachidonic acid, but exerted little effect on ristocetin-induced aggregation, and there was no correlation between platelet aggregation thresholds to arachidonate and to ristocetin. Incubation with indomethacin abolished the generation of thromboxane B2 after stimulation with arachidonate, but had no effect on the stimulation with ristocetin, during which no TxB2 was produced. The nephrotic patients had elevated factor VIII-related antigen (Factor VIII R:Ag) concentrations in their plasma, but in addition both decreased serum IgG and platelet-associated IgG were found which were correlated. The hyperaggregability of nephrotic platelets to ristocetin may relate to the elevated factor VIII R:Ag levels, or to the low platelet-associated IgG, since platelet IgG Fc receptors and von Willebrand factor receptors are spatially close or identical.