CAJ | 학술논문

目的：观察尿激酶或纤溶酶冲击治疗对IgA肾病患者的肾脏保护作用。方法：对84例IgA肾病患者资料进行回顾性分析，并根据是否使用促纤溶药物及使用药物的种类将患者分为对照组（n＝23）、尿激酶组（n＝32）和纤溶酶组（n＝29），比较分析治疗6个月、1年3组患者的24 h尿蛋白定量、血生化、肾小球滤过率、凝血像。结果：3组患者24 h尿蛋白定量在治疗6个月和1年均较治疗前有统计学差异（P＜0．01）；组间比较：尿激酶组在治疗6个月及治疗1年时较对照组有统计学差异（P＜0．01）；纤溶酶组和对照组在治疗1年时有统计学差异（P＜0．05）。在治疗1年时，尿激酶组肾小球滤过率改善，较对照组有统计学差异（P＜0．05）。结论：在中重度IgA肾病患者，促纤溶治疗有独立于激素和免疫抑制剂之外的减少蛋白尿和肾脏保护作用。
목적：관찰뇨격매혹섬용매충격치료대IgA신병환자적신장보호작용。방법：대84례IgA신병환자자료진행회고성분석，병근거시부사용촉섬용약물급사용약물적충류장환자분위대조조（n＝23）、뇨격매조（n＝32）화섬용매조（n＝29），비교분석치료6개월、1년3조환자적24 h뇨단백정량、혈생화、신소구려과솔、응혈상。결과：3조환자24 h뇨단백정량재치료6개월화1년균교치료전유통계학차이（P＜0．01）；조간비교：뇨격매조재치료6개월급치료1년시교대조조유통계학차이（P＜0．01）；섬용매조화대조조재치료1년시유통계학차이（P＜0．05）。재치료1년시，뇨격매조신소구려과솔개선，교대조조유통계학차이（P＜0．05）。결론：재중중도IgA신병환자，촉섬용치료유독립우격소화면역억제제지외적감소단백뇨화신장보호작용。
Objective To investigate the protective effect of fibrinolytic therapy on renal function in patients with IgA nephropathy. Methods The clinical data of 84 patients with idiopathic IgA nephropathy were analyzed in a retrospective cohort study. According to different drugs of fibrinolytic therapy, the patients were divided into three groups including control group(n=23), urokinase group (n=32) and fibrinogenase group (n=29). Twenty-four-hour urine protein excretion, serum albumin, estimated glomerular filtration rate (eGFR), prothrombin time and fibrinogen level between the three groups after 6-month and 1-year treatments were compared. Results Compared to the group before treatment, the urine protein excretions were decreased in all 3 groups with 6-month and 1-year treatments (P<0.01). The urine protein excretion in the urokinase group with 6-month and 1-year treatments were lower than that in the control group (P<0.01). The urine protein excretion in the fibrinogenase group with 1-year treatment were lower that in the control group (P<0.05). After 1-year treatment, the eGFR in urokinase group was significantly increased compared with the control group (P<0.05). Conclusion Fibrinolytic therapy can decrease the 24-hour urine protein excretion and improve the renal fuction in those patients with idiopathic IgA nephropathy independent of glucocorticoids and immunosuppressive agents.