AT1RA应用于慢性肾功能不全失代偿期的临床评价

目的：探讨血管紧张素受体拮抗剂（AT1RA）芦沙坦（科素亚）对慢性肾功能不全患者肾脏的保护作用；方法：将42名病人平均分为血管紧张素转换酶抑制剂（ACE）治疗组和芦沙坦治疗组，检测各组治疗前和治疗后（4－6）周的血压、血糖、血肌酐、尿蛋白等；结果：芦沙坦治疗前后尿蛋白排泄量明显减少（P＜0.05），血肌酐下降（P＜0.05），芦沙坦治疗组ACEI治疗组尿蛋白排泄量、血肌酐改善情况明显；结论：芦少坦对慢性肾功能不全患者的肾脏病变有部分保护作用。     

慢性肾功能不全失代偿的可逆因素

目的 :探讨慢性肾功能不全失代偿的可逆因素和及时发现并纠正可逆因素的重要性。方法 :回顾我院泌尿科1 990年～ 2 0 0 2年收治的 569例慢性肾功能不全失代偿期、(尿毒症 )中经临床证实存在可逆因素且经恰当处理后解除失代偿状态 ,病情逆转的 1 0 2例患者的临床资料并进行分析。结果 :常见的可逆因素为原发病活动、感染、水电解质紊乱、心衰、高血压、肾毒性药物的使用等等 ,一般经过积极的非透析治疗可解除失代偿的临床状况 ,维持正常或基本正常生活。结论 :病情急剧恶化 ,Cr<433 1 6μmol/L ,Bμm/Cr>1 0 0者及肾脏体积不缩小的尿毒症患者非常可能存在可逆性因素 ,尤对新收治的慢性肾功能不全失代偿患者应高度重视寻找可逆因素并及时妥善处理     

应用前列腺素E1治疗慢性肾功不全的临床观察

目的探讨前列腺素E1治疗慢性肾功能不全的疗效。方法将CRF患者随机分为治疗组和对照组,治疗组静点前列腺素E1(凯时)15d,其余治疗方法与对照组相同,测治疗前后血肌酐值及24h尿量进行统计学分析。结果治疗组患者经静脉滴注前列腺素E1(凯时)15d后,血肌酐水平下降,24h尿量增多。结论前列腺素E1能改善CRF患者的肾功能,保护残余肾功能。     

前列腺素E1对糖尿病肾病患者肾动脉血流动力学的影响

目的:了解前列腺素E1(PGE1)对糖尿病肾病(DN)患者肾动脉血流动力学的影响. 方法:利用彩色多普勒观察95例DN患者经PGE1治疗前后的肾动脉血流动力学的变化. 结果:DN患者肾动脉血流动力学的各项参数,特别是肾动脉内径、时间速度积分、阻力指数变化显著(P<0.01);PGE1治疗后,其各项参数均有明显的变化(P<0.05);同时BUN, Cr水平由治疗前的(10.1±5.4)mmol/L, (194±51)μmol/L降至(7.9±6.0) mmol/L, (99±35)μmol/L,尿量由(948±128)mL/d 增至(1242±373)mL/d ,均有明显的改善(P<0.05). 结论:DN时多伴有凝血、纤溶障碍所导致的肾动脉血流动力学的变化,应用PGE1治疗有益于延缓肾功能的恶化.     

前列腺素E_1对慢性肾功能不全氮质血症患者的肾保护作用

目的 :探讨前列腺素E1 (PGE1 )对慢性肾功能不全患者的肾保护作用。方法 :测量我院 3年来 78例慢性肾功能不全患者用前PGE1 治疗前后的肾功能、2 4h尿蛋白 ,并用彩色多普勒监测其肾血流变化。结果 :78例经PGE1 治疗后肾血流明显改善 ,肾功能好转 ,尿蛋白减少。结论 :PGE1 具有改善肾血流、保护慢性肾功能不全患者残肾功能效果显著且副作用小的优点 ,是治疗慢性肾功能不全的理想药物     

前列腺素E1对慢性肾功能不全临床疗效观察

目的 :探讨前列腺素E1对早期、中期慢性肾功能不全的疗效。方法 :将 70例慢性肾功能不全随机分为两组 ,对照组采用 (低盐低磷低蛋白饮食 )慢性肾功能不全非透析综合疗法 ,治疗组加用前列腺素E1治疗 ,2 1d为一疗程 ,观察治疗前后两组血BUN ,Scr,Ccr ,Alb ,Hb的变化。结果 :两组治疗后血BUN ,Scr下降 ,治疗组下降明显 ;两组治疗后Ccr,Alb均明显上升 ,治疗组上升明显。两组疗效有显著性差异。对照组Hb上升不明显 ,P >0 .0 5 ,治疗组Hb上升明显 ,P <0 .0 5。两组疗效有显著性差异。结论 :PGE1能延缓慢性肾功能不全进展 ,保护残余肾单位的储备功能 ,改善肾功能。     

慢性肾功能不全失代偿的可逆因素探讨

目的探讨慢性肾功能不全失代偿的可逆因素，促进肾功能衰竭逆转。方法回顾该科1994-2005年收治的260例慢性肾功能不全失代偿期经临床证实存在可逆因素且经恰当处理后解除失代偿状态，病情逆转的40例患者的临床资料并进行分析。结果常见的可逆因素为原发病活动、感染、水电酸碱平衡紊乱、心衰、高血压、肾毒性药物的使用等。一般经过中西医结合治疗可解除失代偿的临床状况，维持正常或基本正常生活。结论病情急剧恶化、病程短、肾脏体积无明显缩小的尿毒症患者可能存在可逆性因素，尤其对新收治的慢性肾功能不全失代偿期患者应重视寻找可逆性因素并及时妥善处理。临床医师要重视尿毒症可逆因素的分析，对部分早、中期尿毒症患者不宜过早替代治疗，以免残余肾功能过早丧失。     

Effect of medical ozone therapy on renal blood flow and renal function of patients with chronic severe hepatitis

Background Medical ozone therapy system was reported to have certain effects on the treatment of severe hepatitis, but its mechanism is not very clear. One of the causes of death of severe hepatitis is complication of renal damage or hepatorenal syndrome. The present study aimed to observe effects of medical ozone therapy system on plasma renin activity （PRA）, angiotensin II （All）, aldosterone （ALD）, renal blood flow and renal function of patients with chronic severe hepatitis and explore mechanisms of medical ozone therapy in the treatment of severe hepatitis. Methods Eighty-five cases with chronic severe hepatitis were randomly divided into ozone therapy group （43 cases） and control group （42 cases）. The patients in the ozone therapy group were treated with basic treatments plus ozone therapy system. Basic autohemotherapy was used. One hundred milliliter venous blood was drawn from each patient, and was mixed with 100 ml （35 pg/ml） medical ozone and then was returned the blood to the patient intravenously, once every other day for 20 days. Only the basic treatments were given to the control group. PRA, All, ALD, renal blood flow and damage to renal function of the two groups before treatment and 20 days after treatment were compared. Survival rates were also compared. Results Twenty days after the treatment, in ozone therapy group, PRA was （1.31±0.12） ng.m^-1.h^1, All （111.25±17.35） pg/ml, ALD （251.31±22.60） pg/ml, which decreased significantly compared with those before treatment （PRA （2.23±0.13） ng.ml^-1.h^-1, All （155.18±19.13） pg/ml, ALD （405.31±29.88） pg/ml, t=4.67-14.23, P 〈0.01 ）, also lower than those of control group 20 days after the treatment （PRA （2.02±0.11） ng.ml^-1.h^-1, All （162.21±15.32） pg/ml, ALD （401.20±35.02） pg/ml, t=4.97-15.61, P 〈0.01）; renal blood flow was （175.15±28.20） ml/min, which increased compared with that before the treatment （（125.68±21.25） ml/min） and was higher than that of control group 20 days after the treatment （（128.59±23.15） ml/min, t=4.78, 4.61, P 〈0.01）. Renal damage occurred in 2 cases （5%） in ozone therapy group, less than that in control group （9 cases, 21%） （X^2=5.295, P 〈0.05）. Thirty-three cases （77%） in ozone therapy group vs. 16 cases （38%） in control group survived （X^2=12.993, P 〈0.01 ）. Conclusions Basic treatment plus medical ozone therapy for patients with chronic severe hepatitis could decrease PRA, All and ALD levels significantly increase renal blood flow, prevent renal damage to certain extent and improve survival rate of the patients.     

Effect of Heme Oxygenase-1 Inducer Hemin on Chronic Renal Failure Rats

The role of HO-1 inducer, hemin, in chronic renal failure (CRF) rats and its possible mechanism of action was studied. 5/6 subtotal nephrectomy was performed to establish chronic renal failure model. Rats were randomly assigned to 4 groups: sham-operated group, CRF group,ferrous gluconate group and heroin group. At the 10th week after operation, serum creatinine,BUN, RBC, HGB and HCT were measured. Renal pathologic changes were observed. RT-PCR and immunohistochemistry were used to detect the expression and distribution of HO-1. RT-PCR and radioimmunoassay was used to determine the expression of ET-1 in the kidney and plasma. The results showed that as compared with CRF group, serum creatinine and BUN in hemin group were reduced significantly and nephrogenic anemia was improved markedly. Glomerular mesangial proliferation and interstitial lesion were also ameliorated significantly. Heroin not only increased the expression of HO-1 but also reduced the expression of ET-1 in the kidney. The level of ET-1 protein in the plasma was also reduced after heroin treatment. Most of these indexes were not obviously changed in ferrous gluconate group. It was suggested that through inducing the expression of HO-1 and reducing the level of ET 1 in the kidney and plasma, heroin plays an important protective role in 5/6 subtotal nephrectomized rats.     

慢性肾衰竭从瘀论治

瘀血与慢性肾衰竭(CRF)关系密切,在CRF发病过程中,无论正气虚损,还是实邪蕴结,最终都可导致瘀血的发生.在CRF治疗中活血化瘀应贯穿始终,无论病人有无瘀血证临床表现,应用活血化瘀治疗,均可取得较好疗效.应用时应根据病情轻重缓急,灵活施治、随证求因、审因论治,才能达到活血除瘀之目的.若不审病因,一味活血破血,不仅无效,反而徒伤正气,促使病情恶化,临证时当引以为戒.     

益肾排毒方对腺嘌呤所致慢性肾衰竭大鼠肾功能的影响

目的 观察益肾排毒方对腺嘌呤所致慢性肾衰竭大鼠肾功能的影响.方法 103只清洁级Wister雄性大鼠,随机分为正常组、模型组、对照组(尿毒清颗粒)、治疗组(低、中、高剂量)6组,除正常组外,其余组均给予1.5％腺嘌呤混悬液按300 mg/(kg·d)剂量灌胃给药,造模3周.造模成功后,按大鼠体质量2 mL/100 g,灌胃1次/d,连续8周.正常组、模型组给予自来水灌胃,对照组灌胃尿毒清颗粒混悬液,治疗组分别按相当于人用药剂量的0.5、1、2倍量灌胃中药煎剂益肾排毒方.给药8周后观察各组大鼠一般情况、肾功能(BUN、Scr)指标、免疫(α-SMA)指标、电镜下肾脏组织超微结构形态变化.结果 与正常组相比,其余各组BUN、Scr水平均显著升高(P＜0.01);与模型组相比,其余各组BUN、Scr水平均显著下降(P＜0.01);与模型组相比,其余各组α-SMA水平均有下降趋势,治疗组(高剂量)水平显著下降(P＜0.01);电镜下,模型组均有不同程度肾损伤,对照组和治疗组肾损伤有所改善.结论 益肾排毒方可降低慢性肾衰竭大鼠血BUN、Scr水平,下调α-SMA的表达,改善修复受损肾脏组织,改善肾间质纤维化的程度,延缓慢性肾衰竭的进程.     

低蛋白饮食疗法对慢性肾小球肾炎导致的慢性肾衰竭患者肾功能进展的延缓效果

目的探讨低蛋白饮食疗法对慢性肾小球肾炎（CGN）导致的慢性肾衰竭（CRF）患者肾功能进展的延缓效果。方法对54例CGN导致的CRF患者给予低蛋白饮食,通过检测24 h尿素氮排泄量计算实际蛋白质摄入量,观察不同的实际蛋白质摄入量对CRF进展的影响。结果实际蛋白质摄入量〈0.7 g/（kg.d）者39例,CRF进展为（-0.09±0.20）ml/min/月;实际蛋白质摄入量〉0.8 g/（kg.d）者15例,CRF进展为（-0.46±0.40）ml/min/月,两者比较,差异有统计学意义（P〈0.01）。结论低蛋白饮食疗法确实可以延缓CGN导致的CRF患者肾功能的进展,但应严格控制实际蛋白质摄入量。     

慢性肾功能衰竭(CRF)患者红细胞和血小板参数分析

目的 :探讨 CRF患者红细胞参数和血小板参数临床意义。方法 :分析 6 0例 CRF患者血常规。结果 :1CRF患者 RBC、HB、HCT明显低于对照组 (P<0 .0 1) ,而 MCV、MCH、MCHC与对照组无显著性差别 ;2 CRF患者血小板参数 PL T、MPV、PDW明显低于对照组。结论 :1CRF患者的贫血为正细胞正色素性 ;2血小板参数可以做为 CRF患者血小板功能评价的简单、快捷的方法     

普罗布考对甲基胍加重残余肾功能损害的干预研究

目的 观察甲基胍加重肾衰大鼠残余肾功能损害,以及普罗布考的干预作用.方法 大鼠随机分为假手术组A(正常对照)和5/6肾切除肾衰模型(B、C、D),B组:给予生理盐水灌胃.C组:给予甲基胍.D组:甲基胍+普罗布考组,检测各组血清尿素氮、肌酐,观察肾脏组织的病理改变,免疫组化法检测肾组织内转化生长因子(TGF-β1)、结缔组织生长因子(CTGF)、纤维结合蛋白(FN)的表达水平,TUNEL观察细胞的凋亡.结果 模型组(B、C、D)较A组血清尿素氮、肌酐显著升高(F =93.355,192.336,P＜0.05),肾小球体积增大、系膜细胞及基质明显增生,免疫组化染色显示阳性面积TGF-β1、CTGF、FN表达显著增强(F =2064.459,814.527,91.021,P＜0.05),细胞凋亡率显著增加(F=118.97,P＜0.05).加入甲基胍后血清尿素氮、肌酐较模型组明显升高(F =93.355,192.336,P＜0.05),肾小球体积较模型组明显增大、系膜细胞及基质较模型组增生严重,免疫组化染色显示TGF-β1、CTGF、FN均较模型组表达增强(F=2064.459,814.527,91.021,P＜0.05),细胞凋亡率较模型组显著增加(F=2064.459,814.527,91.021,P＜0.05),而加入普罗布考后血清尿素氮、肌酐明显下降(F=93.355,192.336,P＜0.05),肾小球体积小于甲基胍组、系膜细胞及基质增生小于甲基胍组,免疫组化显示TGF-β1、CTGT、FN表达减弱(F =2064.459,814.527,91.021,P＜0.05),细胞凋亡率显著降低(F =118.97,P＜0.05).结论 甲基胍可促进肾衰大鼠残余肾细胞的凋亡和纤维化相关因子的表达,普罗布考有一定的拮抗作用.     

Yishen huanshuai recipe retard progression of chronic renal failure

ObjectiveTo investigate the effect of Yishen Huanshuai recipe (YSHSR) on the progression of chronic renal failure (CRF). MethodsForty-six patients with CRF were divided into two groups group A (self-controlled group, n=18), whose treatment plan was subdivided into two phases. During the first phase, the patients treated with low protein diet and controlling blood pressure, while in the second phase, YSHSR was given. Group B (n=28), whose treatment plan was similar with that of group A in the second phase. The rate of progression of CRF was estimated by slope of the creatinine reciprocal (dl/mg) with time (month). Results Mean slope of the creatinine reciprocal with time from the group A during the first phase was -0.0104±0.0021, while during the second phase, it was -0.0034±0.0018. There was significant difference between them (P<0.05). Mean slope from the group B was -0.0047±0.0020. There was also significant difference between that from the group B and that from the group A during the first phase (P<0.05). Conclusion Low protein diet and controlling blood pressure combined with YSHSR therapy could markedly retard the rate of progression of CRF.