Abnormal platelet function in children with chronic renal failure undergoing hemodialysis

Abstract

In order to evaluate the hemostatic disturbance of uremic children, twenty-two patients undergoing hemodialysis were investigated for their platelet aggregation faculty, the amount of malondialdehyde (MDA) generated from washed platelets, a by-product of arachidonic acid cascade of metabolism to form thromboxane A2 (TxA2) and the capacity of uremic plasma to stimulate the production of prostacyclin (PGI2) activity from a rabbit exhausted aortic ring. Platelet aggregation responding to lower concentrations of ADP was enhanced in uremic children as compared with the controls. On the contrary, it was depressed when induced by arachidonic acid (AA) . The amount of MDA generated from washed platelets of patients was significantly reduced. The plasma of patients produced more PGI2 activity from a rabbit aortic ring than that of controls. These results suggested that in uremic children, platelet aggregation pathway is intrinsically disturbed but uremic plasma contains several unknown factors which modulate ADP induced aggregation and PGI2 production to which paradoxical episodes of thrombotic and hemorrhagic complications might be attributable.