[Changes in platelet sensitivity to thromboxane A2 in pediatric patients with nephrotic syndrome]

For the purpose of clarifying the changes occurring in thromboxane (TX)A2 metabolism in the platelet of nephrosis patients, we investigated the changes in platelet sensitivity to TXA2 and the changes in TXA2 production in pediatric patients with nephrotic syndrome (N.S.) using STA2 which is an analogue of TXA2 and ONO 3708 which is a TXA2 receptor antagonist. The subjects investigated in the present study consisted of 11 cases with initial onset of N.S. (onset group), 15 relapse patients (relapse group) and 15 children with N.S. without any recurrence in the past 6 months (remission group) as well as 25 normal children (control group). The results were as follows: (1) Platelet aggregation attributable to STA2 stimulation was enhanced at the onset and relapse of N.S. (2) Sensitivity to TXA2 was enhanced in the platelets of patients in the relapse group. (3) Though some demonstrated enhanced platelet sensitivity to TXA2, while others in the onset group did not, enhanced sensitivity was observed in all the patients along with an improvement in hypoalbuminemia. (4) The amount of daily urinary excretion of TXB2 and 11-dehydro-TXB2 in the onset group and relapse group was increased in comparison with the status in the remission group and control group. The above results demonstrated enhanced platelet sensitivity to TXA2 and increased biological production of TXA2 in patients with N.S., suggesting that TXA2 metabolism in the platelet is deeply involved in the pathophysiology of N.S.