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中华肾脏病杂志

中华肾脏病杂志

北大核心

CSCD

CSTPCD

Chinese Journal of Nephrology
1985年创刊，中国科协主管，中华医学会主办，中山大学附属第一医院承办。本刊是我国内儿科肾脏病学科领域高水平的专业期刊，对促进肾脏病学术交流及发展，起着重要的指导作用。本刊报道我国肾脏病领域领先的科研成果及临床诊疗经验。主要栏目有述评、论著、短篇论著、讲座、综述、临床病理（病例）讨论、病例报告、经验交流、会议纪要、国际学术动态。本刊的办刊宗旨：理论与实践相结合，基础与临床相结合，普及与提高相结合，为培养我国的肾脏病医学人才服务，为我国肾脏病患者的健康服务。读者对象：内科及儿科肾脏病临床和先关科研教学人员。
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  • 发文量：4923
  • 被引量：2122
  • H指数：3
  • 开始收录时间：1989,5(1)
  • CNKI综合因子：0.98
  • 维普期刊影响因子： 1.269
  • 万方期刊影响因子：1.26
  • 创刊时间：1985
  • 国内刊号/CN：44-1217/R
    国际刊号/ISSN：1001-7097
  • 发行周期：月刊
    邮发代号：46-106
  • 主管单位：中国科学技术协会
    主办单位：中华医学会
中华肾脏病杂志-联系信息
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  • 电话：020-87331532
  • 邮箱：cmaszb@mail.sysu.edu.cn
  • 地址：广州市越秀区中山二路58号
  • 邮编：510080
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中华肾脏病杂志 >2023年第12期
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  • 摘要：目的探讨酮酸联合低蛋白饮食对糖尿病肾病（DN）患者肾脏局部肾素-血管紧张素系统（RAS）活性和足细胞脱落的影响。方法随机选择上海4家医院共68例2型DN患者进入本研究,最终完成疗程且资料完整的患者61例,均属慢性肾脏病3~4期。61例患者被分为低蛋白饮食组（LPD,31例）和酮酸联合低蛋白饮食组（LPD+KA,30例）,随访12个月。依据临床及生化等指标评价患者肾功能、尿蛋白和营养状态等改善情况;应用探针荧光定量反转录PCR方法检测患者尿沉渣足细胞标志物nephrin、podocin和synaptopodin的mRNA表达改变;酶联免疫吸附法（ELISA）测定患者尿血管紧张素原（AGT）/肌酐比值。分析酮酸联合低蛋白饮食对DN患者足细胞丢失和尿AGT改变的影响。结果随访12个月后,两组间GFR下降差异无统计学意义（P＞0.05）;与LPD组相比,LPD+KA组患者尿蛋白量明显降低（P＜0.01）,血清白蛋白和前白蛋白浓度明显升高（P＜0.05）。进一步研究发现,患者尿AGT/肌酐比值的基线值与GFR（r=-0.437,P=0.001）、Scr（r=-0.733,P=0.000）、尿蛋白量（r=-0.851,P=0.000）等呈负相关;尿沉渣中podocin和synaptopodin mRNA表达与尿蛋白量呈正相关（r=0.340,P=0.012;r=0.333,P=0.014）,与GFR、Scr无相关。随访12个月后,LPD+KA组患者尿AGT/肌酐值明显低于LPD组（P＜0.05）;尿沉渣podocin和synaptopodin mRNA的表达显著低于LPD组（P＜0.05）。相关分析结果提示,治疗前后尿沉渣podocin和synaptopodin mRNA表达的变化值与尿AGT/肌酐值变化值呈正相关（r=0.305,P=0.026;r=0.281,P=0.04）。结论酮酸联合低蛋白饮食的降尿蛋白作用可能与其降低肾脏局部组织RAS活性,抑制足细胞脱落有关。
  • 摘要：目的以嘌呤霉素（PAN）损伤足细胞,以地塞米松（DEX）干预,观察不同时间点瞬时受体电位阳离子通道蛋白6（TRPC6）表达和分布的变化,探讨在足细胞损伤过程中,DEX对TRPC6表达与分布的影响及与足细胞损伤的关系。方法体外培养足细胞,设立对照组、PAN刺激组和DEX干预组。对照组用含0.02%二甲亚砜（DMSO）的RPMI1640培养液培养,PAN刺激组加入PAN（50μg/ml）,DEX干预组同时加入PAN（50μg/ml）和溶解于0.02%DMSO的DEX（1μmol/L）,处理8 h、24 h、48 h后观察细胞形态并拍摄,采用图像处理软件分析各组细胞形态及胞体面积的差别。采用流式细胞仪检测足细胞凋亡率,采用实时荧光定量PCR、Western印迹和间接免疫荧光染色检测各时间点TRPC6的mRNA、蛋白表达及分布变化。结果经PAN刺激后细胞体显著缩小（P＜0.05）,足突回缩、消失,细胞间失去相互连接,刺激后48 h足细胞凋亡率显著升高（P＜0.05）。PAN刺激组在刺激24 h和48 h后TRPC6 mRNA及蛋白表达量显著上升（P＜0.05）,TRPC6在足细胞上的分布亦出现异常。DEX干预后细胞胞体显著大于PAN刺激组（P＜0.05）,可维持正常的足突形态;干预48 h后足细胞凋亡率显著低于PAN刺激组,TRPC6 mRNA及蛋白的表达、分布均趋于正常水平。结论 DEX通过稳定重要的足细胞分子TRPC6的表达及分布来抑制足细胞损伤,从而发挥保护足细胞和抗蛋白尿的作用。
  • 摘要：＜正＞尿调蛋白由uromodulin（UMOD）基因编码,在肾脏特异性表达,与慢性肾脏病（CKD）的发生与进展相关[1]。2009年欧洲全基因组的研究结果显示,UMOD基因启动子区单核苷酸多态性（SNP）与CKD的发生和肾小球滤过率（eGFR）相关[2-3]。目前有关UMOD基因启动子区的SNP与CKD患者肾脏生存预后关系的研究较少。本研究探讨了UMOD启动子区SNP与CKD患者5年肾脏生存预后的关系。
  • 摘要：＜正＞碘中毒在生活中较为少见,关于碘中毒的表现、疾病发展过程尤其是肾衰的发展过程、治疗的疗效等文献报道很少。近期我科收治一名碘中毒致急性肾衰竭、肝衰竭的病例,报道如下。患者男性,26岁,因"吸入碘蒸汽3 h伴血尿、腹部不适2天"于2013年9月24日入院。既往有"脂肪肝"病史,肝功能正常。患者2日前吸入碘蒸汽约3 h,之后半小时
  • 摘要：Objective To assess the efficacy and safety of ACD-A solution as anticoagulant during continuous renal replacement therapy (CRRT) in high risk of bleeding patients.Methods Forty high risk bleeding patients on continuous veno-venous hemofiltration (CVVH) were randomly divided into two groups:ACD-A group (22 patients,61 cases) and heparin-free group (18 patients,47 cases).Serum creatinine,function of the coagulation system,electrolyte and acid-base were monitored pre-and post-CVVH.The vital signs of the patients during treatment,dialyser clotting and the incidence of bleeding episodes were recorded.Results (1) The serum level of creatinine decreased significantly after treatment in both groups,but the rate of decrease was obviously higher in ACD-A group than that in heparin-free group[(55.4± 10.2)％ vs (42.0±5.2)％,P=0.031].(2) The average duration of CVVH treatment was (17.3±3.8) h in ACD-A group and (9.7±4.5) h in heparin-free group.There was significant difference between them (P =0.019).The frequency of dialyzer clotting was much higher in heparin-free group than that in ACD-A group (88％ vs 4.9％,P ＜ 0.001).(3) There was no significant difference in the function of the coagulation system between pre-and post-CVVH in either group (P ＞ 0.05).(4) Electrolyte,acid-base and glucose tended to be stable during the treatment in ACD -A group.(5) The vital signs were kept stable and no bleeding episodes were found in all patients of two groups.Conclusions Anticoagulation with ACD-A is safe,effective and convenient for CRRT in critically ill patients at high risk of bleeding.The occurrence of complications can be reduced by configurating appropriate replacement fluid and close laboratory monitoring.%目的 探讨枸橼酸-葡萄糖抗凝溶液(ACD-A)在高危出血患者实施连续性肾脏替代治疗(CRRT)中的有效性和安全性.方法 选择40例行CRRT治疗的高危出血患者,随机分为ACD-A组(22例,行CRRT 61例次)和无肝素组(18例,行CRRT 47例次).治疗模式为连续性静脉-静脉血液滤过(CVVH).监测治疗前后血肌酐、凝血功能、电解质、酸碱指标变化.记录患者生命体征、血滤器凝血情况及临床出血事件.结果 (1)两组患者治疗后血肌酐均显著下降,ACD-A组下降率明显高于无肝素组[(55.4±10.2)％比(42.0±5.2)％,P=0.031].(2)ACD-A组平均治疗时间为(17.3±3.8)h,无肝素组为(9.7±4.5)h,两组比较差异有统计学意义(P=0.019).ACD-A组滤器Ⅱ级以上凝血发生率明显少于无肝素组(4.9％比88％,P＜0.001).(3)与治疗前相比,两组患者治疗后凝血功能均无明显变化(均P＞0.05).(4)ACD-A组治疗过程中血清电解质、酸碱指标及血糖均趋于稳定.(5)两组患者治疗过程中生命体征稳定,均无出血事件发生.结论 ACD-A应用于高危出血病人的CRRT抗凝治疗安全、有效、方便.通过配置适宜的置换液和严密的实验室监测,可防止代谢紊乱的发生.
  • 摘要：目的 描述Ⅰ型原发性高草酸尿症(PHI)一家系3例同胞患者的临床特征并进行致病基因AGXT突变分析.方法 通过直接测序法分析该家系AGXT基因突变位点及次要等位基因状态.以100名健康人作为对照.结果 AGXT基因分析发现2个新的错义杂合突变和1个既往报道过的突变:1号外显子第49位蛋氨酸突变为亮氨酸(p.M49L,c.145A＞C),2号外显子第72位天冬酰胺突变为异亮氨酸(p.N72I,c.215A＞ T),以及10号外显子第333位密码子的无义杂合突变(p.R333*).p.M49L和p.R333*均与次要等位基因IVS1+74 bp呈顺式构型,在中国人群中该次要等位基因型频率远高于高加索人.结论 新发现的2个突变位点可能与PHI有关,但其致病性和分子致病机制尚需进一步研究.这是国内首次对PHI的致病基因分析研究.%Objective To describe the clinical characteristics,and to analyze the AGXT gene mutation in three siblings with primary hyperoxaluria type I (PHI).Methods AGXT gene mutation was analyzed by direct sequencing analysis in this family,and the minor allele status was also tested.One hundred unrelated healthy subjects were also analyzed as controls.Results Three mutations in AGXT were identified in each of three patients including two novel heterozygous missense mutations and one previously reported variant.One mutation was a methionine to leucine substitution at position 49 (p.M49L,c.145A ＞ C) in exon 1,one was an asparagine to isoleucine transition at codon 72 (p.N72I,c.215A ＞ T) in exon 2,and another was a heterozygous nonsense mutation at codon 333 (p.R333*).Both p.M49L and p.R333* occured in cis configuration with the minor allele IVS1 +74 bp.Conclusions Two novel mutations are identified probably in association with PHI,however their pathogenicity and potential molecular mechanisms should be explored by further investigations.This is the first investigation on mutant gene analysis of PHI in China.
  • 摘要：Objective To compare the characteristics of renal disease based on renal biopsy data between the Tibetan plateaus and the plain.Methods 160 chronic kidney diseases patients underwent renal biopsy from the plain and 80 cases from Tibet plateau were compared by parallel controlled manner.The relationship of renal pathology and clinical signs were also compared.Results (1) The male to female ratio was quite different between Tibet plateau and plain groups (0.60∶1 vs 1.11 ∶ 1,P ＜ 0.01).(2) The distribution of pathological types between two groups was quite different.The main reason of primary renal disease at Tibet plateau was minimal change disease (51.39％ vs 14.53％,P ＜ 0.01),but at plain it was IgA nephrology (49.57％ vs 6.94％,P ＜ 0.01).Meanwhile,the LN ratio in the secondary glomerulonephritis at the plateau region was significantly lower than those in the plain region (12.6％ vs 34.9％,P ＜ 0.05).Conclusions The most common reason of primary glomerular disease in plateau region is minimal change,and the most common clinical manifestation is nephrotic syndrome.IgA nephropathy in the plain is the most frequent primary renal disease.In terms of the secondary renal diseases,allergic purpura nephritis is dominated in the plateau region,whereas LN is frequently found in the plain.%目的 探讨我国西藏高原地区与内地平原地区慢性肾脏病患者肾脏病理类型特点的差异.方法 采用回顾性对照研究,比较西藏高原地区80例与内地平原地区160例肾活检患者的一般情况及病理类型分布特点,以及病理与临床表现的关系.结果 (1)高原组与平原组男女比例存在明显差异(0.60∶1比1.11∶1,P＜0.01).(2)两组患者的病理类型分布存在明显差异,高原地区的原发性肾小球肾炎以微小病变为主(51.39％比14.53％,P＜0.01),而平原地区则以IgA肾病为主(49.57％比6.94％,P＜ 0.01),同时继发性肾小球肾炎中狼疮肾炎(LN)比例明显低于平原组(12.6％比34.9％,P＜0.05).结论 西藏高原地区最常见的临床表现是肾病综合征,最常见的原发性肾小球肾炎病理类型为微小病变,内地平原地区则以IgA肾病最为常见.西藏高原地区的继发性肾脏病以过敏性紫癜性肾炎为主,平原地区以LN为主.
  • 摘要：Objective To observe the effects of metformin on expression of Adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK),nuclear factor-κB (NF-κB) and transforming growth factor β1 (TGF-β1) in cultured rat glomerular mesangial cells (MCs),and explore its renoprotective mechanisms.Methods MCs were cultured in the medium with normal glucose (group NG,5.6 mmol/L),high glucose (group HG,25mmol/L) and different concentrations of metformin (group M1,M2,M3).After 48 h exposure,the supernatants and MCs were collected.The expression of NF-κB and TGF-β1 mRNA was analyzed by real time-PCR.Total-AMPK,phospho-Thr-172 AMPK (p-AMPK),NF -κB p65 and TGF-β1 were visualized by Western blot.Results The real time-PCR and Western blot result showed MCs could express AMPK,NF-κB and TGF-β1 mRNA and protein.After stimulated by HG,the levels of intracellular NF-κB and TGF-β1 expressions were significantly increased compared with group NG (P ＜ 0.05); The levels of NF-κB and TGF-β1 were significantly decreased in group M1,M2 and group M3 compared with group HG in a dose-dependent manner.After stimulated by HG,the level of intracellular p-AMPK were down-regulated compared with group NG(all P ＜ 0.05); The expression of p-AMPK increased with the rising of metformin concentration,presenting the opposite trend (P ＜ 0.05),while the level of total-AMPK protein was unchanged with exposure to HG or different concentrations of mefformin(P ＞ 0.05).Conclusion Metformin can suppress the expression of NF-κB and TGF-β1 of glomerular MCs induced by HG via AMPK activation,which may partly contribute to its reno-protection.%目的 观察二甲双胍对大鼠肾小球系膜细胞(MCs)腺苷酸活化蛋白激酶(AMPK)、核因子κB (NF-κB)和转化生长因子β1(TGF-β1)表达的影响,探讨其肾脏保护机制.方法 体外培养MCs,随机分为正常糖浓度(NG)组、高糖(HG)组及高糖+不同浓度二甲双胍(M1、M2、M3)组,48 h后收获各组细胞及上清液.采用荧光实时定量PCR法检测细胞NF-κB、TGF-β1的mRNA含量;Western印迹法检测细胞磷酸化AMPK (p-AMPK)、总AMPK、NF-κB p65及TGF-β1的蛋白表达水平.结果 肾小球系膜细胞可表达AMPK,NF-κB和TGF-β1.与NG组相比,HG组MCs的NF-κB、TGF-β1 mRNA和蛋白表达水平升高(均P＜0.05);二甲双胍干预组MCs的NF-κB、TGF-β1的mRNA和蛋白表达水平降低(均P＜0.05),且呈浓度依赖性.与NG组相比,HG组MCs的p-AMPK蛋白表达水平降低(P＜0.05);二甲双胍组MCs的p-AMPK蛋白表达水平升高(P＜0.05),且呈浓度依赖性;各组总AMPK表达量的差异无统计学意义(均P＞ 0.05).结论 二甲双胍可激活肾小球系膜细胞的腺苷酸活化蛋白激酶,抑制NF-κB及其下游产物TGF-β1的合成,此作用可能与其肾脏保护机制相关.
  • 摘要：目的 通过检测不明原因的不典型膜性肾病(UAMN)患者血清中M型磷脂酶A2受体(PLA2R)抗体及肾组织中IgG亚型的分布,研究UAMN患者血清中PLA2R抗体及肾组织中IgG亚型的分布特点.方法 入选2004年2月至2011年11月于北京大学人民医院肾内科诊断为UAMN的患者20例.对照组包括特发性膜性肾病(IMN)患者20例,继发性膜性肾病(SMN)患者13例.其中SMN组中包括狼疮膜性肾病(LMN)5例,乙肝病毒相关性膜性肾病(HBV-MN)8例.分析入选患者的临床及病理资料,检测血清PLA2R抗体及肾组织中IgG亚型的分布特点.结果 (1) UAMN组患者肾活检时平均年龄为(37.9±3.8)岁,IMN组为(50.1±3.0)岁,SMN组为(49.5±4.5)岁,其中UAMN组平均年龄显著低于IMN组(P=0.0178).UAMN组、IMN组和SMN组的女/男比例分别为0.8:1、0.7∶1和0.6∶1,差异无统计学意义.(2)与SMN组比较,UAMN组24 h尿蛋白定量更低(3.47g比7.89g,P=0.023),大量蛋白尿患者的比例也更低(50.0％比84.6％,P=0.043),血清IgG水平更低[(8.40±3.58) g/L比(10.09±4.69) g/L,P=0.025],血清ANA阳性率也更低(10.0％比53.8％,P=0.006).人血白蛋白、血肌酐、eGFR、血清HBsAg阳性率、血清HBeAg阳性率、血清抗HCV阳性率以及低白蛋白血症、肾病综合征患者比例在3组中的差异均无统计学意义.(3)肾脏病理免疫荧光结果示,与IMN组比较,UAMN组IgA、IgM和C1q荧光阳性率更高,差异有统计学意义(均P＜ 0.01);与SMN组比较,则两组的IgA、IgG、IgM、C1q和C3荧光阳性率及荧光强度差异均无统计学意义.(4)在所有53例患者血清中,仅有10例IMN组患者血清抗PLA2R自身抗体检测为阳性,在IMN组PLA2R自身抗体检出率为50％.3组间的PLA2R自身抗体检出率差异有统计学意义(P＜0.01).(5)对肾组织IgG亚型的检测:UAMN组中IgG1亚型阳性率最高(40％),IgG3亚型阳性率最低(15％).IMN组中,IgG4亚型阳性率最高(60％),其次为IgG1(15％),IgG2及IgG3亚型阳性率最低(均为5％).SMN组中,IgG1亚型阳性率最高(76.9％),IgG4亚型阳性率最低(30.8％).UAMN组IgG1、IgG3亚型阳性率与IMN及SMN组比较差异均无统计学,IgG2亚型阳性率表现出与SMN组差异有统计学意义(30.0％比69.2％,P＜0.05),IgG4亚型阳性率与IMN组差异有统计学意义(20％比60％,P＜0.05).SMN组IgG1、IgG2和IgG3亚型的阳性率均显著高于IMN组(分别为76.9％、69.2％、46.2％比15％、5％、5％,均P＜0.01).IMN组IgG4亚型在肾小球沉积的阳性率高于SMN及UAMN组,但仅与UAMN组差异具统计学意义(P=0.0225).UAMN组显示出了与IMN及SMN组的不同,更类似于SMN组特点.结论 UAMN组患者抗PLA2R自身抗体检测均为阴性,肾组织以IgG1亚型沉积为主,表现了类似SMN的特点,但在临床指标上又显示了与SMN的不同.因此要加强临床的长期随访,深入对这一类疾病的研究.%Objective To investigate the characteristic of autoantibodies of M-type phospholipase A2 receptor (PLA2R) in serum and the glomerular IgG subclass deposits in undetermined atypical membranous nephropathy (MN) patients.Methods From Feb 2004 to Nov 2011,53 cases diagnosed as MN by kidney puneture biopsy in our hospital were included into the study.There were 20 undetermined atypical membranous nephropathy (UAMN),20 idiopathic membranous nephropathy (IMN) and 13 secondary membranous nephropathy (SMN) which were composed of lupus membranous nephropathy (LMN) and HBV related membranous nephropathy (HBV-MN).Clinlical and pathological characteristics were analyzed.The autoantibodies of PLA2R in serum were detected and the glomerular IgG subclass deposits were observed.Results (1) The average age underwent renal biopsy was (37.9±3.8) years of UAMN,(50.1±3.0) years of IMN and (49.5±4.5) years of SMN.The difference in onset average age at disease was significant between UAMN and IMN (P =0.0178).The female/male ratio (F/M) in UAMN,IMN and SMN was 0.8∶ 1,0.7∶1 and 0.6∶ 1(P ＞ 0.05).(2) Compared with SMN,the level of 24-hours urinary protein excretion (3.47 g vs 7.89 g,P =0.023),the ratio of amount urinary protein patients (50.0％ vs 84.6％,P=0.043),the level of serum IgG [(8.40±3.58) g/L vs (10.09±4.69) g/L,P =0.025] and the positive rate of ANA in serum (10.0％ vs 53.8％,P =0.006) in UAMN were all much lower.There were no significant statistical differences in serum albumin,serum creatinine,eGFR,positive rate of HBsAg,HBeAg or HCV,as well as the ratio of hypo-albuminemia and nephrotic syndrome among the three groups.(3) IF positive rate of IgA,IgM and C1q in UAMN were all significantly higher than that in IMN (P ＜ 0.01).There were no significant differences in IF positive rate of IgA,IgM,C1q,IgG and C3 between UAMN and SMN.The IF strength of IgA,IgG,IgM,C3 and C1q in UAMN showed no significant differences between UAMN and SMN.(4) The serum autoantibodies of PLA2R were only detected in 10 cases of IMN group (50％) with all the other cases negative.This detection rate of serum autoantibodies of PLA2R showed significant statistical differences among the three groups (P ＜ 0.01),but no differences between UAMN and SMN (the detection rate in both groups were 0％).(5) IgG1 deposits was the dominant IgG on the glomeruli in UAMN group (40％),as well as in SMN group (76.9％).IgG4 deposits was the dominant IgG on the glomeruli in IMN group (60％).The positive rate of IgG1 and IgG3 in UAMN showed no significant statistical differences when compared with IMN or SMN.The positive rate of IgG2 in UAMN was significantly lower than in SMN (30.0％ vs 69.2％,P ＜ 0.05).The positive rate of IgG4 in UAMN was significantly lower than in IMN (20％ vs 60％,P ＜ 0.05).The positive rate of IgG1,IgG2 and IgG3 in SMN were all significantly higher than in IMN.Conclusions None of the UAMN group had autoantibodies of PLA2R in serum,and IgG1 deposits was the dominant IgG subclass on the glomeruli which indicated the similarity with the SMN group.At the same time,UAMN was significantly different from SMN in clinical manifestations.
  • 摘要：Objective To investigate the effect of active vitamin D (VD) on macrophage M1 and M2 phenotype and its role in protecting podocyte impairment in diabetic nephropathy (DN).Methods Diabetes mellitus rats were established by intraperitoneal injection with streptozocin.Rats were randomly divided into four groups:normal-1 (NC-1,n=8),normal-2 (NC-2,n=8,normal rats treated with calcitriol 0.1 μg· kg-1 · d-1 by gavages),DN (n=24) and VD (n=24,DN+calcitriol 0.1 μg· kg-1 · d-1 by gavages).Blood glucose and body weight were assessed,and 24-hour urine was collected regularly.Blood and urine samples were taken for biochemical study,and kidney tissues were used for PAS staining to assess histological changes.Immunohistochemical staining was used to detect number of CD68 + macrophage.Western blotting was used to detect protein expressions of nephrin,podocin,CD68,M1 specific marker of inducible nitric oxide synthase (iNOS),TNF-α and M2 specific marker of CD163,arginase 1 (Arg-1),mannose receptor (MR).Results (1) In DN group,levels of BUN,Scr,urinary protein and glomerular mesangial matrix proliferation were significantly higher (P ＜ 0.05),and the expressions of nephrin,podocin were significantly decreased compared with NC groups (P ＜ 0.05).These above changes were significantly improved in VD group (P ＜ 0.05).(2)Number of CD68 + macrophage infiltration in DN group was increased in a time dependent manner compared with NC groups,which was significantly reduced in VD group (P ＜ 0.05).(3)To further definite M1 and M2 macrophage activation phenotype,the protein expressions of iNOS and TNF-α was increased in DN group at 8th,14th,18th weeks compared with NC groups (P ＜ 0.05),which were significantly decreased in VD group (P ＜ 0.05).Although,there were no significant difference of protein expressions of CD163,Arg-1 and MR between VD and DN group at both 8th and 14th week (P ＞ 0.05),the protein expressions of CD163,Arg-1 and MR were higher in VD group at 18th week than that in DN group (P ＜ 0.05),and the ratio of CD163/CD68 was also enhanced in VD group (P ＜0.05).(4)Moreover,the protein expression of iNOS was negatively correlated with expression of either nephrin or podocin (r =-0.707,P ＜ 0.01; r =-0.712,P ＜ 0.01),whereas the protein expression of CD163 was positively correlated with expression of either nephrin or podocin (r =0.627,P＜ 0.01; r=0.613,P ＜ 0.01).Conclusion Vitamin D can regulate macrophage phenotype,via inhibiting M 1 macrophage activation and enhancing M2 macrophage activation to protect podocyte impairment.%目的 探讨活性维生素D(VD)能否通过调节肾组织巨噬细胞M1及M2表型活化从而防治糖尿病肾病(DN)大鼠足细胞损伤.方法 利用腹腔注射链脲菌素(STZ)建立糖尿病大鼠模型.将SD雄性大鼠按随机数字表法分为4组:对照组1(NC-1组,n=8)、对照组2(NC-2组,n=8,对照+骨化三醇0.1μg·kg-1·d-1灌胃)、DN组(n=24)、DN+VD干预组(VD组,n=24,DN+骨化三醇0.1 μg· kg-1·d-1灌胃),定期检测血糖、体质量,收集尿标本,分别于干预后8周、14周、18周末处死动物,检测Scr、BUN和尿蛋白变化;PAS染色观察肾脏病理改变;免疫组化法检测肾组织CD68+巨噬细胞浸润数量;Western印迹法检测nephrin、podocin、CD68以及M1巨噬细胞特异性标志物诱导型氮氧化物合酶(iNOS)、肿瘤坏死因子α(TNF-α)和M2巨噬细胞特异性标志物CD163、精氨酸酶1(Arg-1)、甘露糖受体(MR)表达.结果 (1)与两对照组相比,DN组Scr、BUN、24 h尿蛋白量及肾小球系膜基质增生程度显著增加(P＜0.05),podocin、nephrin蛋白表达下降(P＜0.05).VD干预后能明显改善上述病理现象(均P＜0.05).(2)与两对照组相比,DN组肾组织CD68+巨噬细胞浸润数量明显增加,呈时间依赖性.VD干预后能显著减少CD68+巨噬细胞浸润数量(P＜0.05).(3)进一步确定肾组织巨噬细胞M1、M2活化表型发现,8周、14周、18周末DN组iNOS、TNF-α蛋白表达较对照组显著升高(均P＜0.05),VD干预后能明显抑制同期DN肾组织iNOS、TNF-α表达(均P＜0.05);8周、14周末VD组CD163、Arg-1、MR蛋白表达与DN组相比差异无统计学意义(均P＞0.05),而18周末VD组CD163、Arg-1、MR蛋白表达较DN组显著升高(均P＜0.05),CD 163/CD68蛋白表达比例亦显著增加(P＜0.05).(4)相关分析显示,M1标志物iNOS与nephrin、podocin蛋白表达均呈负相关(r=-0.707,P＜0.01;r=-0.712,P＜0.01);M2标志物CD163与nephrin、podocin蛋白表达均呈正相关(r=0.627,P＜ 0.01;r=0.613,P＜ 0.01).结论 活性维生素D具有调节巨噬细胞表型活化的能力,通过抑制巨噬细胞M1型活化并增强M2型活化,进而发挥足细胞保护作用.
  • 摘要：目的 探讨NADPH氧化酶系统(NOXs)对单侧输尿管梗阻(UUO)大鼠肾间质纤维化的影响.方法 雄性Wistar大鼠按随机区间法分为假手术组(Sham,n=8)、假手术+夹竹桃麻素(apocynin)治疗组(SA,n=8)、UUO组(n=8)和UUO+夹竹桃麻素治疗组(UA,n=8).SA及UA组自手术日起每天给予夹竹桃麻素100 mg/kg灌胃治疗,Sham组和UUO组给予等量清水灌胃.术后第7天处死取材,采用ELISA及Western印迹法分别检测肾脏组织超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活性,8-异构前列腺素F2α(8-iso-PGF2α)浓度,NOX2、NOX4及α平滑肌肌动蛋白(α-SMA)、Ⅰ型胶原(COL-Ⅰ)的表达,ERK1/2激酶的活化.结果 与Sham组相比,UUO大鼠第7天NOX2、NOX4表达及8-iso-PGF2α水平显著升高(P＜0.05),同时伴有肾组织COL-Ⅰ和α-SMA表达升高、ERK1/2激酶活化增加(P＜0.05).夹竹桃麻素治疗显著降低NOX2、NOX4的表达及8-iso-PGF2α水平(P＜0.05),同时大鼠肾组织α-SMA及COL-Ⅰ表达显著下降、ERK1/2活化降低(P＜0.05).夹竹桃麻素治疗对肾组织SOD及CAT活性无明显影响.结论 NADPH氧化酶系统通过促氧化应激参与梗阻性肾病大鼠肾间质纤维化的进展,抑制该系统可能作为抑制肾间质纤维化的治疗靶点.%Objective To clarify whether the NADPH oxidases (NOXs) family contributed to the reactive oxygen species (ROS) production and subsequent interstitial fibrosis in unilateral ureter obstruction (UUO) rats.Methods Male Wistar rats were randomly divided into sham operation group (n =8),sham operation + apocynin treatment group (n =8),UUO operation group (n =8) and UUO operation+apocynin treatment group (n =8).Either vehicle or apocynin (100 mg/kg per day) were given by gavage for 7 days after surgery.Rats were sacrificed at 7th day.ELISA was used to detect the activity of superoxide dismutase (SOD) and catalase (CAT),and the level of 8-iso-prostaglandin F2alpha (8-isoPGF2α) in renal tissue.Western blotting was used to detect the protein expressions of NADPH oxidase subunit NOX2 and NOX4,α-smooth muscle actin(α-SMA),collagen Ⅰ (COL-Ⅰ) and the level of ERK1/ 2 phosphorylation (p-ERK1/2).Results UUO rats with vehicle displayed increased oxidative stress,as measured by renal tissue 8-iso-PGF2α,accompanied with increased renal expression of NADPH oxidases (NOX2,1.5-fold and NOX4,1.7-fold,respectively),compared with sham-operated rats (P ＜0.05).Furthermore,vehicle treated UUO rats showed increased renal COL-Ⅰ and α-SMA levels,compared with sham-operated rats (P ＜ 0.05).ERK1/2 was also activated as detected by p-ERK1/2 expression in UUO rats with vehicle (P ＜ 0.05).Apocynin treatment significantly decreased renal tissue 8-iso-PGF2α level and expressions of NOX2 (-28.7％) and NOX4 (-31.0％) in UUO rats,respectively,compared with vehicle treated rats (P ＜ 0.05).And significant decrease of COL-Ⅰ (-26.4％) and α-SMA expression (-80.0％) were also observed (P ＜ 0.05).The activation of ERK1/2 in UUO rats was greatly inhibited by apocynin treatment (P ＜ 0.01).Despite the pronounced dysregulation of pro-oxidative NOXs family,no compensatory increase of antioxidative enzyme activities occurred.Conclusion The NOXs family contributes largely to the production of ROS and subsequent interstitial fibrosis after ureter ligation,and inhibition of the NOXs family may be a choice for preventing interstitial fibrosis.
  • 摘要：Objective To investigate the effect of fluvastatin on TGF-β1 expression in a rat model of peritoneal dialysis(PD).Methods A rat model of PD was built by intraperitoneal injection of 2.5％ or 4.25％ peritoneal dialysate.SD rats were randomly divided into 7 groups:(1) Normal control group; (2)Saline control group:saline 100 ml/kg intraperitoneal injection(IP) each day; (3) Fluvastatin treatment group:fluvastatin intragastrically administration 10 mg/kg each day; (4) 2.5％ PD group:2.5％ peritoneal dialysate IP 100 ml/kg everyday; (5)4.25％ PD group:4.25％ peritoneal dialysate IP 100 ml/kg everyday; (6)2.5％ PD plus fluvastatin treatment group:2.5％ peritoneal dialysate IP 100 ml/ kg plus fluvastatin 10 mg/kg everyday; (7)4.25％ PD plus fluvastatin treatment group:4.25％ peritoneal dialysate IP 100 ml/kg plus fluvastatin 10 mg/kg everyday.The rats were sacrificed at 6 weeks and peritoneal tissues were dissected.The expressions of TGF-β1 and FN were examined by RT-PCR and immunohistochemical analysis.Masson staining was used for histological examination.Results Masson staining showed that the peritoneum thickened in 2.5％ and 4.25％ PD group than in normal control group and saline control group.The fluvastatin treatment ameliorated the thickening of peritoneum induced by PD.RT-PCR and immunohistochemical analysis showed that the mRNA and protein expression of TGF-β1 and FN increased in 2.5％ and 4.25％ PD group than in normal and saline control group (all P ＜ 0.05).The fluvastatin treatment ameliorated the increased expression of TGF-β1 and FN induced by PD.There was no statistically significant difference among normal control group,saline control group and fluvastatin treatment group in both peritoneal thickness and the expression of TGF-β1 and FN.Conclusion Fluvastatin can reduce the increased expressions of TGF -β1 and FN in rat peritoneum and ameliorate the thickening of peritoneum induced by PD.%目的 探讨氟伐他汀对腹膜透析大鼠腹膜组织转化生长因子β1(TGF-β1)表达的影响.方法 每日腹腔注射2.5％或4.25％的葡萄糖腹透液建立腹膜透析大鼠模型.SD雄性大鼠(体质量180 ～ 200 g)随机分为7个组:(1)正常对照组;(2)生理盐水组;(3)氟伐他汀组;(4) 2.5％PD组;(5)4.25％PD组;(6)氟伐他汀干预的2.5％PD组;(7)氟伐他汀干预的4.25％PD组.6周后留取大鼠壁层腹膜组织,光镜观察各组大鼠壁层腹膜形态学的变化,RT-PCR法及免疫组化法分别测定各组大鼠腹膜TGF-β1及纤维连接蛋白(fibronectin,FN)的mRNA及蛋白的表达量.结果 光镜下Masson染色显示4.25％PD组与2.5％PD组大鼠腹膜较正常对照组明显增厚;氟伐他汀干预的42％PD组和2.5％PD组的壁层腹膜厚度薄于相应未干预的PD组,但仍厚于正常对照组;生理盐水组和氟伐他汀组大鼠腹膜的厚度较正常对照组未见明显改变.2.5％PD组与4.25％PD组的TGF-β1和FN的mRNA及蛋白的表达量均明显高于正常对照组(均P＜ 0.05),氟伐他汀干预的2.5％PD组和4.25％PD组的TGF-β1和FN的mRNA及蛋白表达量较无氟伐他汀干预的2.5％PD组和4.25％PD组均有显著减少(均P＜0.05).生理盐水组和氟伐他汀组大鼠腹膜TGF-β1和FN的mRNA及蛋白表达量与正常组比较,差异无统计学意义.结论 氟伐他汀能改善高糖腹透液环境下大鼠腹膜的厚度,同时降低高糖腹透液诱导的大鼠腹膜TGF-β1和FN mRNA及蛋白的表达,对腹膜有保护作用.
  • 摘要：@@
  • 摘要：Objective To explore the effects of physiological intrauterine hypoxia on the mammal kidney development in ex vivo model.Methods Kidney rudiments were micro-dissected from embryonic day 13.5 SD rat embryos.They were pooled and assigned randomly to control group (normoxia,21％ O2) and experimental groups(hypoxia,3％-5％ O2).For conventional culture,the rudiments were placed on 0.4 μm pore-size polycarbonate filters at the bottom of a well insert in a six well plate and incubated at 5％ CO2 at 37℃.The hypoxia micro-environment was created in an incubator through injecting N2 Immunostaining was carried out to label the structure of developing kidney and pictures were taken by a laser confocal microscope.TdT-mediated dUTP nick end labeling was used to detect cell apoptosis while EdU (5-Ethynyl-2'-deoxyuridine) was added to the medium for cell proliferation detection during kidney development.After culture kidneys of both groups were processed and the changes of genes expression were measured by real time PCR.Results Kidney development was significantly suppressed under hypoxia condition with decreased ureteric buds as well as nephrons compared with that under normoxia condition (P＜0.05).Hypoxia inhibited the proliferation of cultured kidneys while reduced the apoptosis of their cells (P ＜ 0.05).Six2-positive progenitors were better maintained within kidneys cultured under low O2 (P ＜ 0.05).Moreover,genes regulating metanephric mesenchymal to epithelial transformation such as Wnt9b and Wnt4 were down-regulated while genes functioning to maintain metanephric mesenchymal progenitors such as Six2,Wt-1 and Pax2 were up-regulated in hypoxia.Conclusion Physiological intrauterine hypoxia as an important microenvironment factor may suppress mammal kidney development through inhibiting the proliferation and differentiation of embryonic kidney progenitors while maintain their undifferentiated status and self-renewal,thus contributing to the balance between differentiation and maintenance of a mesenchymal progenitor cell pool which determines the final number of nephrons in adult kidneys.%目的 研究宫内生理性低氧微环境对哺乳动物胚胎早期肾脏发育的影响.方法 采用大鼠胚胎肾脏体外培养的方法建立肾脏发育模型,应用低氧培养箱模拟胚胎发育早期宫内生理性低氧微环境,免疫荧光染色技术标记胚肾输尿管芽分枝和后肾间充质向上皮转分化过程,激光共聚焦显微镜观察胚肾发育形态学变化;原位末端转移酶标记技术(TUNEL法)检测胚肾细胞凋亡的变化,胸腺嘧啶核苷类似物(EdU)掺入法检测胚肾细胞增殖的变化,实时荧光定量PCR法检测胚肾发育相关基因表达的变化.结果 体外培养条件下低氧(3％～5％O2)微环境显著抑制胚肾发育,输尿管芽分枝和肾小球数目均减少(P＜0.05).低氧(5％O2)条件下胚肾细胞的凋亡程度较常氧下显著减轻,细胞增殖则受到了显著抑制(P＜0.05).低氧增强胚肾后肾间充质Six2阳性干细胞的自我更新,上调Six2、Wt-1等发育重要相关基因的表达,下调Wnt9b和Wnt4等诱导分化相关基因的表达.结论 宫内生理性低氧微环境可能通过影响哺乳动物胚肾发育相关信号通路抑制胚肾干细胞的增殖和分化,从而促进胚肾干细胞维持自我更新.
  • 摘要：Objective To finding out the characters of vascular remolding after the establishment of native arteriovenous fistula on the wrist,and exploring the influential factors.Methods Doppler ultrasound was used to monitor the diameter of cephalic vein,brachial artery,radial artery and ulnar artery at the time before the surgery and one day,one week,two weeks,four weeks and eight weeks after the surgery respectively.The tendency of the diameter change was analyzed.Results Twenty eight patients completed the whole monitor session,in which eleven were female.The average age of those patients was (53.68 ± 2.61) years old.Twelve of them were diabetic nephropathy.The diameters of all vessel were increased more rapidly at the first day than any other days after surgery(all P ＜ 0.01).The patients were divided into two groups depending on whether diabetic nephropathy.No significant difference was found between the two groups on the tendency of diameter change in cephalic vein and brachial artery (all P ＞ 0.05).However,the tendency of diameter change in radial artery and ulnar artery was statistically significant difference between the two groups (all P ＜ 0.05).Conclusions Cephalic vein,brachial artery,radial artery and ulnar artery are all apparently dilated on the first day after the surgery.The vascular dilation and diameter increasing become much slower after the period,the diameter tend to be stable.The primary diseases may affect the tendency of the diameter change in radial artery as well as ulnar artery.%目的 观察血液透析患者前臂腕部动静脉内瘘建立前后头静脉、肱动脉、桡动脉及尺动脉的血管内径变化,探讨内瘘建立后的血管重构特点及影响因素.方法 选择2010年10月至2011年10月在河北医科大学第三医院接受腕部自体动静脉内瘘成形术患者为研究对象.应用彩色多普勒超声技术测量患者术前及术后1d、1周、2周、4周、8周时头静脉、肱动脉、桡动脉及尺动脉的血管内径,观察其变化趋势.结果 28例患者平均年龄(53.68±2.61)岁.原发病为糖尿病肾病者12例.彩色多普勒超声检查结果显示:术后1d组各血管的扩张幅度最大,明显大于其余各时间段组,组间比较差异有统计学意义(均P＜ 0.01).其余时间段组的血管内径变化率的组间比较差异无统计学意义(均P＞ 0.05).依据患者原发病是否为糖尿病肾病分组后发现,两组患者的头静脉、肱动脉变化趋势差异无统计学意义(P＞0.05);而桡动脉、尺动脉变化趋势的组间差异有统计学意义(均P＜ 0.01).结论 前臂自体动静脉内瘘建立后,头静脉、肱动脉、桡动脉及尺动脉均于术后1d发生明显扩张,内径迅速增大.此后上述血管内径扩张缓慢,逐步趋向稳定.原发病不同对桡动脉及尺动脉内径的变化趋势产生影响.
  • 摘要：＜正＞目前普遍观点认为氧化应激参与了糖尿病肾病的发生和发展[1]。解耦联蛋白2（uncoupling protein 2,UCP2）是解耦联蛋白家族的一员,位于线粒体内膜上,可以增加线粒体内膜对质子的通透性,使呼吸作用中的氧化与磷酸化解耦联,使能量以热能形式释放。研究表明UCP2与氧化应激密切相关[2]。目前尚未见关于UCP2在糖尿病肾组织表达的相关研究。本研究主要观察糖尿病大鼠肾脏中UCP2的表达情况,并观察抗氧化剂普罗布考对UCP2表达的影响及对肾脏的保护作用。
  • 摘要：＜正＞患者,男,48岁,因"维持性血液透析（MHD）1年,间断发热伴胸闷1个月"入院。1年前诊断为慢性肾小球肾炎、慢性肾脏病5期,行左前臂自体动静脉内瘘术后予常规MHD治疗。近1个月患者无明显诱因出现间断发热,多为血液透析（HD）时发生,体温最高39℃,发热前感畏寒,无寒战及盗汗,伴阵发性胸闷、气促、乏力,活动后气急,无咳嗽咳痰,期间自行不规则口服多种抗生素,体温明显高时在当地医院曾应用地塞米松,可退热数日;1 d前因乏力、胸闷、气促加重入院。否认糖尿病和心脏疾病史,长
  • 摘要：＜正＞患者,女,68岁,农民。因"发作性胸闷、心悸4个月余,纳差、乏力、低热1周",于2013年5月27日入住本院心内科。既往体健。查体主要发现低热,体温37.3℃,余未见明显异常。入院后主要检查结果:尿蛋白阳性,血沉偏快,贫血,肾功能异常,先后两次核周型抗中性粒细胞胞质抗体（p-ANCA）及髓过氧化物酶（MPO）-ANCA阳性。考虑"系统性血管炎",转入肾内科进一步行肾活检,穿刺标本送第二军医大学附属长征医院检验。病理:光镜下共13个小球,未见小球硬化,其中1个肾小球毛细血管袢皱缩,
  • 摘要：目的探讨6分钟步行试验（6-minute walk test,6MWT）在腹膜透析（腹透）患者中的应用及其对腹透患者预后的预测作用。方法入选2010年5月1日至2011年4月30日在本院腹透中心规律随访、病情稳定、能耐受6MWT的患者。入选患者均行6MWT,记录6分钟步行距离（6MWD）。按6MWD的中位数值将患者分成高6MWD组和低6MWD组。同时检测患者临床生化指标及检查心脏彩色超声波改变。前瞻性随访所有患者,终点事件为患者死亡、退出腹透或研究终止。logistic回归法分析6MWD的影响因素;多因素Cox风险比例模型法分析6MWD与患者全因死亡的关系。结果共145例患者入选本研究。与高6MWD组相比,低6MWD组患者年龄较大;收缩压、舒张压、左室射血分数（LVEF）、蛋白质分解率均较低（均P＜0.01）。高敏C反应蛋白（hs-CRP）、低密度脂蛋白较高（均P＜0.05）。logistic回归分析结果显示高龄（OR=1.040,P=0.018）、低舒张压（OR=0.948,P=0.007）、低LVEF（OR=0.927,P=0.042）是影响腹透患者6MWD降低的独立危险因素。至研究终点,高6MWD组有6例（8.3%）患者死亡,低6MWD组15例（20.5%）死亡,低6MWD组患者的1年存活率明显低于高6MWD组患者（Log-rank=4.983,P=0.026）。心血管并发症[95%CI（1.098~8.952）,P=0.033],6MWD[95%CI（0.104~0.964）,P=0.043]是影响腹透患者全因死亡的独立危险因素。低6MWD组患者技术存活率明显低于高6MWD组（Log-rank=4.838,P=0.028）。两组患者无腹膜炎生存时间的差异无统计学意义,但低6MWD组腹膜炎患者转血透的比例明显高于高6MWD组患者（25.0%比4.2%,P=0.013）。结论年龄、舒张压以及左室功能是腹透患者6MWD的独立影响因素,6MWT操作简单、安全,可作为预测腹透患者预后的一项指标。
  • 摘要：目的对肾小球轻微病变（glomerular minor lesion,GML）进行临床及电镜病理的分类总结,进一步明确该病理表现的性质及意义,探讨其与临床表现的相关性。方法纳入北京协和医院2003年1月7日至2008年12月2日经光镜及免疫荧光病理诊断为GML、同时电镜病理资料完整的患者148例,回顾性分析其临床及病理资料。结果孤立性血尿是患者最常见的临床表现,其次为血尿合并少量蛋白尿及单纯蛋白尿,部分患者可并存高血压、特殊自身免疫表现、肝炎标志物阳性等。经电镜检查明确,GML可最终呈现各种不同的病理表现:薄基底膜肾病（66.2%）、系膜增生性肾小球肾炎（20.3%）、Alport综合征（2.7%）、膜性肾病（3.4%）以及正常组织（4.7%）等。结合临床与病理,表现为孤立性血尿的GML患者,经电镜病理检查诊断为薄基底膜肾病的可能性最大（76.9%）。部分患者存在蛋白尿、高血压等提示不良预后的情况。结论GML只是一种对肾脏病理表现的粗泛描述,对应的电镜病理具有较大异质性,临床意义各异,需积极完善电镜病理,结合临床特点,明确最终诊断,指导治疗。
  • 摘要：目的探讨维持性血液透析（MHD）患者外周血胱抑素C（Cys-C）及氨基末端脑利钠肽前体（NT-proBNP）水平与心血管（CV）事件发生的相关关系,以期寻找一种有效的预测心血管疾病（CVD）的生物学标志物。方法从3个血液净化中心的452例MHD患者中筛选出无冠心病、心力衰竭、心律失常病史,血甲状旁腺激素、血红蛋白、血脂等指标正常的患者126例,采用血液透析、血液透析加滤过及血液灌流等3种透析方式,治疗前及治疗期间每3个月检测透析前血Cys-C、NT-proBNP、血磷、血全段甲状旁腺素（iPTH）、血红蛋白、心电图;每6个月行超声心动检查,观察时间24个月,随访3年,记录患者的心血管事件发生情况及检查结果。应用多因素logistic回归分析上述各指标与CV事件发生的相关性。血Cys-C、NT-proBNP预测效能用受试者工作特征（ROC）曲线下面积（AUC）评价。结果126例患者试验及随访期间发生CV事件18例次,其中心力衰竭8例次,心肌梗死4例次,心律失常6例次。发生CV事件患者血Cys-C中位数[M（1/4,3/4）]为8.59（9.74,7.10）mg/L,NT-proBNP中位数为7739（9 887,6736）ng/L。多因素非条件logistic回归分析结果显示,Cys-C、NT-proBNP、iPTH、透析低血压、透析期间体质量增长是CV事件发生的独立危险因素。血Cys-C和NT-proBNP水平在预测MHD患者CVD发生的AUC分别为0.64（95%CI 0.53~0.71,P＜0.05）和0.79（95%CI 0.72~0.89,P＜0.01）。以Cys-C中位数8.59 mg/L、NT-proBNP中位数7739ng/L作为临界值,其预测CV事件的灵敏度为84.3%,特异度为92.7%。结论血清Cys-C、NT-proBNP是预测血液透析患者心血管事件发生的有效生物学标志物。
  • 摘要：目的探讨白藜芦醇（RSV）对自发性高血压大鼠肾损害的保护作用及对炎性因子白细胞介素6（IL-6）、胞间黏附分子1（ICAM-1）的影响。方法雄性8周龄自发性高血压大鼠（SHR）按随机数字表法分为2组:模型组（SHR组,n=6）和RSV干预组（RSV组,n=6）,另取同龄雄性正常血压（Wistar-Kyoto）大鼠作为对照组（WKY组,n=6）。RSV组每天予RSV（20 mg/kg）灌胃持续20周,SHR组与WKY组同时予等量生理盐水灌胃。代谢笼收集8 h尿液检测尿微量白蛋白（mALB）和尿β2微球蛋白（β2-MG）,收集血和肾组织标本检测血肌酐、尿素氮以及肾脏组织病理改变,免疫组化法观察各组大鼠肾组织纤连蛋白、Ⅰ型胶原、IL-6、ICAM-1变化;实时定量PCR及Western印迹法检测肾组织IL-6、ICAM-1 mRNA和蛋白表达。结果与WKY组相比,SHR组尿mALB和尿β2-MG水平显著增高（P＜0.05）,RSV干预可显著减少尿mALB和β2-MG排泄（P＜0.05）。免疫组化结果显示,SHR组大鼠肾组织纤连蛋白、Ⅰ型胶原、IL-6、ICAM-1的表达较WKY组增加,RSV干预能显著减轻上述改变。同时SHR组大鼠肾组织IL-6、ICAM-1mRNA和蛋白表达较WKY组显著升高（P＜0.05）,RSV干预可显著降低IL-6、ICAM-1的表达（P＜0.05）。结论RSV可减轻自发性高血压大鼠尿mALB、尿β2-MG水平,改善肾脏纤维化等指标,其作用机制可能与抑制IL-6、ICAM-1的表达有关,提示炎性反应可能是高血压肾损害潜在的干预靶点。
  • 摘要：目的观察富含半胱氨酸蛋白61（Cyr61）对缺氧后人肾小管上皮细胞（HK-2）氧化应激的影响,探讨Cyr61对HK-2的保护机制。方法将HK-2细胞分为5组:空白组、Cyr61处理组、MAPK抑制剂组（Cyr61+PD98059预处理）、p38抑制剂组（Cyr61+SB203580预处理）、PI3K抑制剂组[Cyr61+渥曼青霉素（Wortmannin）预处理]。各组细胞预处理12 h后进行缺氧培养。采用四甲基偶氮唑盐（MTT）法检测缺氧前后细胞存活率,流式细胞术检测细胞凋亡率,双氯荧光黄乙酸乙酯（[DCFH-DA）染色检测细胞内活性氧簇（ROS）的生成量,比色法检测细胞中超氧化物歧化酶（SOD）、过氧化氢酶（CAT）活性,Western印迹法检测细胞磷酸化（p）Akt及细胞核内Nrf2蛋白表达水平。结果缺氧培养后空白组HK-2细胞内ROS含量和Nrf2蛋白表达增加,SOD、CAT活性下降,同时细胞存活率下降,凋亡率增高（均P＜0.05）。Cyr61处理组缺氧后存活率、细胞内SOD、CAT活性和p-Akt、Nrf2蛋白显著高于空白组,同时其凋亡率及ROS含量明显低于空白组（均P＜0.05）。与Cyr61处理组相比,缺氧后PI3K抑制剂组HK-2细胞存活率、细胞内SOD、CAT活性和p-Akt、Nrf2蛋白显著下降,凋亡率及ROS含量显著增加（均P＜0.05）;而MAPK抑制剂组和p38抑制剂组HK-2细胞的各项指标同Cyr61处理组相比差异无统计学意义（均P＞0.05）。结论Cyr61可通过PI3K途径促进Nrf2表达,增强抗氧化物质SOD、CAT产生,减少ROS生成,在缺氧诱导的HK-2细胞氧化应激损伤中发挥保护作用。

    中华肾脏病杂志的期刊信息

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    中华肾脏病杂志的获奖情况

    中华肾脏病杂志的收录情况

    • • 北大核心期刊（1992版）
    • • 北大核心期刊（1996版）
    • • 北大核心期刊（2000版）
    • • 北大核心期刊（2004版）
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    • • 北大核心期刊（2011版）
    • • 北大核心期刊（2014版）
    • • 北大核心期刊（2017版）
    • • 化学文摘（网络版）
    • • 中国科学引文数据库（2011-2012）
    • • 中国科学引文数据库（2013-2014）
    • • 中国科学引文数据库（2015-2016）
    • • 中国科学引文数据库（2017-2018）
    • • 中国科学引文数据库（2019-2020）
    • • 日本科学技术振兴机构数据库
    • • 中国科技核心期刊

    中华肾脏病杂志的投稿信息

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