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动物实验表明,肾组织受损时影响血管扩张剂——前列腺环素和血管收缩剂血栓素A_2(TxA_2)的合成。在免疫或中毒引起肾小球损害时,肾TxA_2可影响肾小球通透性导致蛋白丢失。在成人微小病变型肾病中,TxA_2合成明显增加,作为肾TxA_2标志物的血栓素B_2(TxB_2)在尿中排泄增加,用TxA_2合成的抑制剂可减少尿TxB_2的排泄和蛋白尿。本文旨在研究微小病变型肾病综合征(MCNS)患儿尿TxB_2排泄,并阐明尿TxB_2与肾小球丢失蛋白之间的关系。 5例MCNS患者,年龄6～12岁,男性4例,女性1例。患者对激素治疗均有效,其中4例为反复发作性MCNS,1例为激素依赖性MCNS。观察期间有2例复发2次,余者各复发1次。5次复发经强的松2 mg/Kg/d治疗后缓解,
Animal experiments show that the renal tissue damage affects the vasodilator - prostacyclin and vasoconstrictor thromboxane A_2 (TxA_2) synthesis. When immune or poisoning causes glomerular damage, kidney TxA_2 can affect glomerular permeability leading to protein loss. In adult minimal change nephropathy, TxA 2 synthesis was significantly increased, as a marker of renal TxA 2 thromboxane B 2 (TxB 2) excretion increased in the urine, with TxA 2 synthesis inhibitors can reduce urinary TxB 2 excretion and proteinuria. This article aims to investigate urinary TxB 2 excretion in children with minimal-neoplastic nephrotic syndrome (MCNS) and to elucidate the relationship between urinary TxB 2 and glomerular loss of protein. Five cases of MCNS patients, aged 6 to 12 years, 4 males and 1 female. Patients were effective hormone therapy, including 4 cases of recurrent MCNS, 1 case of hormone-dependent MCNS. During the observation period, 2 cases relapsed 2 times and the others relapsed 1 time. 5 relapse after prednisone 2 mg / Kg / d treatment remission,