ANALYSIS OF PLATELET ABNORMALITIES IN UREMIA WITH AND WITHOUT GLANZMANNS-THROMBASTHENIA

Uremia causes a bleeding tendency associated with platelet dysfunction , and previous studies have shown abnormalities of platelet glycoprote in (GP) Ib or GPIIb/IIIa and a tendency for platelet activation in ure mia. The present study compared the abnormalities of platelet function in uremia with (n=1) or without (n=18) associated Glanzmann's thromba sthenia. There was a significant difference between ristocetin-induced agglutination of platelets from the uremic patients without Glanzmann 's thrombasthenia and platelets from healthy controls (n=15). In addit ion, a reduction of GPIb expression by uremic platelets along with nor mal GPIIb/IIIa expression was confirmed using flow cytometry. Many coa gulation markers were increased in the uremic patient with Glanzmann's thrombasthenia, suggesting that the coagulation was enhanced and the platelets were prone to activation. However, the thrombasthenic platel ets actually showed little increase in the binding of a monoclonal ant i-CD63 antibody directed against lysosomal integral membrane protein ( which is expressed after platelet activation), while uremic platelets showed a marked increase. In addition, the expression of GPIb, by thro mbasthenic platelets was normal, while that of GPIIb/IIIa was markedly decreased. Our results suggest that thrombasthenic platelets are resi stant to activation and to the degradation of GPIb under uremic condit ion and that this difference from 'ordinary' uremic platelets be relat ed to the difference in GPIIb/IIIa.