中文摘要：

目的：探讨原发性肾小球疾病患者血清中血管紧张素II1型受体自身抗体（AT1-AA）的表达及其临床意义。方法：采用ELISA，对326例原发性肾小球疾病患者与同期收集的197例健康对照者进行血清AT1-AA的检测。将原发性肾小球疾病患者分为AT1-AA阴性组和AT1-AA阳性组，比较两组的临床和病理指标。结果：（1）原发性。肾小球疾病患者血清中AT1-AA阳性率为35．58％（116／326），明显高于正常对照组的9．64％（19／197）（P〈0．01）；（2）原发性肾小球疾病患者中有免疫抑制剂用药史的患者AT1-AA阳性率明显低于无用药史的患者（P〈0．05）；（3）原发性肾小球疾病患者中无高血压组和有高血压组的AT1-AA阳性率均显著高于正常对照组（P〈0．01），但无高血压组和有高血压组之间AT1-AA阳性率的差异并无统计学意义（P〉0．05）；（4）AT1-AA阳性组中女性患者所占比例和血清球蛋白水平高于AT1-AA阴性组（P〈0．05）。结论：AT1-AA在原发性肾小球疾病患者血清中明显增高，提示与其它经典的自身免疫抗体相似，AT1-AA可能也是肾小球疾病的重要致病因素，抑制AT1-AA的表达可能成为预防和治疗原发性肾小球疾病的新手段。

英文摘要：

AIM： To investigate the expression of angiotensin II type 1 receptor agonistic autoantibodies （ AT1- AA） in serum from patients with primary glomendopathies and its clinical significance. METHODS： Clinicopathological data of the patients with primary glomerulopathies （n = 326） and the healthy controls （n = 197） were collected. The level of AT1-AA in serum samples was detected by enzyme-linked immunosorbent assay （ELISA）. The patients were divided into AT1-AA positive and negative groups according to ELISA result, and their clinicopathological data between the two groups were compared. RESULTS： The positive rate of AT1-AA in the patients with primary glomerulopathies was 35.58% （ 116/326）, which was much higher than that in the healthy controls [9.64% （ 19/197）, P 〈0.01 ]. The positive rate of AT1-AA in the patients with the history of immunosuppressant medication was significantly lower than that in the patients without the history. There was no significant difference of AT1-AA positive rate between the patients complicated with hy-pertension and without hypertension （ P 〉 0.05 ）, The positive rate of AT1 -AA in female patients was much higher than that in male patients （ P 〈 0.05 ）. The level of serum globulin in AT1 -AA-positive patients was significantly higher than that in AT1 -AA-negative patients （ P 〈 0.05 ）. CONCLUSION： The serum level of AT1 -AA significantly increases in the patients with primary glomerulopathies, indicating that AT1-AA might be an important pathogenic factor of glomerulopathies, similar to the other classic autoimmune antibodies. Specific inhibition of AT1-AA would serve as a new strategy for prevention and treatment of primary glomerulopathies. [