慢性肾小球肾炎患者血清抗α1受体和血管紧张素Ⅱ1受体自身抗体与肾损害程度的分析

目的探讨慢性肾小球肾炎（chronic glomerulonephritis，CGN）患者血清中抗血管紧张素Ⅱ1受体自身抗体（AT1受体抗体）和抗α1肾上腺受体自身抗体（α1受体抗体）产生的阳性率与血清肌酐水平的关系。方法以合成的AT1和α1受体多肽片段为抗原，应用酶联免疫吸附测定（ELISA）技术，检测111例慢性。肾小球肾炎患者（CGN），61例高血压无肾损害患者，40例正常人血清中抗AT1和α1受体自身抗体。结果①CGN抗AT1和α1受体自身抗体阳性率分别为68．5％（76／111）和56．8％（63／111）明显高于单纯高血压组的34：4％（21／61）、27．9X（17／61）和正常对照组（分别为10．0％和12．5％）（P〈0．05，P〈0．01）；②CGN患者亚组比较，早期肾衰期抗AT1和α1受体自身抗体的检出阳性率最高，与晚期肾衰和尿毒症期比较具有显著性统计学意义（P〈0．01）；③血清肌酐水平比较分析（血清肌酐高于正常但〈450μmol／L组）抗AT1和抗α1受体自身抗体的检出阳性率，明显高于血清肌酐水平450～707μmol／L组和〉707μmol／L组，比较具有统计学意义（P〈0．01）。结论CGN发病与血清抗AT1和α1受体自身抗体产生有关，血清抗AT1和α1受体自身抗体与血清肌酐水平有关，免疫学机制可能参与CGN发病。

Relationship between Autoantibodies against Angiotensin AT1 Receptor and a1 Receptor and Rental Damaga Degree in Chronic Glomerulonephritis

Objective To explore the relationship between autoantibodies against angiotensin Ⅱ type 1 receptor （AT1-receptor） and α1-adrenergic receptor （al-receptor）, and sera CER level in patients with chronic glomerulonephritis （CGN）. Methods The epitopes of the second extracellular loop of AT1-receptor （165-191） and α1receptor （192-218） were synthesized and used respectively to screen sera autoantibodies of patients with CGN （CGN, n = 111）, hypertenson without renal failure （HT, n = 61） and healthy blood donors as normal control （NC, n = 40） by enzyme-linked immu- nosorbent assay （ELISA）. Results In CGN patients, the positive rates of autoantihodies against ATe-receptor and α1-receptor were 68. 5% and 56. 8% respectively, higher than those of HT patients （34. 4%,27. 9%）, and healthy donors （10. 0%, 12. 5%） （P〈0. 011. For patients whose sera CER levels were above normal and lower than 450μmol/L, the positive rates of autoantibodies against ATl-receptor and α1-receptor were 68. 5% and 56. 8% respectively, higher than those for the patients whose sera CER levels were between 450 and 707μmol/L or above 707 μmol/L （P〈0. 01 ）. Conclusion The instance of CGN is related with autoantibodies against ATe-receptor and α1-receptor, which are relerant with sera CER levels. Immunological mechanisms may participate in CGN.