益气养阴活血方治疗IgA肾病气阴两虚证的疗效以及对血清Gd-IgA1水平的影响

Efficacy of Yiqi Yangyin Huoxue Decoction in Treating IgA Nephropathy with Qi-yin Deficiency Syndrome and its Effect on Serum Gd-IgA1 Levels

目的:观察益气养阴活血方治疗IgA肾病气阴两虚证的疗效以及对血清Gd-IgA1水平的影响。方法:将40例IgA肾病患者随机分成对照组和治疗组各20例。对照组予以控制饮食、血压,纠正贫血等对症治疗;治疗组在对照组组治疗基础上加服益气养阴活血方,连续治疗3个月。记录治疗前后两组患者中医证候积分以及估计肾小球滤过率(eGFR),检测血肌酐(Scr)、尿素氮(BUN)、24 h尿蛋白(UTP)、尿红细胞(URBC)以及血清Gd-IgA1水平。结果:治疗后治疗组疗效明显优于对照组(P<0.01);两组中医证候积分以及URBC、Scr、BUN、UTP、血清Gd-IgA1等水平明显下降(P<0.05),eGFR明显上升(P<0.05),且治疗组优于对照组(P<0.05);治疗前后血清Gd-IgA1水平与eGFR呈负相关。结论:益气养阴活血方治疗气阴两虚型IgA肾病疗效确切,其机制可能与下调血清Gd-IgA1水平有关。

Objective:To observe the clinical efficacy of Yiqi Yangyin Huoxue Decoction in treating IgA nephropathy with TCM Qi-yin deficiency syndrome and its effect on serum Gd-IgA1 levels.Methods:40 patients with IgA nephropathy were randomly divided into the control group and the treatment group with 20 cases each.The control group were given symptomatic treatments such as controlling diet,blood pressure and correcting anemia.The treatment group were treated with Yiqi Yangyin Huoxue Decoction on the basis of the treatment of the control group for 3 months.The scores of TCM syndrome and estimated glomerular filtration rate(eGFR)were recorded before and after treatment.Serum creatinine(Scr),urea nitrogen(BUN),24 h urine protein(UTP),urine red blood cell(URBC)as well as serum Gd-IgA1 levels were tested before and after treatment.Results:The clinical efficacy of the treatment group was significantly better than that of the control group after treatment(P<0.01).The scores of TCM syndrome,Scr,BUN,UTP,URBC and serum Gd-IgA1 levels were significantly reduced in the two groups(P<0.05),GFR was significantly increased(P<0.05),and the treatment group was better than the control group(P<0.05).The serum Gd-IgA1 levels were negatively correlated with GFR before and after treatment.Conclusion:Yiqi Yangyin Huoxue Decoction has a remarkable clinical curative effect on treating IgA nephropathy with Qi-yin deficiency syndrome,its mechanism may be related to the down-regulation of serum Gd-IgA1.