肾愈Ⅱ号颗粒治疗慢性肾炎的临床研究
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摘要
目的
     通过运用中药肾愈Ⅱ号颗粒治疗慢性肾炎(CGN)的临床研究,观察肾愈Ⅱ号颗粒治疗CGN的疗效,探讨其作用机制,探寻中医药治疗CGN的有效方法。
     方法
     将已确诊为CGN的患者随机分为2组:肾愈Ⅱ号颗粒治疗组(简称A组),肾炎四味片对照组(简称B组),每组各30例。两组均根据病情需要采用对症治疗的基础上,A组予肾愈Ⅱ号颗粒口服,每次10g,每日2次;B组口服肾炎四味片,每次8片,每日3次,疗程为2个月。实验前后查Hb、24hupq、BUN、Scr、ALB、ALT及血清sIL-2R和血浆TXB_2及6-Keto-PGF_(1α)等指标,并记录患者临床症状的变化,作出疗效评价。
     结果
     1 A组总有效率为86.67%,B组总有效率为66.67%,A组总体疗效优于B组(p<0.05)。
     2 A组在改善患者临床症状,降低症状积分明显优于B组,二者相比亦有显著性差异(p<0.01)。
     3 A组在降低24hupq、升高Alb及Hb方面明显优于B组,二者相比有显著性差异(p<0.01或p<0.05)。A组能显著降低患者BUN、Scr(p<0.01),且降低BUN明显优于B组,二者相比有显著性差异(p<0.05)。
     4 实验结果表明,二组CGN患者血中sIL-2R、TXB_2含量均明显高于正常,而血中6-Keto-PGF_(1α)低于正常。治疗后A组sIL-2R有显著性降低(p<0.01),B组无显著性变化(p>0.05),A组和B组比较,有显著性差异(p<0.05);治疗后A组TXB_2有显著降低(p<0.05),6-Keto-PGF_(1α)显著性升高(p<0.05),而B组无显著性变化(p>0.05),二组相比有显著性差异(p<0.05);A组治疗后TXB_2/6-Keto-PGF_(1α)非常显著降低(p<0.01),B组治疗后TXB_2/6-Keto-PGF_(1α)显著性降低(p<0.05),二组比较差异不明显(p>0.05)。
     5 实验结果表明,A组对不同中医证型的患者治疗前后BUN、Scr、sIL-2R均有显著性降低(p<0.01或p<0.05);B组脾肾气虚兼水湿型治疗后BUN、Scr较治疗前比较有显著性降低(p<0.05);但B组脾肾气虚兼水湿型治疗后sIL-2R及脾肾气虚兼瘀血型BUN、Scr、sIL-2R较治疗前比较无显著性差异(p>0.05);A组脾肾气虚兼瘀血型BUN、Scr、sIL-2R治疗后较B组脾肾气虚兼瘀血型比较有显著性差异(p<0.05);但A组脾肾气虚兼水湿型BUN、Scr、sIL-2R治疗后较B组脾肾气虚兼水湿型比较无显著性差异(p>0.05)。
     6 实验结果提示,患者血清sIL-2R与BUN、Scr有明显的相关性(r=0.58,r=0.55;P<0.01)。
     结论
     sIL-2R及TXA_2-PGI_2平衡失调在CGN发病中起重要作用,肾愈Ⅱ号颗粒能够改善肾功能,减少尿蛋白,改善患者临床症状,降低sIL-2R含量,调节TXA_2-PGI_2的平衡,从而有效延缓CGN的进展,其机理可能于与调节免疫及改善肾脏组织血流动力学有关。
OBJECTIVE
    The goal of this clinical experiment is to probe the mechanism and therapeutic effect of Shenyu II infusing Prescription(SYP) on treating Chronic Glomerulonephritis (CGN), and search an effectual method of TCM in treating CGN.
    METHODS
    60 patients with CGN were divided into 2 groups at random: SYP therapeutic group(Group A, n=30). Four Tastestablet for Nephritis control group (Group B, n=30). According to the requirement of disease both groups were treated with controlling blood pressure and diuresis. Group A took SYP two times daily, lOg each time. Group B took Four Tastestablet for Nephritis three times daily,8 tablets each time.The therapeutic period was two months. Before and after experiment, we assayed the patient's Haemoglobin, 24hupq, ALB, ALT, BUN, Scr, blood soluble interleukin-2 receptor (sIL-2R), blood thromboxane B2(TXB2)and 6-keto-prostaglandin F1a (6-k-PGF1a). Recorded the change of patients' clinical symptoms. at last, observed the difference of therapeutic effect between group A and group B.
    RESULT
    Result of the study could be summarized as:
    1 The total effective rate of group A was 86. 67%,while group B was 66. 67%, the total therapeutic effect of group A was better than that of group B (p<0. 01).
    2 SYP could improve the patients'clinical symptoms, the effects was better than group B (p<0. 01) .
    3 SYP could decrease urinary protein, BUN, Scr. increase ALB and Hb signif icantly( p<0. 01). The effects of decrease urinary protein, Bun, Scr and increase ALB,Hb was better than group B (p<0. 01 or p<0. 05) .
    4 All patients' blood sIL-2R, TXBa were higher and 6-keto-PGF1a, was lower than that of general persons. SYP could decrease blood sIL-2R, TXB2 and increase blood 6-keto-PGF1a significantly (p<0. 01 or p<0. 05) . It is effects was better than group B (p<0. 05) .
    5 SYP could decrease the patients' BUN, Scr, sIL-2R of two symptom-complexs (Qi-def iciency of both spleen and kidney coexisting blood statis and coexisting water) significantly (p<0. 01 or p<0. 05 ) . To the symptom-complexs (Qi-def iciency of both spleen and kidney coexisting blood statis. The SYP's effective of decrease BUN, Scr, sIL-2R was better than group B (p<0. 05) .but that is not to the symptom-complexs of Qi-def iciency of both spleen and kidney coexisting water (p>0. 05).
    6 The result of experiment indicated: there were significantly interrelation between blood sIL-2R and BUN, between sIL-2R and Scr (r=0. 58, r=0.55; P< 0. 01) .
    
    
    CONCLUSION
    The alteration of sIL-2R and TXA2-PGI2 could play a important role in CGN. SYP could improve renal function and clinical symptoms, decrease proteinuria and sIL-2R, adjust the balance of TXA2-PGI2. SYP therapy could markedly retard the rate of progression of CGN. The mechanism may be concerned with it is regulating immunity and improving renal dynamics of blood flow.
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