呈发作性肉眼血尿的IgA肾病22例临床分析

目的:总结伴有肉眼血尿的IgA肾病患者临床及病理特点。方法:选取经肾活检病理诊断为IgA肾病的患者76例,根据患者病程中是否出现肉眼血尿分为研究组22例和对照组54例。应用Katafuchi半定量积分法分析患者肾脏病变程度,比较2组患者病理学改变及临床特点。结果:①研究组患者前驱感染发生率显著高于对照组,高血压发生率及血肌酐水平低于对照组,平均病程短于对照组(均P<0.05)。2组患者24h尿蛋白排泄量无统计学差异(P>0.05)。②研究组患者肾脏病理积分、血管积分、球硬化积分及血管壁增厚积分低于对照组(均P<0.05)。结论:伴有肉眼血尿的IgA肾病患者发病期多伴有前驱感染,病程中高血压发生率、血肌酐水平较不伴有肉眼血尿的IgA肾病患者低;病理改变较不伴有肉眼血尿的IgA肾病轻,预后相对较好。     

126例IgA肾病伴高血压患者血压昼夜节律异常的危险因素分析

目的 分析IrA肾病伴高血压患者血压昼夜节律异常的危险因素.方法 收集成人IrA肾病伴高血压患者126例,均行肾活检及动态血压监测,排除服用降压药物、糖皮质激素者.采用单因素及多因素Logistic回归分析血压昼夜节律异常的危险因素.结果 (1)成人IgA肾病伴高血压患者非勺型血压患病率为73.8％;(2)与勺型血压组比较,非勺型血压患者总胆固醇、血尿酸、血清肌酐、尿蛋白/肌酐、夜间尿钠、尿氯排泄水平均显著增高,肾小球滤过率(eGFR)水平显著降低;(3) Logistic回归分析显示,高尿酸、尿蛋白/肌酐≥1.84 mg/mg、24小时尿钠＞62.5mmol/L、eGFR ＜60 ml/min/1.73 m2是IgA肾病伴高血压患者血压昼夜节律异常的危险因素.结论 肾脏损害不仅是导致高血压的重要原因,在血压节律调控异常中也发挥了重要作用.     

影响IgA肾病预后的危险因素分析

目的通过分析IgA肾病患者的临床资料及病理特征,探讨影响IgA肾病患者长期肾存活率的危险因素。方法分析724例肾活检确诊为IgA肾病患者肾活检时的临床资料及病理特征。对所有患者进行随访,每3~6个月检测尿蛋白、血肌酐(Scr)等指标,以Scr值比基础值升高1倍以上为观察终点。随访时间>6个月者才纳入成功随访病例。用非参数乘积限估计法(Kaplan-Meier法)分析生存率,用Cox回归模型分析影响预后的危险因素。结果共有317例IgA肾病患者成功随访,肾活检后平均随访时间为(43·5±32·2)个月。有39例(12·3%)患者进入随访终点,其1、3、5、10年肾存活率分别为99·5%、93·1%、84·5%和60·1%。Cox比例风险模型单因素分析发现病程长、肾活检时血Scr>115μmol/L、尿蛋白>1·0g/24h、高血压、Lee氏分级Ⅳ级或Ⅳ级以上、中重度肾小球硬化、新月体形成、中重度肾间质纤维化和肾小血管损害是影响IgA肾病预后的危险因素;多因素分析结果显示,蛋白尿、血Scr水平、肾小球硬化、新月体形成、肾间质纤维化是影响IgA肾病预后的独立危险因素。结论蛋白尿、肾功能不全、肾小球硬化、新月体形成和肾间质纤维化是影响IgA肾病预后的独立危险因素。     

狼疮性肾炎合并高血压的临床表现及病理

目的 高血压是狼疮性肾炎(LN)常见并发症,而且是加速LN患者向终末期肾病发展的独立危险因素.本文总结LN合并高血压患者临床及病理特征,探讨高血压发生的相关因素. 方法 回顾性分析伴或不伴高血压的LN病例,比较两组临床特点、实验室检查和肾脏病理的差别. 结果 本组81例病人,LN正常血压51例,LN合并高血压30例(37.0%),两组患者24 h尿蛋白排泄量、肾功能、血尿酸、血红蛋白、活动性和慢性化指数存在显著差异,男性、年龄(≥45岁)、病程(≥1年)、有高血压家族史、血肌酐(≥133μmol/L)、尿蛋白排泄量(≥2 g/24 h)、小管间质指数(≥5)、肾小球硬化指数(≥1)以及合并小动脉壁增厚者高血压发生率更高. 结论 高血压是LN患者常见并发症,伴高血压的LN患者临床表现和肾脏病变较重,高血压是LN预后不良的重要指标.     

高尿酸血症对IgA肾病临床病理特征和疾病进展的影响

目的分析IgA肾病(IgA nephropathy, IgAN)伴高尿酸血症的临床和病理特征,并探讨高尿酸血症对IgAN进展的影响。方法以2006年1月至2016年12月福建医科大学附属第一医院行肾组织活检确诊为IgAN的患者为研究对象,根据血尿酸水平分为高尿酸血症组和尿酸正常组,比较分析两组患者临床和病理特征。以血肌酐倍增或进入终末期肾病(ESRD)或进入肾脏替代治疗为观察终点,用Kaplan-Meier法比较两组患者的肾脏生存率,并用逐步Cox回归模型分析影响IgAN进展的危险因素。结果进入终点事件或未进入观察终点但随访时间2年的231例IgAN患者纳入研究,其中伴高尿酸血症组92例(39.8%),血尿酸正常组139例(60.2%)。两组在性别、血压、血肌酐、血尿素氮、24 h尿蛋白、估算的肾小球滤过率(eGFR)、病理分级、肾小管萎缩/间质纤维化程度方面差异有统计学意义(P0.05)。29例进入终点事件,单因素COX回归分析显示肾小球硬化、肾小管萎缩/间质纤维化、24h尿蛋白定量、高尿酸血症、贫血、高血压病、血肌酐、血尿素氮在进展组与非进展组间差异有统计学意义(P0.05);Kaplan-Meier生存曲线提示,IgAN伴高尿酸血症组肾脏存活率较低。逐步校正的多因素COX回归分析显示贫血、24 h尿蛋白、肾小球硬化、血肌酐是IgAN进展的独立危险因素。结论伴高尿酸血症的IgAN患者临床表现和肾脏病理损害更重,肾小管萎缩/肾间质纤维化程度更高,肾脏存活率更低。     

血液透析在糖尿病肾病治疗中的效果观察

目的分析血液透析在糖尿病肾病治疗中的效果。方法选取该院2017年1月—2019年1月收治的68例糖尿病肾病患者,行血液透析治疗,6个月后对比治疗前后患者的肾功能以及并发症发生率。肾功能指标包括血尿素氮、血肌酐、24 h尿蛋白定量。结果治疗前,患者血尿素氮水平为(26.6±9.7)mmol/L,血肌酐水平为(815±263)mmol/L,24 h尿蛋白定量为(8.5±1.3)g。治疗后,患者血尿素氮水平为(15.7±6.6)mmol/L,血肌酐水平为(602±143)mmol/L,24 h尿蛋白定量为(4.8±1.4)g。前后对比,差异有统计学意义(t=46.012、286.993、16.023,P<0.05)。患者并发症发生率为22.05%(15/68)。结论在糖尿病肾病治疗中,血液透析可缓解患者病情,确保治疗流程化、高质量进行也能控制并发症发生率。     

妊娠期高血压的危险因素

目的探讨妊娠期高血压的危险因素,为预防妊娠期高血压发病提供参考依据。方法采用1∶2配对病例对照研究方法,入选2010年3月至2013年3月福建医科大学附属第一医院住院分娩的妊娠期高血压患者372例(病例组)和同期足月分娩健康新生儿的非妊娠期高血压者744名(对照组)作为研究对象。采用问卷调查和查阅临床资料相结合的方式,收集两组的基础资料,并对危险因素进行单因素和多因素非条件Logistic回归分析。结果与对照组相比,病例组年龄较大;24h尿白蛋白含量、血肌酐水平较高;孕前体质量指数(BMI)≥24kg/m2、糖化血红蛋白(HbA1c)在6.0%~6.5%、孕妇情绪焦虑和妊娠≥2胎者所占的比例较高;孕期检查≥6次所占的比例较低(均P0.05)。单因素Logistic回归分析显示:年龄、孕前BMI、HbA1c、24h尿白蛋白含量、血肌酐水平、孕期检查次数、孕妇情绪、多胎妊娠是妊娠期高血压的危险因素(均P0.05)。多因素非条件Logistic显示:年龄(OR=1.317)、孕前BMI(OR=1.183)、HbA1c(OR=1.303)、24h尿白蛋白(OR=2.847)、血肌酐(OR=1.102)是妊娠期高血压发生的独立危险因素。结论年龄较大、孕前BMI≥24kg/m2、HbA1c在6.0%~6.5%、24h尿白蛋白含量和血肌酐水平较高的孕妇,容易发生妊娠期高血压。     

冠状动脉介入术导致对比剂肾病危险因素分析

目的探讨冠状动脉介入术患者对比剂肾病的危险因素。方法收集我院2008年1月~2009年12月期间住院的172例接受冠状动脉介入术患者的临床资料,比较对比剂使用剂量,测定介入治疗前后血清肌酐,分析发生对比剂肾病危险因素。结果 172例患者发生对比剂肾病32例,发生率18.61%(32/172),肾小球滤过率>60 mL/min患者发生对比剂肾病21例(13%),肾小球滤过率<60 mL/min患者发生对比剂肾病19例(40%)(P<0.001),年龄≥75岁、3支病变、左心室射血分数<40%、血清肌酐>133μmol/L及对比剂剂量>300 mL与对比剂肾病相关(P<0.001)。糖尿病或高血压合并肾功能不全对比剂肾病发病率高于单纯糖尿病或高血压患者(P<0.01)。结论介入治疗术前肾功能受损及其损害程度是术后出现对比剂肾病的最主要危险因素,肾功能不全、年龄≥75岁、多支冠状动脉病变、左心室射血分数<40%、对比剂剂量>300 mL均为对比剂肾病的独立危险因素。糖尿病或高血压病合并肾功能不全可以增加对比剂肾病的临床风险。     

IgA肾病肾功能正常期高血压的发生特点及相关因素分析

目的探讨IgA肾病患者肾功能正常期高血压的发生特点。方法2002—2006年中山大学附属第一医院肾内科住院,经肾活检确诊为IgA肾病,肾小球滤过率(eGFR)≥90mL/(min.1.73m2)的患者507例,根据血压高低分为高血压组(93例)和血压正常组(414例),分析高血压的发生与临床、病理各项指标之间的关系。结果IgA肾病肾功能正常期高血压的发生率18.3%,部分患者尿检改变轻微甚至以高血压为主要症状;单因素分析显示男性、年龄大、体重指数(BMI)高、血三酰甘油、胆固醇升高是高血压发生的临床危险因素,多因素回归分析表明男性、年龄大、BMI高,肾小动脉病变、球性硬化是高血压发生的独立危险因素,少新月体形成亦与高血压发生独立相关。结论IgA肾病肾功能正常期患者高血压的发生并不少见;提高对早期肾性高血压及相关危险因素的认识,有助于原发性肾脏病的诊治。     

IgA肾病合并高血压患者的临床与病理特点分析

目的探讨IgA肾病合并高血压患者的临床与病理特点。方法根据血压状况将317例IgA肾病患者分为高血压组119例和非高血压组198例,分析两组临床和病理特点。结果高血压组肾功能不全的发生率明显高于、血尿的发生率明显低于非高血压组(P<0.05);高血压组24 h尿蛋白定量、尿NAG酶、血肌酐、血尿酸及年龄均显著高于非高血压组,血浆白蛋白水平显著低于非高血压组(P均<0.05);高血压组肾小球硬化指数、间质指数和血管指数均高于非高血压组,病理损害程度为重度者的比例明显高于非高血压组(P均<0.05)。结论合并高血压的IgA肾病患者临床上高尿酸血症、贫血、肾功能不全等的发生率高,肾脏病理损害程度较重,其可能的临床风险因素是高蛋白尿及高血肌酐水平;可能的病理风险因素为肾小球硬化、间质小管病变及肾血管病变。     

IgA肾病预后不良因素与肾血管病变相关性分析

目的：探讨IgA肾病（IgAN）肾血管病变的危险因素。方法选择宁夏人民医院肾脏内科2010年10月至2013年7月经肾活检确诊的原发性IgAN患者100例,并将其分为肾血管病变组和无肾血管病变组,进行对照研究,比较肾血管病变与各项临床指标、病理改变之间的关系。结果100例IgAN患者中有肾血管病变者70例（70%）,无肾血管病变者30例（30%）。单因素分析结果表明,肾血管病变组24h尿蛋白、血尿酸、血肌酐均高于无肾血管病变组（P＜0.05）,血清白蛋白低于无肾血管病变组（P＜0.05）;病理学检查显示肾小球硬化、肾间质纤维化、新月体形成、炎性细胞浸润、肾小管萎缩严重病理表现发生率,肾血管病变组明显高于无肾血管病变组（P＜0.05）。多因素非条件logistic回归分析结果表明,高血压（OR＝7.728,95%CI 1.708～34.964）、24h尿蛋白定量（OR＝20.022,95%CI 3.869～103.623）、肾小球硬化（OR＝12.093,95%CI 2.431～60.149）、肾间质纤维化（OR＝8.511,95%CI 1.332～54.396）是IgAN肾血管病变加重的危险因素。结论 IgAN预后不良因素为高血压、24h尿蛋白定量、肾小球硬化、肾间质纤维化,上述指标与IgAN肾血管病变密切相关,进一步证实了肾血管病变可作为判断预后的一项重要病理指标。     

伴高尿酸血症的IgA肾病临床与病理分析

目的 探讨血清尿酸对IgA肾病临床、病理及预后的影响.方法 回顾性分析我院2007年1月至2010年10月456例经肾穿刺活检病理确诊为原发性IgA肾病住院患者的临床和肾脏病理特点资料.采用t检验和x2检验进行统计学处理.结果 456例IgA肾病患者中高尿酸血症者127例,发生率为27.9％,高尿酸血症组平均年龄、男性所占比例、高血压发生率、血清胆固醇、甘油三酯、体质量指数、肌酐、尿蛋白定量(24h)水平显著高于血尿酸正常组(P＜0.05,P＜0.01);高尿酸血症组肾组织病理病变程度显著重于血尿酸正常组(P＜0.01),分别为肾小球积分(8.1±0.8和5.3±0.9),肾小管间质积分(4.2±0.4和2.7±0.4),血管病变积分(1.43±0.60和0.76±0.29).结论 高尿酸水平对IgA肾病有明显影响,积极降低血清尿酸,有效控制上述临床指标,可望减轻肾组织损害,延缓IgA肾病的进展.     

拟诊高血压肾硬化的非良性肾小动脉硬化症的临床及病理学分析

目的探讨拟诊高血压肾硬化（HN）患者的临床特征,以期提高对良性肾小动脉硬化症（BN）及类似疾病的认识.方法回顾性分析我科63例HN患者年龄、性别、家族史、血压、尿蛋白排泄、血清学各项指标以及眼底、心脏结构等临床参数.通过肾脏病理学检查明确诊断,分析比较各组间临床参数差异及组织学特征.结果依据病理诊断将患者分为BN（35例）、恶性肾小动脉硬化症（MN,12例）、原发性肾炎（PN,10例）、局灶节段性肾小球硬化症（FSGS,6例）四组.10例PN患者中IgA肾病7例（11.1%）,系膜增生性肾炎2例（3.2%）,间质性肾炎1例（1.6%）,HN诊断符合率为74.6%.BN组患者男性居多,年龄高于PN、FSGS组;高血压家族史及高血压病程均较PN、FSGS高;血尿发生率及血尿程度均低于另两组;蛋白定量亦低于PN、FSGS组,尤其与FSGS组比较差异有统计学意义;HN组左心室心肌重量指数（LVMI）明显高于PN、FSGS组,且与PN组差异有统计学意义（P〈0.05）.但BN组与上述两组相差不显著.BN组视网膜病变主要为0～Ⅱ级,占76%,而MN、FSGS则以Ⅲ～Ⅳ级病变为主.组织学显示PN组球性硬化的肾小球比率高于HN、FSGS组,小管慢性化指标PN组高于HN组,但无明显统计学意义.HN、BN组肌内膜细胞增殖、小动脉玻璃样变等血管病变较FSGS组明显,尤以BN组病变最显著.结论临床拟诊HN患者不能排除PN、FSGS.部分BN、MN与PN患者临床特征相似,单纯依据病史、化验等手段难以鉴别,肾组织病理检查是明确诊断的最佳手段.     

高尿酸血症与IgA肾病临床病理的相关性分析

目的 探讨高尿酸血症与IgA肾病临床病理的相关性.方法 选取2007年1月至2010年12月在吉林大学第一医院肾内科肾活检确诊为IgA肾病患者148例,根据血尿酸水平分为血尿酸正常组(107例)和血尿酸增高组(41例),并对两组年龄、性别、高血压、病程、体重指数、生化指标及病理情况进行比较.结果 二组患者间性别、年龄等差异均无统计学意义(P>0.05).血尿酸增高组患者高血乐发病率、病程(月)、体重指数(kg/m2)、血尿素氮(mmol/L)、肌酐(μmol/L)、TG (mmol/L)及24 h尿蛋白定量(mg/24 h)分别为63.4%、18.90 ±10.12、22.81±3.60、8.93±4.28、155.96±107.72、2.11±1.06和4328.16±1434.25,而血尿酸止常组分别为38.3%、9.46±3.91、15.32±2.54、5.21±2.18、79.52±40.01、1.86±1.20和2885.10±1388.15,两组患者差异均有统计学意义(P值均<0.05).Lee's分级血尿酸增高组I+Ⅱ级占12.2%、IV+V级占39.0%,而血尿酸正常组I+Ⅱ级占25.2%、IV+V级占16.9%,两组患者差异均有统计学意义(P值均<0.05).肾小管间质损害(TIL)分级血尿酸增高组以Ⅲ十Ⅳ级多见,占68.3%,而血尿酸正常组以Ⅱ级多见,占76.6%.肾小动脉病变分级血尿酸增高组以Ⅱ+Ⅲ级多见,占73.2%,而血尿酸止常组以0+I级多见,占69.2%.结论 IgA肾病患者血尿酸水平与24 h尿蛋白定量、血压、肾功能损害相关,血尿酸升高者Lee's分级、TIL分级及肾小动脉病变分级较差.

Abstract：

objective To analyze the correlation between the level of serum uric acid and the clinical and pathological features of IgA nephropathy.Methods Totally 148 patients diagnosed as IgA nephropathy by renal biopsy in our hospital from January 2007 to December 2010 were divided into hyperuricaemic group(41 cases)and non-hyperuricaemic group(107 cases)according to the level of serum uric acid.The clinical parameters and renal pathology grade were compared.Results There were significant differences between hyperuricaemic group and non-hyperuricaemic group in the incidences of hypertension(63.4%vs 38.3%),disease duration[(18.90±10.12)months vs(9.46±3.91)months]and body mass index[(22.81±3.60)kg/m2vs(15.32±2.54)kg/m2](all P<0.05),while no differences in age and sex(both P>0.05).The blood urea nitrogen(BUN)[(8.93±4.28)mmol/L vs (5.21±2.18)mmol/L],creatinine(Cr)[(155.96±107.72)μmol/L vs(79.52±40.01)μmol/L],serum triglycerides[(2.11±1.06)mmoVL vs(1.86±1.20)mmol/L]and 24-hour urine protein amount [(4328.16±1434.25)mg/24 h vs(2885.10±1388.15)mg/24 h]were significantly different between the two groups(all P<0.05).The percentage of Lee's grade I+Ⅱin hyperuricaemic group was 12.2%,and IV+V grade was 39.0%,while percentage of Lee's grade I+Ⅱin non-hyperuricaemic group was 25.2%,and IV+V grade was 16.9%(P<0.05).Tubulointerstitial lesions(TIL)gradeⅢ+IV was more in hyperuricaemic group,which was 68.3%,while TIL grade II was more in non-hyperuricaemic group,which was 76.6%.Renal artery damage grade II+Ⅲ was more in hyperuricaemic group.which was 73.2%,while renal artery damage grade 0+1 was more in non-hyperuricaemic group,which was 69.2%.Conclusion The level of serum uric acid was related with 24-hour urine protein amount,blood pressure and kidney function in IgA nephropathy,and Lee's grade,TIL grade and renal artery damage grade were severe in hyperuricaemic group.     

Acute Kidney Injury in Immunoglobulin A Nephropathy: Potential Role of Macroscopic Hematuria and Acute Tubulointerstitial Injury

The aim of our retrospective study was to analyze the clinical course and outcome of patients with immunoglobulin A (IgA) nephropathy who presented with macroscopic hematuria and acute kidney injury (AKI). During the period from 1990 to 2005, seven out of 584 adult patients with IgA nephropathy (1.2%) fulfilled the criteria for macroscopic hematuria‐induced AKI. There was an equal gender distribution among our patients, and a rather high average age at presentation (55.7 ± 10.9 years). Four patients who were oliguric upon admission to hospital needed hemodialysis treatment. The average serum creatinine at the time of kidney biopsy was 429.8 ± 377 µmol/L (median value 378). The percutaneous kidney needle biopsies showed focal proliferative crescentic glomerulonephritis of subclass III, according to the Haas scheme, associated with prominent red blood cell tubular casts and acute tubulointerstitial nephritis. Four patients with the most prominent crescents and tubulointerstitial involvement were treated with methylprednisolone. All patients, treated and untreated, recovered their kidney function (the serum creatinine at a median follow‐up of 15 months was 111.7 ± 38 µmol/L). In conclusion, AKI in IgA nephropathy accompanied by macroscopic hematuria appears to have been a reversible condition in our series of patients. Regarding pathogenesis, the kidney biopsy study points to the important role of glomerular bleeding with consequent, widespread obstructive red blood cell tubular casts accompanied by tubular injury and interstitial nephritis.     

Pathological regression by angiotensin II type 1 receptor blockade in patients with mesangial proliferative glomerulonephritis.

Although angiotensin II type 1 receptor blocker (ARB) therapy reduces proteinuria and retards the progression of renal injury in patients with glomerulonephritis, whether these drugs actually ameliorate pathological damages in human glomerulonephritis has not been determined. Fifteen patients with biopsy-proven mild-to-moderate mesangial proliferative glomerulonephritis (10 with immunoglobulin A [IgA] nephropathy and 5 with non-IgA mesangial proliferative glomerulonephritis) received ARB monotherapy. In these patients, repeated renal biopsy was performed after a mean of 28.1 months, and pathological changes (including the mesangial matrix expansion ratio and interstitial fibrosis expansion ratio) were quantitatively examined using an image analyzer. Clinical markers were also evaluated, including the serum creatinine, serum IgA, creatinine clearance (Ccr), 24-h urinary protein excretion, urinary N-acetyl-beta-D-glucosaminidase (NAG), and blood pressure. ARB therapy significantly reduced urinary protein excretion (0.68+/-0.63 to 0.20+/-0.32 g/day, p=0.016) and the blood pressure (systolic: 133.3+/-18.2 to 123.4+/-10.5 mmHg, p=0.041; diastolic: 79.4+/-11.9 to 72.0+/-8.2 mmHg, p=0.038). Although the global glomerular sclerosis ratio was unchanged (6.3+/-8.5% to 10.7+/-16.1%, p=0.33), the mesangial matrix expansion ratio (33.1+/-10.8% to 22.7+/-7.8%, p=0.001) and the interstitial fibrosis ratio (19.9+/-5.8% to 13.8+/-4.4%, p=0.034) were significantly reduced by ARB treatment. The levels of pathological improvement were similar between patients with IgA nephropathy and those with non-IgA mesangial proliferative glomerulonephritis. The results of the present study strongly suggest that ARB monotherapy can significantly reverse pathological changes, including mesangial matrix expansion and interstitial fibrosis, in human glomerulonephritis.     

Obesity as a risk factor of chronic kidney disease in patients undergoing primary angioplasty

The number of patients with chronic kidney disease-CKD is still growing. Overweight and obesity present also an important problem of world public health. However, there are not many data showing possible association between obesity and incresing risk of development of renal failure recently it has been demonstrated that in obese patients secondary focal segmental glomerulosclerosis and glomerular hypertrophy appear more frequently. The aim of this study was to estimate glomerular filtration rate-GFR in patients with normal serum creatinine concentration undergoing primary angioplasty according to body mass index. The study included 1413 patients udergoing primary angioplasty for acute myocardial infarction. The following parameters were assessed: age, gender, family history of cardiovascular disease, risk factors of cardiovascular disease (hypertension, diabetes mellitus, obesity etc.), previous myocardial infarction, pre-existing heart failure, treatment given, localization of infarct, coronary stenting, serum creatinine before angioplasty, cholesterol, LDL, HDL, triglycerides, glucose, blood pressure. Of a total of 1413 patients, 1337 (94.62%, 943 M, 394 F) had correct serum creatinine concentration (below 1.5 mg/dl for men, below 1.2 mg/dl for women). Glomerular filtration rate was calculated from serum creatinine levels by using the simplified Modification of Diet in Renal Disease Study formula--MDRD, Cockcroft-Gault equation and Jeliffe formula. An average value of GFR in study group was 79.94 +/- 24.51 ml/min (Cockcroft-Gault equation), 73.02 +/- 21.96 ml/min (Cockcroft-Gault adjusted to weight), 90.37 +/- 25.1 ml/min (MDRD equation) and 77.67 +/- 21.65 ml/min (Jeliffe formula). A significant lower serum creatinine levels and GFR (assessed by 3 formulas and Cockcroft-Gault using adjusted weight) were observed in women group. In the whole study group (with normal serum creatinine levels) substantial correlation was found between age and serum creatinine concentration (r = 0.13, p > 0.001), GFR (MDRD, r = -0.37, p < 0.001, Cockcroft-Gault, r = -0.62, p < 0.001, adjusted to weight r = -0.64, p < 0.001, Jeliffe r = -0.61, p < 0.001) and also between BMI and GFR (MDRD r = 0.28, p < 0.001, Cockcroft-Gault, r = 0.31, p < 0.001, adjusted to weight r = 0.08, p < 0.001, Jeliffe r = 0.341, p < 0.001), but not with serum creatinine concentration (r = 0.03, p = 0.3). In patients with normal serum creatinine levels percentage of patients with GFR below 60 ml/min ranges from 4.79% up to 30.74%. In patients with higher BMI, higher GFR may be partially caused by glomerular hyperfiltration. Overweight or obesity are significant, but potentially changeable risk factors for development of chronic renal failure. However, chronic kidney disease is one of the complications of obesity.     

基质金属蛋白酶-9和金属蛋白酶组织抑制物-1在IgA肾病肾组织中的表达

目的 探讨基质金属蛋白酶－9（MMP－9）／金属蛋白酶组织抑制物－1（TIMP－1）系统在IgA肾病肾组织中的表达及其对IgA肾病的进展的影响。方法 采用免疫组织化学和原位杂交技术,分别在蛋白质和基因水平检测38例IgA肾病患者肾组织中的MMP－9和TIMP－1的变化。结果 MMP－9在正常肾脏肾小球的脏层上皮细胞和内皮细胞有少量表达,在肾小管上皮细胞和间质血管壁也有少量表达;在IgA肾病中,MMP－9在系膜增殖性肾小球和间质血管壁的表达均明显增多（P＜0．001）,而在硬化肾小球内的表达则明显减少,肾小管细胞的MMP－9表达无明显变化。TIMP－1在正常肾组织中不能检出,在IgA肾病患者具有系膜增殖性病变的肾小球中有微量表达,在增殖在很重但尚未完全硬化的肾小球内表达增多,在肾小管间质表达最为明显（P＜0．001）,其主要见于肾小管细胞、间质细胞和血管内皮细胞。肾组织中的TIMP－1表达与血清肌酐水平呈显著相关（P＜0．05）,与肾小管间质的纤维化和炎细胞浸润程度亦明显相关（P值均＜0．01）。肾小球中的MMP－9表达与尿蛋白无明显相关性,但与血清肌酐水平呈显著负相关（P＜0．05）。结论 MMP－9和TIMP－1的异常表达可能是影响IgA肾病进展的因素之一。     

Microalbuminuria in hypertensive patients with electrocardiographic left ventricular hypertrophy: the LIFE study

OBJECTIVES : Left ventricular hypertrophy and albuminuria have both been shown to predict increased cardiovascular morbidity and mortality. However, the relationship between these markers of cardiac and renal glomerular damage has not been evaluated in a large hypertensive population with target organ damage. The present study was undertaken to determine whether albuminuria is associated with persistent electrocardiographic (ECG) left ventricular hypertrophy, independent of established risk factors for cardiac hypertrophy, in a large hypertensive population with left ventricular hypertrophy who were free of overt renal failure. METHODS : Patients with stage II-III hypertension were enrolled in the study if they had left ventricular hypertrophy on a screening ECG by Cornell voltage-duration product and/or Sokolow-Lyon voltage criteria, and clinic blood pressures between 160 and 200/95-115 mmHg and plasma creatinine < 160 mmol/l. A second ECG and morning spot urine were obtained after 14 days of placebo treatment. Renal glomerular permeability was evaluated by urine albumin/creatinine (UACR, mg/mmol). Microalbuminuria was present if UACR > 3.5 mg/mmol and macroalbuminuria if UACR > 35 mg/mmol. RESULTS : The mean age of the 8029 patients was 66 years, 54% were women. Microalbuminuria was found in 23% and macroalbuminuria in 4% of patients. Microalbuminuria was more prevalent in patients of African American (35%), Hispanic (37%) and Asian (36%) ethnicity, heavy smokers (32%), diabetics (36%) and in patients with ECG left ventricular hypertrophy by both ECG-criteria (29%). Urine albumin/creatinine was positively related to Sokolow-Lyon voltage criteria and Cornell voltage-duration product criteria. In multiple regression analysis, higher UACR was independently associated with older age, diabetes, higher blood pressure, serum creatinine, smoking and left ventricular hypertrophy. Patients smoking > 20 cigarettes/day had a 1.6-fold higher prevalence of microalbuminuria and a 3.7-fold higher prevalence of macroalbuminuria than never-smokers. ECG left ventricular hypertrophy by Cornell voltage-duration product or Sokolow-Lyon criteria was associated with a 1.6-fold increased prevalence of microalbuminuria and a 2.6-fold increase risk of macroalbuminuria compared to no left ventricular hypertrophy on the second ECG. CONCLUSIONS : In patients with moderately severe hypertension, left ventricular hypertrophy on two consecutive ECGs is associated with increased prevalences of micro- and macroalbuminuria compared to patients without persistent ECG left ventricular hypertrophy. High albumin excretion was related to left ventricular hypertrophy independent of age, blood pressure, diabetes, race, serum creatinine or smoking, suggesting parallel cardiac damage and albuminuria.