论文部分内容阅读
目的探讨慢性肾小球肾炎血浆纤溶酶原激活物及其受体和纤溶酶原激活物抑制剂(PAI-1)的变化意义,血管紧张素转换酶抑制剂(ACEI)治疗的干预影响。方法测定78例慢性肾小球肾炎患者的血浆组织型纤溶酶原激活物(tPA)、尿激酶型纤溶酶原激活物(uPA)及其受体(uPAR)和PAI-1的水平,与健康成年人43人作对照;并观察经ACEI治疗8周后各项指标的改变。结果78例患者血浆uPAR水平明显高于对照组(P<0.05),PAI-1水平显著高于对照组(P<0.01)。予以ACEI(福辛普利)10～20mg/d治疗8周后,ACEI治疗组患者PAI-1水平较常规治疗组患者明显下降(P<0.05)。结论慢性肾小球肾炎患者血浆PAI-1水平明显升高,细胞外基质(ECM)的转化受到抑制;ACEI治疗可降低PAI-1水平,促进ECM的转归,延缓肾脏纤维化。
Objective To investigate the significance of the changes of plasma plasminogen activator and its receptor and plasminogen activator inhibitor (PAI-1) in chronic glomerulonephritis and the intervention of angiotensin converting enzyme inhibitor (ACEI) treatment . Methods The plasma level of tissue plasminogen activator (tPA), urokinase-type plasminogen activator (uPA) and its receptor (uPAR) and PAI-1 in 78 patients with chronic glomerulonephritis were measured. Compared with 43 healthy adults; and observed the change of each index after 8 weeks of treatment with ACEI. Results The plasma levels of uPAR in 78 patients were significantly higher than those in the control group (P <0.05), and the PAI-1 levels were significantly higher than those in the control group (P <0.01). After treated with ACEI (fosinopril) 10 ~ 20mg / d for 8 weeks, PAI-1 in ACEI group was significantly lower than that in the conventional treatment group (P <0.05). Conclusions Plasma PAI-1 levels are significantly elevated in patients with chronic glomerulonephritis, and the transformation of extracellular matrix (ECM) is inhibited. ACEI treatment can reduce the level of PAI-1, promote the outcome of ECM, and delay renal fibrosis.