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。     

老年IgA肾病患者的临床病理特点和长期预后的相关危险因素分析

目的:探讨老年IgA肾病(IgAN)患者的临床病理特点、长期预后及其相关危险因素. 方法:选取2003年1月至2012年12月在南京军区南京总医院肾脏科经肾活检确诊为IgAN且年龄≥65岁的患者82例,随机选取同期经肾活检确诊为IgAN且年龄在18～64岁的患者328例作为对照组,回顾性分析这些患者的临床及随访资料. 结果:老年IgAN患者与对照组相比,肾活检时平均动脉压(MAP) (P=0.001)、24h尿蛋白定量(P=0.011)、血清肌酐(P＜0.001)、估算的肾小球滤过率(eGFR)(P＜0.001)、血尿酸(P=0.012)、总胆固醇水平(P＜0.001)均存在统计学差异.老年IgAN肾小球硬化比例(P=0.001)及肾小管萎缩/间质纤维化(P=0.009)、肾小球节段硬化(P＜0.001)和动脉硬化(P＜0.001)等慢性化病变的发生率均明显高于对照组.老年IgAN患者3年和8年累计肾脏存活率分别为(89.6％和37.7％,P=0.000 2),显著低于对照组(96.5％和79.4％,P=0.000 2).多因素COX回归分析结果表明,肾活检时蛋白尿(HR 1.847;P=0.011)、eGFR(HR 1.080;P=0.006)水平及存在肾小管萎缩/间质纤维化(HR 5.850; P=0.007)是老年IgAN患者肾脏预后的独立危险因素. 结论:本研究表明,老年IgAN患者高血压、血清肌酐升高及肾病范围蛋白尿的发生率均高于同期行肾活检的非老年IgAN患者,肾脏组织的慢性化病变突出.肾活检时蛋白尿、eGFR水平及存在肾小管萎缩/间质纤维化是影响老年IgAN患者预后的独立危险因素.     

成人过敏性紫癜肾炎预后及其危险因素分析

目的 探讨成人过敏性紫癜肾炎(Henoch-Schnlein nephritis,HSPN)预后及其危险因素。方法 对福建医科大学附属第二医院2002年1月至2011年10月经肾活检证实的76例过敏性紫癜肾炎预后及其危险因素进行回顾性分析。结果 平均随访57个月,10例(13.2%)进入终末期肾脏疾病(end-stage renal failure,ESRD)。单因素分析显示,起病时伴高血压、肾功能损害、随访时24 h尿蛋白定量≥1 g和肾小管间质慢性化指数是肾脏预后不良的危险因素,肾脏预后不良与性别、年龄、肾外表现、起病时肉眼血尿、就诊时24 h尿蛋白定量≥1.0 g、肾小球活动及慢性化指数和免疫抑制剂治疗无关。多因素分析显示,肾脏预后不良危险因素包括起病时肾功能损害(OR=10.96,95%CI 1.56~77.26,P<0.05)和肾小管间质慢性化指数(OR=2.77,95%CI 1.20~6.39,P<0.05)。结论 成人HSPN预后较差,预后不良危险因素包括起病时肾功能损害及肾小管间质慢性化指数。     

IgA肾病预后及危险因素分析

目的:探讨影响IgA肾病患者预后的危险因素。方法:选取诊断为IgA肾病患者622例的基本资料,肾脏终点为患者肾小球过率(eGFR)下降50%或发生终末期肾病(ESRD)。采用Kaplan-Meier方法计算生存率,使用单因素及多因素COX回归分析影响IgA肾病患者预后的危险因素。结果:全部患者1年、3年、5年肾脏生存率分别为99.6%,98.4%,91.9%。多因素COX回归分析结果显示患者肾活检时慢性肾脏病(CKD)分期(HR:4.79,95%CI:1.25~18.36,P=0.022)、24 h尿蛋白定量(HR:5.08,95%CI:1.04~24.83,P=0.045)和血清补体C3(HR:0.01,95%CI:0.01~0.59,P=0.016)是IgA患者疾病进展的独立危险因素。结论:8.1%的IgA肾病患者在5年之内eGFR下降50%或进展为ESRD,肾活检时肾功能不全、高24 h尿蛋白定量以及低血清补体C3是预后的独立危险因素。     

狼疮性肾炎患者肾脏远期生存率及影响因素

目的:分析狼疮性肾炎(LN)患者的临床特征和肾脏远期预后,并对影响肾脏预后的危险因素进行评估. 方法:收集本中心经肾活检明确诊断为LN,随访时间≥1年汉族患者的资料,观察终点为进入终末期肾病(ESRD). 结果:本研究共纳入患者1 814例,其中男性253例(13.9％),女性1 561例(86.1％);肾脏病理改变为Ⅱ型患者127例(7.0％)、Ⅲ型244例(13.5％)、Ⅲ+Ⅴ型202例(11.1％)、Ⅳ型711例(39.2％)、Ⅳ+Ⅴ型284例(15.7％)和Ⅴ型246例(13.6％);LN患者5年、10年、15年、20年和25年肾脏生存率分别为93.1％、87.9％、81.0％、68.3％和58.7％;患者的性别、LN病程、平均动脉压、尿蛋白定量、血清肌酐、血红蛋白、血清补体水平及病理类型是ESRD的独立危险因素.随访指标时间平均尿蛋白和时间平均平均动脉压均为ESRD的独立危险因素,且其预测价值分别高于基线尿蛋白和平均动脉压. 结论:结果显示中国汉族LN患者远期预后良好.肾脏预后和病理类型相关,Ⅳ型和Ⅳ+Ⅴ型LN患者肾脏预后最差.病程中应积极控制尿蛋白和血压以减少ESRD的发生.     

Th1/Th2平衡关系与IgA肾病临床、病理表现的相关性分析

目的探讨辅助性T（Th）1/Th2细胞平衡与IgA肾病（IgAN）临床、肾脏病理表现的相关性。方法采用流式细胞术检测40例IgAN患者与20例健康人对照组外周血Th1、Th2值;收集IgAN患者慢性扁桃体炎史和反复发作性肉眼血尿史,血清胆固醇（Tch）、三酰甘油（TG）、IgG、IgA、内生肌酐清除率（Ccr）,24 h尿蛋白及肾脏病理表现;并了解IgAN患者以上情况与Th1/Th2比例的相关性。结果 IgAN患者外周血中Th2细胞比例为（1.77±0.90）%,较健康对照组的（1.18±0.15）%升高（P〈0.01）。慢性扁桃体炎对Th1/Th2比例无明显影响;有反复发作性肉眼血尿的IgAN患者Th1细胞比例（8.50±4.68）%及Th1/Th2值（4.10±2.01）均较无反复发作性肉眼血尿IgAN患者高（P〈0.05）,24 h尿蛋白定量大于1.0 g/d IgAN患者的Th1细胞比例（2.55±1.20）%及Th1/Th2值（1.58±0.43）均较小于1.0 g/d的患者（P〈0.01）;多元线性回归分析显示IgAN患者外周血Th1/Th2比值与血清中IgG/IgA值存在着正相关关系。结论 IgAN患者存在Th2细胞型免疫表达增强,可能与IgA肾病的免疫机制有关;反复发作性肉眼血尿及24 h尿蛋白小于1.0 g/d的IgAN患者外周血的Th细胞亚群呈Th1偏移;IgAN患者的血清中IgG/IgA值对外周血中Th1/Th2比值存在着正相关影响。     

肥胖相关性肾病的远期预后及危险因素分析

目的:研究肥胖相关性肾病(ORG)患者长期预后及相关危险因素。方法:选取东部战区总医院国家肾脏疾病临床医学研究中心ORG随访登记数据库,分析2003年1月至2015年12月经肾活检确诊为ORG患者的随访资料。利用Kaplan-Meier法计算肾脏累积生存率,并利用COX回归模型分析预后危险因素。结果:共227例患者纳入本研究,中位随访时间61月,随访期间37例(16. 3%)新发糖尿病,14例(6. 2%)进展至终末期肾病(ESRD),18例(7. 9%)患者发生终点事件[估算的肾小球滤过率(e GFR)下降50%或进入ESED]。患者肾活检后5年、10年累积肾脏生存率分别为93. 6%和89. 9%。多因素COX回归分析结果表明活检时肾功能不全(HR=6. 140,P=0. 001)、重度间质纤维化(HR=9. 102,P=0. 045)和时间平均蛋白尿(HR=1. 578,P=0. 000)是肾脏预后的独立危险因素。调整活检时肾功能不全、时间平均蛋白尿后,重度间质纤维化较无间质纤维化,终点事件风险增加9. 102倍(P=0. 045)。结论:本研究结果表明ORG患者5年、10年肾脏累积生存率分别为93. 6%和89. 9%。活检时肾功能不全、重度间质纤维化、时间平均蛋白尿是ORG患者预后的独立危险因素。     

以毛细血管内皮细胞弥漫增生为主要表现的IgA肾病的临床病理特点及其预后

目的探讨以毛细血管内皮细胞弥漫性增生为主要表现的IgA肾病(EPIgAN)的临床、病理特点和预后。方法分析北京大学第一医院近15年来IgA肾病(IgAN)的临床和病理资料,比较EPIgAN与非EPIgAN临床病理特点和肾脏存活率;分析EPIgAN预后及其影响因素;观察激素治疗对EPIgAN预后的影响。结果920例IgAN中符合EPIgAN47例,占5·1%。EPIgAN与非EPIgAN相比,肾穿时尿蛋白升高、高血压和水肿多见,细胞新月体明显,而肾小球硬化和肾间质纤维化则较轻;对所有研究对象进行随访,其中36例EPIgAN患者完成随访,平均随访62个月。100例非EPIgAN患者完成随访,平均随访时间64个月。两组共7例到达随访终点。Kaplan-Meier分析两组自然预后差异无显著性(LogRank,P=0·52);Cox回归分析内皮弥漫增生不是影响IgAN预后的危险因素(P=0·27);激素治疗能降低EPIgAN尿蛋白,但随访期内肾脏存活率与对照组差异无显著性。结论EPIgAN肾穿时临床表现重、组织活动性病变多而慢性化指标少,内皮弥漫增生不是影响IgAN预后的危险因素。     

抗中性粒细胞胞质抗体相关血管炎肾脏病理改变与肾脏预后的关系

目的:探讨抗中性粒细胞胞质抗体(ANCA)相关血管炎(AAV)不同肾脏病理类型的远期肾脏预后及影响预后的危险因素。方法:205例AAV患者,其中男性89例,女性116例,中位年龄52岁(37~59)岁,基线血清肌酐(SCr)380.1μmol/L(194.5~583.4μmol/L),其中84例(41.0%)需行肾脏替代治疗(RRT)。肾脏病理类型包括局灶型(n=23)、混合型(n=71)、新月体型(n=47)和硬化型(n=64)。回顾性分析不同病理类型AAV的肾脏预后及影响因素。结果:34例(40.5%)摆脱RRT(中位时间1月),局灶型、混合型、新月体型和硬化型摆脱RRT比例分别为100%、54.5%、48.0%和22.9%。随访3~160月(中位时间22月),26例(12.7%)死亡,92例(44.9%)进入终末期肾病(ESRD)。局灶型、混合型、新月体型和硬化型的5年肾存活率分别为92.3%、60.8%、42.8%和28.7%(P0.01)。多因素COX回归分析显示病理类型、基线SCr和血清白蛋白水平为影响肾存活的独立危险因素,局灶型(HR 0.1,P=0.01)、混合型(HR 0.4,P=0.002)和新月体型(HR 0.5,P=0.005)较硬化型进入ESRD的风险显著低。SCr≥442μmol/L(HR 4.9,P=0.00)和病变与正常肾小球比例≤10%(HR 2.1,P=0.04)是硬化型AAV进展至ESRD的独立风险因素。结论:欧洲血管炎研究小组病理类型能预测AAV患者远期肾脏预后,除病理类型外,SCr和血清白蛋白水平也为影响肾存活的独立危险因素;对硬化型AAV要结合SCr水平和病变与正常肾小球比例判断肾脏疾病预后。     

泌尿系统疾病

口服氯沙坦50mg/d,治疗8周;然后增至100mg/d,再治疗8周。A组18例16周均维持在50mg/d。B组137例有130例随访至试验终点。结果:A组尿蛋白<3.5g/24h者,治疗8周后尿蛋白较入选时下降(31.9±6.2)％,16周后下降(47.8±6.6)％,均P<0.001。B组患者尿蛋白≥     

Relationship between serum IgA/C3 ratio and progression of IgA nephropathy

OBJECTIVE: The serum IgA/C3 ratio might be considered to serve as a diagnostic marker for patients with IgA nephropathy (IgAN), but its value as a marker of the severity of histological lesions or prognosis is unknown. METHODS: We studied the serum IgA/C3 ratio, using standardized reference material, in 86 patients with IgAN and in 32 with non-IgAN. The patients with IgAN were divided according to the severity of histological lesions (mild IgAN, n=29 and severe IgAN, n=57) based on Japanese clinical guidelines. RESULTS: The serum IgA level was significantly higher, while its C3 level was lower in patients with severe IgAN compared to those with non-IgAN. However, these levels were not different between patients with mild IgAN and non-IgAN. In contrast, the serum IgA/C3 ratio obviously differed among the three groups (2.47+/-0.96 vs. 3.63+/-1.44 vs. 4.72+/-1.86; p<0.01, ANOVA). Kaplan-Meier analysis of the patients with IgAN classified according to the mean serum IgA/C3 ratio revealed that the group with high serum IgA/C3 (4.5 and above) had a significantly poorer renal outcome (p<0.05, log-rank test), since the cumulative renal survival rate at 5 years was 84.4% vs. 100%. The ratio (%) of patients with severe IgAN in whom hematuria disappeared, was significantly higher in the low, than in the high serum IgA/C3 group (41.9% vs. 15.4%; p<0.05, t-test). CONCLUSION: The serum IgA/C3 ratio appears to reflect the histological severity of IgAN and could serve as a marker of the progression of IgAN.     

Role of genetic polymorphism in the SA gene on the blood pressure and prognosis of renal function in patients with immunoglobulin A nephropathy.

The SA gene has been shown to be much more highly expressed in the kidneys of spontaneously hypertensive rats than in the corresponding wild-type strain. Genetic polymorphism of this gene has been shown to play a role in human hypertension, although the details of this association remain controversial. We investigated the possible associations between SA gene polymorphism and both hypertension and the prognosis of renal function in patients with immunoglobulin A nephropathy (IgAN). Genomic DNA was isolated from the peripheral blood of 367 individuals, including 274 patients with histologically proven IgAN and 100 controls without any history of renal disease. The SA genotype was determined by polymerase chain reaction (PCR)-restriction fragment length polymorphism (RFLP) with Pst I. The frequencies of genotypes and alleles were not different between the patients with IgAN and those without renal disease. In the group without renal disease, the SA gene polymorphism was not associated with hypertension. However, in the patients with IgAN the A1 allele frequency was significantly higher in the hypertensives than in the normotensives. The renal survival of the patients with the A2 allele tended to be better than that of those without the A2 allele. The findings thus suggest that SA gene polymorphism may be associated with the renal prognosis of IgAN through its effect on blood pressure. Further, they suggest that the sensitivity to this gene polymorphism increases in patients with renal injury.     

Heterogeneity of prognosis in adult IgA nephropathy, especially with mild proteinuria or mild histological features

OBJECTIVE: The present study was undertaken to clarify the clinical course and prognosis of adult patients with primary IgA nephropathy (IgAN), especially with mild proteinuria or mild histological alternations. PATIENTS AND METHODS: A population of 735 IgAN patients whom we were able to observe for more than two years was examined. RESULTS: A total of 115 patients (15.6%) was on dialysis during the observation period. The overall 5-year renal survival rate was 92.0%. On the other hand, 166 patients (22.6%) were in clinical remission. A group with mild proteinuria included 197 patients (26.8%). Forty-seven patients of this group showed minor glomerular abnormalities, whereas 12 patients with mild proteinuria showed severe mesangial involvement. Three patients with mild proteinuria were on dialysis during the observation period, whose proteinuria was increased during the clinical course. A group with minor glomerular abnormalities included 82 patients (11.2%). Forty-seven patients of this group showed mild proteinuria, of whom 12 patients showed moderate proteinuria. However, three patients with minor glomerular abnormalities who were not on dialysis showed loss of renal function. CONCLUSION: These results indicated the heterogeneity of the course and prognosis in IgAN. Even if a patient's initial clinical or histological findings are comparatively mild, strict follow-up management is needed.     

Clinical course and prognostic factors of clinical early IgA nephropathy

BACKGROUND: Immunoglobulin A nephropathy (IgAN) is prevalent in many countries including China. At the time of diagnosis many IgAN patients present with normal renal function, proteinuria of 0.4 g/d or less, and normal blood pressure and they are classified as clinically early IgAN patients. However, the natural history of clinically early IgAN and prognostic factors has not yet been clarified. METHODS: We investigated 177 early IgAN patients (108 males and 69 females) followed up for a mean period of 111 +/- 43 months. RESULTS: During the follow-up period among 177 clinically early IgAN patients, urinary abnormalities disappeared in 9% of the patients; increased proteinuria was present in 79 patients (46%). The prevalence of hypertension was 38% (68 patients), and 24% (43 patients) developed renal insufficiency. Poor renal outcome was associated with haematuria, urinary protein excretion index (UPEI, the product of urinary protein excretion at the time of renal biopsy and prebiopsy duration), and tubulointerstitial lesions. CONCLUSION: Renal outcome is dismal in patients with clinically early IgAN. Haematuria, UPEI, and tubulointerstitial lesions could be useful markers of a progressive course.     

Association of gene polymorphism of polymeric immunoglobulin receptor and IgA nephropathy

OBJECTIVE: In order to explore the possibility that genetic predisposition to dysfunction of mucosal immunity and the IgA processing pathway plays a role in the pathogenesis of mesangial IgA1 deposition in IgAN, we examined the possible association of the gene polymorphism of pIgR in the patients with and without IgAN. SUBJECTS AND METHODS: Genomic DNA of peripheral blood cells was isolated from 372 individuals including 172 histologically confirmed IgAN patients. Segments of the pIgR gene were PCR amplified and restriction fragment length polymorphism was determined as A1 and A2 with and without Pvu II site, respectively. RESULTS: The pIgR genotype distribution was significantly different between the patients with IgAN and those without IgAN. Allele frequency of A2 was higher in IgAN than in other renal diseases (A1 and A2; 0.516 and 0.484 in IgAN, 0.641 and 0.359 in others, chi2 = 9.84, P = 0.0017, Odds ratio = 1.71). Moreover, the subjects with A2A2 genotype were associated with a relatively low level of serum IgA only in the patients with IgAN but not in other renal diseases. The difference of allele frequencies was more remarkable in the patients with a serum IgA level of less than 300 mg/dl (A1 and A2; 0.439 and 0.561 in IgAN, 0.702 and 0.298 in others, chi2 = 12.44, P = 0.0004, Odds ratio = 3.01). CONCLUSION: This is the first demonstration of the pIgR gene polymorphisms in IgAN which are associated with its clinical phenotype. Gene polymorphisms of pIgR may be candidate genetic markers of susceptibility to IgAN.     

肾小球肾炎肾组织megsin的表达及其意义

目的 :观察megsin在肾小球肾炎患者肾小球内表达及其特点 ,对原发性肾小球肾炎 (IgA肾病 ,IgAN)和继发性肾小球肾炎 (狼疮性肾炎 ,LN)进行研究。　 方法 :应用针对人类megsin的多克隆抗体 ,采用免疫组化法检测肾活检组织中肾小球内megsin的表达 ,其中IgAN 10例、LN 2 0例 ,并采用半定量方法与正常肾组织和轻微病变性肾病进行比较。　 结果 :正常肾组织和轻微病变性肾病均可表达一定量的megsin ,而在IgAN和LN的肾小球内megsin均表达明显增加。megsin仅表达于肾小球系膜区域 ,小管间质未见表达。在IgAN系膜增生性病变中megsin表达量较硬化性病变明显增多 (P <0 0 5 )。而在LN肾小球megsin的表达量虽较正常肾组织和轻微病变型肾病显著增多 ,但与原发性肾小球肾炎IgAN相比较 ,其表达量少 ,即使在LNⅣ型时。　 结论 :megsin在原发性和继发性肾小球肾炎均有一定的表达 ,并在其疾病进程中以及肾小球系膜功能调节中起一定作用 ,但在原发性和继发性肾小球肾炎中megsin的表达调节可能存在不同的机制     

Role of hepatitis B virus infection in pathogenesis of IgA nephropathy

AIM: To investigate the role of hepatitis B virus (HBV) in the pathogenesis of IgA nephropathy (IgAN). METHODS: HBV antigens (HBAg, or HBsAg, HBcAg, and HBeAg) in renal tissues with IgAN were detected by immunohistochemical technique. The distribution and localization of HBV DNA were observed by using in situ hybridization. Southern blot analysis was performed to reveal the state of renal HBV DNA. RESULTS: Among 100 patients with IgAN, HBs antigenemia was detected in 18 patients (18.00 %). HBAg in renal tissues was detected in 31 patients (31.00 %), the positive rate of HBAg, HBsAg and HBcAg was 64.52 % (20/31), 32.26 % (10/31), 32.26 % (10/31), respectively in glomeruli. HBcAg was also found in tubular epithelia and interstitia, which was 45.16 % (14/31) and 6.45 % (2/31), respectively. Five out of six cases with positive HBV DNA by in situ hybridization were proved to be HBV DNA positive by Southern blot analysis, and all were of the integrated form. Eight specimens were demonstrated to be HBV DNA positive by in situ hybridization, which was localized in the nuclei of tubular epithelial cells and glomerular mesangial cells as well as in infiltrated interstitial lymphocytes. CONCLUSION: There is a relationship between HBV infection and IgAN. In addition to the humoral immune damage mediated by HBAg-HBAb immune complex, the cellular mechanism mediated by HBV originating from renal cells in situ may be also involved in the pathogenesis of IgAN.     

Renal biopsy in elderly adults over 75 years of age

The results of 177 renal biopsies (RB) in patients over 75 years of age were analysed. The three most frequent histological types were: Overall: membranous nephritis (MN), minimal change disease (MCD) and IgA Nephropathy (IgAN); In nephrotic syndrome (51% of RB): MN (36%), MCD (33%) and amyloidosis (12%); In chronic renal failure without nephrotic syndrome (25% of RB): chronic interstitial nephritis (17%), benign nephrosclerosis (12%) and IgAN (12%); In acute or progressive renal failure (18% of RB): acute tubular necrosis (36%), crescentic GN (16%) and IgAN (12%). Isolated proteinuria was most frequently associated with IgAN. In only 40% of patients was the medical history relevant, and only in selected cases it allowed for accurate prediction of the histological findings. Our data favor a more liberal use of biopsy in the elderly patients.     

Existence and significance of hepatitis B virus DNA in kidneys of IgA nephropathy

AIM: To investigate the existence and significance of hepatitis B virus (HBV) DNA in the pathogenesis of IgA nephropathy (IgAN). METHODS: Fifty cases of IgAN with HBV antigenaemia and/or hepatitis B virus antigens (HBAg, or HBsAg, HBcAg) detected by immunohistochemistry in renal tissues were enrolled in our study. The distribution and localization of HBV DNA were observed using in situ hybridization. Southern blot analysis was performed to reveal the state of renal HBV DNA. RESULTS: Among the 50 patients with IgAN, HBs antigenemia was detected in 17 patients (34%). HBAg in renal tissues was detected in 48 patients (96%), the positive rate of HBAg, HBsAg, and HBcAg was 82% (41/50), 58% (29/50), and 42% (21/50) in glomeruli, respectively; and was 94% (47/50), 56% (28/50) and 78% (39/50) in tubular epithelia, respectively. Positive HBV DNA was detected in 72% (36/50) and 82% (41/50) cases in tubular epithelia and glomeruli respectively by in situ hybridization, and the positive signals were localized in the nuclei of tubular epithelial cells and glomerular mesangial cells as well as infiltrated interstitial lymphocytes. Moreover, 68% (34/50) cases were proved to be HBV DNA positive by Southern blot analysis, and all were the integrated form. CONCLUSION: HBV infection might play an important role in occurrence and progress of IgAN. In addition to humoral immune damages mediated by HBAg-HBAb immune complex, renal tissues of some IgAN are directly infected with HBV and express HBAg in situ, and the cellular mechanism mediated by HBV originating from renal cells in situ may also be involved in the pathogenesis of IgAN.