辛伐他汀与氟伐他汀对高血压肾病患者的疗效

目的：研究辛伐他汀与氟伐他汀对高血压肾病患者的疗效。方法：将2008年4月-2011年4月收治的120例患者作为研究对象,男66例,女54例,年龄45～70岁,病程4—15年,按照数字随机表方式将患者分为观察A组与观察B组,每组60例。观察A组给予辛伐他汀,观察B组给予氟伐他汀,均40mg／d,治疗6个月后,比较两组药物治疗对高血压肾病患者尿蛋白的影响。结果：两组治疗后的总胆固醇（TC）,低密度脂蛋白（LDL—C）,高密度脂蛋白（HDL—C）,三酰甘油（TG）以及血压情况与本组治疗前比较差异有统计学意义（P〈0．05）。治疗后TC,LDL—C两组比较差异无统计学意义（P〉0．05）。结论：高血压肾病患者使用辛伐他汀或者氟伐他汀治疗,均可减少患者的尿蛋白排泄,两种药物效果比较,差异无统计学意义,因此在临床治疗时,选择两种药物中的一种即可。     

氟伐他汀治疗高尿酸血症肾病的临床观察

目的:探讨氟伐他汀治疗慢性尿酸性肾病的疗效及机制。方法:对46例高尿酸血症肾病患者随机分为氟伐他汀治疗组和一般治疗组,3个月后观察两组24 h尿蛋白定量、三酰甘油、血肌酐、尿素氮等指标变化。结果:经3个月治疗,氟伐他汀治疗组的24 h尿蛋白定量、三酰甘油明显下降,两组间差异有统计学意义。肌酐、尿素氮虽均有下降,但差异无统计学意义。结论:氟伐他汀能明显减少慢性高尿酸血症患者尿蛋白排出,同时降低三酰甘油和肌酐、尿素氮,有助于减轻高尿酸血症肾病的肾损害。     

氟伐他汀降肾病高脂血症疗效观察

目的：探讨氟伐他汀对肾病综合征高脂血症的疗效及其副作用和对肝、肾功能的影响。方法检测住院患者６０例应用氟伐他汀为治疗组,４０例应用藻酸双脂钠为对照组,治疗时间为６周。两组治疗前后均查总胆固醇、甘油三脂、高密度脂蛋白胆固醇、低密度脂蛋白胆固醇、肌酐、尿素氮及转氨酶,采用ｔ检验。结果 治疗组应用氟伐他汀（４０ｍｇ／ｄ）后可显著降低高胆固醇及混合性高脂血症,与对照组相比,Ｐ〈０．０１。结论 氟伐他汀对肾     

不同剂量阿托伐他汀和辛伐他汀预防对比剂肾病的临床观察

目的观察不同剂量阿托伐他汀和辛伐他汀用于预防对比剂肾病的效果。方法 550例冠状动脉造影患者和350例行经皮冠状动脉介入治疗(PCI)患者,分为空白对照组、阿托伐他汀和辛伐他汀组,其中阿托伐他汀和辛伐他汀组均细分为:小剂量组、中剂量组和大剂量组,并分别给予不同剂量药物口服。观察2组术后血清肌酐(Scr)、内生肌酐清除率(Ccr)变化,以及对比剂肾病发生情况。结果 1术后1、3、5 d,阿托伐他汀不同剂量组患者的Scr水平均显著低于对照组(P0.05);2术后1、3、5 d,辛伐他汀不同剂量组Scr水平与术前相比,差异无统计学意义(P0.05);不同剂量组患者Scr水平均低于对照组(P0.05);3阿托伐他汀和辛伐他汀中、大剂量组对比剂肾病发生率均低于对照组(P0.01)。结论阿托伐他汀和辛伐他汀均有助于预防对比剂肾病的发生。     

氟伐他汀对糖尿病肾病维持性透析患者微炎症状态的影响

目的:观察氟伐他汀对糖尿病肾病维持性血液透析患者微炎症状态的影响.方法:选择我院因糖尿病肾病行维持性血液透析患者44例,随机分为氟伐他汀治疗组及非氟伐他汀治疗组各22例,2组患者治疗前后3个月分别测定高敏C反应蛋白(hs-CRP)、白介素6(IL-6)、肿瘤坏死因子α(TNF-α)、甘油三酯(TG)及总胆固醇(TC),并与非糖尿病肾病的维持性血液透析患者进行比较.结果:糖尿痛肾病透析患者hs-CRP、IL-6、TNF-α、TG、TC明显高于非糖尿病肾病透析患者;治疗三月后,治疗组hs-CRP、IL-6、TNF-α、TG、TC水平下降,且与治疗前及非治疗组比较,差异有显著性.结论:氟伐他汀能改善糖尿病肾病维持性血透患者微炎症状态.     

氟伐他汀与瑞舒伐他汀对冠心病患者的降脂疗效比较

选取我院2012年10月~2013年8月收治的200例冠心病患者,并随机将所有患者分成2组各100例,其中氟伐他汀组采取氟伐他汀进行治疗,瑞舒伐他汀组采取瑞舒伐他汀进行治疗。对比两组在治疗前后高密度脂蛋白胆固醇(HDL-C)、低密度脂蛋白胆固醇(LDL-C)以及总胆固醇(TC)、三酰甘油(TG)、超敏C反应蛋白(hs-CRP)的水平差别。结果在接受治疗半个月后,两组患者的LDL-C、TC、TG、hs-CRP均有所下降,而HDL-C均有升高,且两组均无不良反应发生,安全可靠,但瑞舒伐他汀对冠心病患者的降脂效果优于氟伐他汀组,且安全可靠,值得在临床上进一步推广。     

阿托伐他汀对高血压肾病患者肾功能的影响

目的:旨在研究阿托伐他汀降脂以外的作用--对高血压肾病患者尿蛋白、肌酐、尿酸的影响及与炎症因子转化生长因子β1(TGF-β1)、白细胞介素-6(IL-6)的关系.方法:选取血压控制达标的高血压肾病患者68例,随机分为治疗组和对照组,治疗组给予阿托伐他汀10 mg/d,治疗24周,检测两组治疗前后TGF-β1、IL-6、24 h尿蛋白、肌酐、尿酸、血脂.结果:治疗组治疗前TGF-β1、IL-6、尿蛋白、尿酸及肌酐与对照组治疗前比较差异无显著性(P＞0.05);治疗组经阿托伐他汀治疗6、12、24周后,TGF-β1、IL-6、尿蛋白明显下降,12周和24周与治疗前水平比较均差异有显著性(P＜0.05),24周与6、12周比较差异亦有显著性(P＜0.05),与对照组治疗后比较差异亦有显著性(P＜0.01),但6周与治疗前比较则差异无显著性(P＞0.05).结论:阿托伐他汀能减轻高血压肾病的蛋白尿,该作用可能通过降脂以外的降低炎症因子TGF-β1、IL-6的抗炎作用实现.     

氟伐他汀治疗糖尿病肾病合并高脂血症的临床观察

糖尿病肾病（Diabetic Nephropathy,DN）是糖尿病的最常见的并发症之一,大量临床与实验研究已经证实,2型糖尿病血脂异常及血液流变学异常与DN的发展密切相关,这些异常的变化往往会加速DN的进展。作使用氟伐他汀治疗DN患取得了一定疗效,现报告如下。     

缬沙坦联合氟伐他汀治疗慢性尿酸性肾病临床观察

目的；观察缬沙坦与氟伐他汀联合应用对慢性尿酸性肾病的疗效。方法；32例患者随机分为两组，每组16例，在高尿酸血症肾病常规治疗基础上，对照组给予缬沙坦80mg1次／d口服，治疗组在对照组的基础上加用氟伐他汀40mg1次／d口服，疗程8周。结果：治疗后两组血压、血尿酸、24h尿蛋白均显著下降．肾功能明显改善，治疗组血脂较对照组下降，两者之间比较有统计学意义（P〈0.01）。结论：缬沙坦与氟伐他汀联合应用能有效减轻尿酸性肾病的肾损害。     

氟伐他汀对自发性高血压大鼠心血管的保护作用

目的：探讨氟伐他汀对自发性高血压大鼠心血管系统的作用。方法：12周龄自发性高血压大鼠30只，随机分成3组，每组10只：安慰剂组给予安慰剂喂养，氟伐他汀组喂养氟伐他汀20mg／(kg-d)：基础组入选后即处死留取血标本检测。分别测量治疗3个月前(后)收缩期血压、体质量、全心质量、左心室质量及血浆血管紧张素Ⅱ、血脂、血糖和尿素氮、肌酐、尿酸水平以及肠系膜三级动脉血管壁／腔面积比。结果：①氟伐他汀组治疗后收缩压(mmHg)均明显下降(163&;#177;4)，与安慰剂组(174&;#177;7)比较，差异有显著性意义(F=3．12，P&;lt;0．05)。②氟伐他汀组全心质量和体质量比及左心室质量和体质量比明显下降(全心重／体质量：0．005l&;#177;0．0003和0．0049&;#177;0．0002；左室质量／体质量：0．0040&;#177;0．0003和0．0039&;#177;0．0001)，与安慰剂组比较，差异有显著性意义(F=2．96，P&;lt;0．05)。③氟伐他汀治疗后血管紧张素Ⅱ(ng／L)水平无明显下降(241．50&;#177;45．68，F=1.26，P&;gt;0．05)。④氟伐他汀治疗后胆固醇(mmol／L)下降(123&;#177;0．46)；三酰甘油水平(mmol／L)也明显变化(1．31&;#177;0．23)，高密度脂蛋白水平(mmol／L)升高(1．20&;#177;0．51)，与安慰剂组比较，差异有显著性意义(F=3．39，P&;lt;0．05)。⑤氟伐他汀治疗后血糖、血浆尿素氮、肌酐、尿酸水平水平无明显降低作用(F=1．76，P&;gt;0．05)。⑥安慰剂组肠系膜动脉壁／腔面积比明显高于氟伐他汀治疗组(0．69&;#177;0．06和0．42&;#177;0．06，F=3．61，P&;lt;0．05)。结论：氟伐他汀治疗可减少高血压对心血管系统的不利影响，对心血管系统有保护作用。     

辛伐他汀治疗早期糖尿病肾病的疗效评价

目的观察辛伐他汀对早期糖尿病肾病患者尿微量白蛋白的影响。方法将确诊的早期糖尿病肾病患者100例随机分成对照组50例和治疗组50例,治疗前均检测血糖、血脂、血压、糖化血红蛋白、尿微量白蛋白和血清肌酐等指标。对照组给予口服降糖药物、抗凝、氯沙坦降压等常规治疗;治疗组除常规治疗外,增加辛伐他汀20mg,口服,每晚1次。治疗1年后,均再次检测上述指标,对比其两组治疗前后的变化。结果两组治疗后尿微量白蛋白均明显减少,其中对照组由（159.7±57.9）mg/24h降至（108.0±44.1）mg/24h（P〈0.01）,治疗组由（160.8±53.2）mg/24h降至（98.8±47.6）mg/24h（P〈0.01）,治疗组较对照组下降更明显（P〈0.01）。排除降脂作用后,治疗组尿微量白蛋白下降值仍明显优于对照组（P〈0.01）。结论辛伐他汀能减少早期糖尿病肾病患者尿微量白蛋白,且独立于其调脂效应外,延缓糖尿病肾病的进展。     

原发性膜性肾病患者外周血淋巴细胞亚群的变化及其与蛋白尿的关系

目的分析原发性膜性肾病(PMN)患者外周血淋巴细胞亚群的变化及其与蛋白尿的关系。方法选取新乡医学院一附院肾内科确诊的PMN患者40例,收集其详细临床资料,并留取外周血应用流式细胞仪测定淋巴细胞亚群(CD3+、CD4+、CD8+、CD4+/CD8+、CD16+CD56+、CD19+),同时选取20例健康志愿者作为健康对照组,比较PMN患者外周血淋巴细胞亚群与健康对照组的差别。根据患者尿蛋白水平,将PMN患者分为大量蛋白尿组(尿蛋白定量大于或等于3.5g/d)及非大量蛋白尿组(尿蛋白定量小于3.5g/d),分析两组患者上述淋巴细胞亚群水平的差异及其可能的临床意义。结果 (1)和健康对照组相比,PMN患者外周血CD4+细胞计数有升高趋势(51.83±6.80 vs.43.5±5.65,P0.05),CD8+细胞计数有降低趋势(28.83±5.60 vs.35.33±5.00,P0.05),而CD4+/CD8+比值较健康对照组明显升高(1.86±0.43 vs.1.27±0.33,P0.01)。与健康对照组比较,PMN患者外周血CD16+56+细胞计数无明显差异,而CD19+细胞计数明显升高(8.00±2.76 vs.7.33±2.66,P0.01)。(2)和非大量蛋白尿组相比,大量蛋白尿组CD19+细胞计数明显高升高(9.80±3.19 vs.7.10±2.23,P0.01),而CD4+细胞、CD8+细胞计数、CD4+/CD8+比值两者间差异均无统计学意义(P0.05)。结论 PMN患者表现出明显的B淋巴细胞异常和CD4+/CD8+细胞比值的偏移,且B淋巴细胞异常程度与蛋白尿量有关,因此,监测PMN患者淋巴细胞亚群变化有助于评估病情、指导治疗。     

羟氯喹联合治疗对IgA肾病残余蛋白尿的影响

目的 探讨羟氯喹(HCQ)联合肾素-血管紧张素系统抑制剂、激素和/或免疫抑制剂对IgA肾病患者残余蛋白尿的影响.方法 纳入2018年9月至2020年8月四川省人民医院活检为IgA肾病的门诊患者,HCQ联合治疗组28例和对照组46例,均随访6个月.比较两组患者随访期间残余蛋白尿下降率以及残余蛋白尿有效下降率的累积频率等....     

Effect of simvastatin on apoprotein B—containing lipoproteins in patients with diabetic nephropathy

Background: Diabetic patients with nephropathy usually have a more atherogenic lipoprotein profile than those without nephropathy, which may be associated with the substantially higher incidence of coronary heart disease (CHD) in this population. Simvastatin has been shown to significantly reduce the incidence of CHD events in diabetic patients.Objective: The purpose of this study was to evaluate the effect of simvastatin (10 mg/d) on atherogenic apoprotein (apo) B—containing lipoproteins in type 2 diabetic patients with nephropathy.Methods: Diabetic patients with nephropathy and a group of healthy control subjects matched for age, sex, and body weight were enrolled. Diabetic patients were administered simvastatin 10 mg/d for 6 months. Apo B—containing lipoproteins were sequentially separated by ultracentrifugation to yield very low-density lipoprotein (VLDL) (density <1.006 g/mL), intermediate-density lipoprotein (IDL) (1.006-1.019 g/mL), light low-density lipoprotein (LDL) (1.019-1.044 g/mL), and dense LDL (1.044-1.063 g/mL) fractions. Apo B in lipoproteins was measured by a sensitive enzyme-linked immunosorbent assay at baseline and after 6 months of simvastatin treatment.Results: A total of 18 patients with diabetic nephropathy and 36 matched controls were enrolled. The diabetic patients had significantly higher levels (P < 0.01) of total cholesterol, LDL cholesterol, triglycerides, and apo B compared with age- and weight-matched control subjects at baseline. The diabetic patients also had significantly higher levels (P < 0.05) of cholesterol and apo B in the VLDL, light LDL, and dense LDL fractions. Treatment with simvastatin for 6 months significantly reduced plasma total cholesterol by 21%, LDL cholesterol by 30%, and apo B by 25% (P < 0.001), but did not affect urinary albumin excretion. Simvastatin significantly decreased both triglyceride and cholesterol levels in VLDL by 18% (P < 0.05), and cholesterol and apo B in IDL by 22% (P < 0.05) and 26% (P < 0.01). Simvastatin decreased both the light and dense LDL subfractions to a similar extent, reducing cholesterol and apo B in light LDL by 27% (P < 0.001) and in dense LDL by 28% (P < 0.01) and 18% (P < 0.05), respectively. The light LDL/dense LDL ratio for apo B and for cholesterol were not altered by simvastatin therapy.Conclusions: The results of this study suggest that simvastatin may reduce levels of atherogenic apo B—containing lipoproteins and small dense LDL in diabetic patients with nephropathy.     

羟苯磺酸钙治疗肾病蛋白尿疗效观察

目的观察羟苯磺酸钙治疗肾病蛋白尿的临床疗效。方法将148例患者随机分为两组,观察组74例在常规综合治疗的基础上服用羟苯磺酸钙0.5 g,每日3次,对照组74例单用常规治疗。结果观察组4周时24小时蛋白尿较治疗前明显下降(2.49±1.02 vs 1.64±0.85)g(P<0.001);对照组4周时24小时蛋白尿较治疗前也有所减少(2.47±1.02 vs 2.20±1.01)g(P<0.01),但12周时高于治疗前水平(2.47±1.02 vs 2.60±0.98)g。两组间比较,4,8,12周差异均有统计学意义(P<0.001)。羟苯磺酸钙治疗蛋白尿的作用对肾功能正常和慢性肾衰竭者都有效,4周后24小时蛋白尿均较治疗前明显减少(2.42±0.91 vs 1.53±0.77;2.50±1.09 vs 1.75±0.93)g,差异均有统计学意义(P<0.001)。此外,该药物还可降低慢性肾衰竭血尿素氮(BUN)、肌酐(Scr)水平。结论羟苯磺酸钙具有减少肾病蛋白尿的作用,该作用对肾功能正常和慢性肾衰竭者都有效,并可降低慢性肾衰竭BUN、Scr水平。     

氟伐他汀及缬沙坦对糖尿病肾病相关炎症因子的影响

目的 比较氟伐他汀及缬沙坦对2型糖尿病早期肾病相关炎症因子的影响及对糖尿病肾病的保护作用.方法 2型糖尿病早期肾病共90例,其中常规降糖治疗组作为对照组(DN1组),在常规降糖治疗基础上加用缬沙坦作为缬沙坦组(DN2组),在常规降糖治疗基础上加用氟伐他汀作为氟伐他汀组(DN3组).分别测定各组患者治疗前后的血糖、血脂、血肌酐(SCr)、C反应蛋白(CRP)、24 h尿蛋白定量、尿白蛋白排泄率(UAER)及数种炎症因子.结果 (1)干预前3组的血清CRP、转化生长因子-β1(TGF-β1)、白细胞介素-6(IL-6)、肿瘤坏死因子-α(TNF-α)、白细胞介素-18(IL-18)浓度差异无统计学意义.DN2组治疗后与治疗前相比,IL-6[(15.99±2.87)ng/L与(17.64±2.91)ng/L,t=-3.091,P<0.01]、TNF-α[(48.72±14.62)ng/L与(52.56±17.02)ng/L,t=-2.131,P<0.05]、TGF-β1[(33.54±10.69)μg/L与(40.11±12.08)μg/L,t=-2.921,P<0.01]、IL-18[(139.65±66.37)ng/L与(158.74±74.20)μg/L,t=-2.053,P<0.05]、CRP[(5.12±3.54)mg/L与(6.08±3.39)mg/L,t=-2.072,P<0.05]均明显降低;DN3组治疗后与治疗前相比,IL-6[(15.39±2.77)ng/L与(16.49±2.81)ng/L,t=-2.071,P<0.05]、TNF-α[(45.89 ±16.22)ng/L与(53.04 ±17.02)ng/L,t=-3.651,P<0.01]、TGF-β1[(31.19±10.48)μg/L与(37.11±11.76)μg/L,t=-2.963,P<0.01]、IL-18[(141.54±66.65)ng/L与(158.01±73.23)ng/L,t=-2.182,P<0.05]、CRP[(4.94±3.61)mg/L与(5.86±3.46)mg/L,t=-2.110,P<0.05]亦均明显降低.DN2、DN3组治疗后的炎症因子含量差异无统计学意义(P>0.05).(2)在DN2、DN3组治疗前后血压均无差异情况下,DN2组治疗后与治疗前比较,UAER[(63.1±31.7)μg/min与(82.9±40.0)μg/min,t=-2.145,P<0.05]、24 h尿蛋白定量[(0.14±0.11)g/24 h与(0.18±0.15)g/24 h,t=-2.438,P<0.05]、尿微量白蛋白/肌酐(ALb/Cr)[(114.7±68.1)mg/g与(162.0 ±83.8)mg/g,t=-2.399,P<0.05]均明显降低,DN3组治疗后与治疗前比较,UAER[(65.5±32.6)μg/min与(83.5±42.1)μg/min,t=-2.131,P<0.05]、24 h尿蛋白定量[(0.15±0.12)g/24 h与(0.18±0.13)g/24h,t=-2.611,P<0.05]、尿ALb/Cr[(119.1±78.2)mg/g与(160.0±82.3)mg/g,t=-2.213,P<0.05]亦均明显降低,但2组治疗后结果 比较差异均无统计学意义(P均>0.05).结论 2型糖尿病肾病患者用缬沙坦、氟伐他汀均能降低尿蛋白,降低相关血清炎症因子含量,提示对肾功能具有保护作用.

Abstract：

Objective To compare the effects of fluvastatin and valsartan on the inflammatory cytokines in the early stage of type 2 diabetic nephropathy and their protective effects on to diabetic nephropathy. Methods Ninety patients with early stage of type 2 diabetic nephropathy were divided into three groups, 30 patients receiving routine hypoglycemic agents (DN1) as control,30 patients receiving routine hypoglycemic agents plus valsartan (DN2) and the other 30 receiving routine hypoglycemic agents plus fluvastatin (DN3). Blood glucose, blood lipid,serum creatinine and C reactive protein(CRP),24-hour urine protein,urinary albumin excretion rate (UAER) and several inflammatory cytokine were measured before and after treatment. Results ( 1 ) No significant difference of the levels of serum CRP,TGF-β1,IL-6,TNF-α, IL-18 at the baseline were observedamong these three groups.In the DN2 group,after treatment,IL.6 was([15.99±2.87]ng/L and[17.64±2. 131 ,P <0. 05) ,TGF-β1 was ( [33.54 ±10. 69] μg/L and [40. 11 ± 12. 08] μg/L,t = -2. 921 ,P <0. 01 ),IL-18 was ( [139.65±66. 37] ng/L and [158.74±74. 20]ng/L,t = -2.053,P <0. 05),CRP was ( [5. 12±3. 54] mg/L and [6. 08 ±3. 39] mg/L, t = - 2. 072, P < 0. 05 ) after and before treatment, respectively. All abovemented indices significantly decreased after treatment. In the DN3 group, IL-6 was ( [15. 39 ±2. 77] ng/L ng/L,t = -3. 651 ,P <0. 01 ) ,TGF-β1 was ( [31.19 ±10. 48] μg/L and [37. 11± 11.76] μg/L,t = -2. 963,P<0.01),IL-18 was ([141.54 ±66.65] ng/L and [158.01±73.23] ng/L,t = -2. 182,P <0.05),CRP respectively. All abovemented indices significantly decreased after treatment No significant difference was observed on inflamaory factors after treatment between the DN2 and DN3 group ( P > 0. 05). (2) In the subgroup that there was no difference in blood pressure between before and after treatment in both the DN2 and DN3 group,in the DN3 group,UAER was ([63. 1 ±31.7] μg/min and[82.9±40.0] μg/min,t = -2. 145,P <0. 05) ,24 h total urokinase protein was ( [0. 14 ±0. 11] g/24 h and [0. 18±O. 15] g/24 h, t = - 2. 438, P <0. 05 ), microalbuminuria/urine creatinine was ( [ALb/Cr] [114. 7±68. 1] mg/g and [162.0±83.8] mg/g,t = - 2. 399, P < 0. 05 ) after and before treatment. All abovemention indices significantly decreased after treatment. In the DN3 group, UAER was ( [65.5 ±32. 6]μg/min and [83.5 ±42. 1]μg/min,t = - 2. 131, P <0. 05 ),24 h total urine protein was ( [0. 14 ±0. 11] g/24 h and [0. 18±0. 15] g/24 h, t = - 2. 438, P < 0. 05 ),0. 05 ) after and before treatment. All abovemention indices significantly decreased after treatment. No significant difference was observed after treatment between the DN2 and ON3 group ( P > 0. 05 ). Conclusion Both valsartan and fluvastatin are able to protect the renal function of patients with type 2 diabetic nephropathy by decreasing the levels of urine proteins and correlated serum inflammatory cytokines.     

高脂血症对轻中度蛋白尿IgA肾病患者临床及病理特征的影响

目的探讨高脂血症对轻中度蛋白尿IgA肾病患者临床及病理特征的影响。方法选取原发性IgA肾病中表现为轻中度蛋白尿的成人患者529例。根据血脂水平分为高脂血症组和血脂正常组,分析2组患者临床与病理差异。比较不同尿蛋白水平的患者高脂血症与临床和病理特征的关系。结果与血脂正常组相比,高脂血症组患者的体质量指数(BMI)、收缩压、舒张压、尿酸(UA)、24 h尿蛋白定量均显著升高,肾小管萎缩间质纤维化、肾间质炎性细胞浸润程度较重(P0.05)。Pearson相关分析表明,高脂血症组总胆固醇(CHOL)与24 h尿蛋白定量、收缩压呈正相关,与血浆白蛋白(ALB)负相关;甘油三酯(TG)与24 h尿蛋白定量、BMI、估算肾小球滤过率(e GFR)呈正相关。高密度脂蛋白胆固醇(HDL)与BMI、ALB、UA、舒张压呈负相关。24 h尿蛋白定量在1~3.5 g的患者中,高脂血症组患者239例(76.6%),与血脂正常者相比,其BMI、收缩压、舒张压、UA、24 h尿蛋白定量均显著升高,系膜增殖、系膜细胞增生程度加重(P0.05)。尿蛋白定量不足1 g的患者中,高脂血症患者132例(60.7%),与血脂正常者相比,前者BMI、UA均升高,吸烟、饮酒多见,间质纤维化程度较重(P0.05)。结论高脂血症患者的BMI、血压、UA、24 h尿蛋白定量均显著升高,肾小管萎缩间质纤维化、肾间质炎性细胞浸润程度较重。24 h尿蛋白定量在1~3.5 g患者中,高脂血症的发生率高于尿蛋白不足1 g患者。     

Effect of fluvastatin on proteinuria in patients with immunoglobulin A nephropathy

3-Hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase inhibitors are established drugs for the treatment of hypercholesterolemia, but several studies have shown that benefits obtained with these drugs are not causally related only to regression of cholesterol lowering. Moreover, in experimental models of progressive renal disease, statins have reduced the extent of glomerulosclerosis. This study evaluated the antiproteinuric effect of a daily dose of 40 mg fluvastatin for 6 months in moderately proteinuric patients with immunoglobulin A nephropathy, stable renal function, and no indicators of poor long-term prognosis. The effects of therapy were evaluated on the basis of 24-hour proteinuria (total proteinuria and albuminuria), albuminemia, creatinine clearance, cholesterol, and triglyceride values. Renal function remained stable in all patients. A significant decrease in proteinuria was observed after 6 months of therapy and persisted for all the observations. An increase in serum albumin was observed after 6 months of therapy. This study suggests that there is an antiproteinuric effect of HMG-CoA reductase inhibitors in moderately proteinuric patients with immunoglobulin A nephropathy.     

Effects of fluvastatin slow-release (xl 80 mg) versus simvastatin (20 mg) on the lipid triad in patients with type 2 diabetes

The lipid triad is the association of small, dense (sd) low-density lipoprotein (LDL), low high-density lipoprotein (HDL), and hypertriglyceridemia, all of which play a role in coronary artery disease in patients with type 2 diabetes. Although statins have demonstrated clear positive effects on cardiovascular morbidity/mortality in patients with diabetes and on single components of the lipid triad, it remains controversial whether they affect all components of the triad in these patients. Therefore, we performed a single-center, parallel-group, prospective, randomized, open-label, blinded-endpoint (PROBE)-type comparison of fluvastatin extended-release (XL) 80 mg (n=48) and simvastatin 20 mg (n=46), each given once daily for 2 months to patients with type 2 diabetes with the lipid triad, who were enrolled after a 1-month lifestyle modification and dietary intervention program. After fluvastatin therapy, LDL (-51%; P > .01), apolipoprotein B (ApoB;-33%; P > .01, intermediate-density LDL (idLDL) (-14.3%; P > .05), sdLDL (-45%; P > .01), and triglycerides (-38%; P > .01) were significantly decreased, and HDL (+14.3%; P > .05) and apolipoprotein A-I (ApoA-I; +7%; P > .05) were increased; large buoyant (lb) LDL did not change (P=NS). Simvastatin therapy decreased LDL (-55.1 %; P > .01), ApoB (-46%; P > .01), lbLDL (-33.3%; P > .05), idLDL (-22.7%; P > .05), sdLDL (-33.3%; P > .05), and triglycerides (-47.9%; P > .01); HDL was not changed (P=NS) after simvastatin, but ApoA-I was increased (+11.3%; P > .01). HDL increases (P > .01) and sdLDL decreases (P > .01) were significantly greater after fluvastatin compared with simvastatin therapy; LDL, triglycerides, ApoB, and idLDL changes were similar after both therapies (P=NS), and lbLDL decreases were greater with simvastatin therapy (P > .05). With both treatments, classic mean LDL and ApoB target levels were achieved in most patients. We conclude that the lipid triad can be controlled with fluvastatin XL 80 mg in patients with type 2 diabetes.