CD71在IgA肾病肾组织中的表达与临床病理关系

目的研究CD71在人类IgA肾病肾组织中的表达强度及与IgA肾病临床病理关系,分析其作为IgA肾病病理和预后标记物的可能性。方法选取该院180例肾穿刺活检为IgA肾病患者,收集患者临床资料,采用光镜、免疫组织化学、免疫荧光、IgA肾病半定量评分等方法检测IgA肾病组肾组织中CD71的表达,并与正常对照组比较;分析CD71与病理严重程度及临床的相关性。结果 (1)在IgA肾病组,CD71的表达明显高于正常对照组(P0.05),且CD71的表达强度随肾组织病理损害加重而增强;(2)IgA肾病肾组织中CD71表达量与IgA肾病组织学半定量评分法中的系膜细胞增生指数(Ms HI)和系膜基质增多指数(Ms MI)呈正相关(P0.05);(3)IgA肾病肾组织中CD71的表达量与患者的蛋白尿水平呈正相关,与肌酐清除率水平呈负相关(P0.05),而与患者血尿水平无明显相关性(P0.05)。结论 CD71在IgA肾病不同病理肾组织表达不同,随病理损害的加重而增强,且CD71的表达与反应系膜细胞和系膜基质增多指数相关,提示CD71与系膜细胞增殖关系密切;另外,CD71表达量与蛋白尿呈正相关,与肌酐清除率呈负相关,提示其与IgA肾病肾功下降及预后不良有关。因此,肾组织CD71的表达可作为判断该症严重程度和预后的生物学标记物之一。     

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。     

IgA肾病临床分型与病理特点的关系

目的探讨IgA肾病患者临床分型、病理特点及其相关性。方法回顾性分析249例原发性IgA肾病患者的临床、病理资料。结果249例IgA肾病患者临床分型以尿检异常型最常见,新月体型者最少见;病理分级以Ⅳ级最多见,Ⅴ级最少见。单纯性镜下血尿型、大量蛋白尿型、尿检异常型及反复发作肉眼血尿型病理分级以Ⅲ、Ⅳ级常见。病理分级与蛋白尿水平、高血压、血肌酐水平呈正相关（r=0.246、0.333、0.312,P均〈0.01）。结论IgA肾病临床表现多样化,以尿检异常型最常见;病理改变以Ⅲ级、Ⅳ级多见。     

HLA-DR基因与广西地区汉族、壮族IgA肾病相关性的研究

目的 探讨广西地区汉族、壮族IgA肾病与HLA-DR基因的相关性.方法 采用聚合酶链反应-序列特异性引物法(PCR-SSP)对87名IgA肾病患者及110名正常对照者的HLA-DR4、-DR12基因频率进行检测.结果 壮族IgA肾病组HLA-DR4的基因频率高于对照组(P＜0.05),HLA-DR4基因阳性组持续性镜下血尿伴蛋白尿的发生率高于阴性组(P＜0.05).汉族IgA肾病组HLA-DR12的基因频率高于对照组(P＜0.01),HLA-DR12基因阳性组持续性镜下血尿伴蛋白尿的发生率高于阴性组(P＜0.01).结论 ①HLA-DR4基因可能是广西壮族IgA肾病的易感基因;HLA-DR12基因可能是广西汉族IgA肾病的易感基因.②HLA-DR4基因与临床表现为持续性镜下血尿伴蛋白尿的广西壮族IgA肾病相关,HLA-DR12基因与临床表现为持续性镜下血尿伴蛋白尿的广西汉族IgA肾病相关.③HLA-DR4、HLA-DR12基因与广西壮族、汉族IgA肾病的不良病理改变均无相关性.     

狼疮性肾炎肾组织CD80与CD86的表达及其意义

目的 研究T淋巴细胞活化分子CD80与CD86在狼疮性肾炎患者肾组织中的表达变化及其与临床指标之间的相关性.方法 肾组织标本来源于2004年12月-2008年10月哈尔滨医科大学附属第一医院住院患者,其中女性44例,男性5例,年龄(28±16)岁.用免疫组织化学法检测狼疮性肾炎及微小病变患者肾组织中的CD80与CD86的表达情况,免疫比浊法检测24 h尿蛋白定量,全自动生化分析仪检测血尿素氮、血肌酐及血浆白蛋白等临床指标.结果 CD80在肾小管上皮细胞、肾间质有阳性表达,在肾小球无表达,而CD86在肾小管上皮细胞、肾间质及肾小球均有表达.CD80与CD86在肾小管间质中的表达水平随着狼疮性肾炎患者肾小管间质病变程度的加重而增强(r=0.574,P<0.001;r=0.534,P<0.001),且CD80的表达与CD86的表达成正相关.CD80与CDB6的表达与患者系统性红斑狼疮疾病活动指数积分(r=0.319,P=0.011;r=0.324,P=0.011)、24 h尿蛋白定量(r=0.424,P=0.003;r:0.408,P=0.004)、肌酐清除率(r=-0.535,P=0.000;r=-0.543,P=0.000)及抗dsDNA抗体滴度(r=0.353,P=0.012;r=0.359,P=0.013)具有明显相关性.结论 CD80与CD86在狼疮性肾炎患者肾组织中的表达水平与肾间质病变具有明显相关性,并且与狼疮性肾炎患者肾活检时的肾功能及活动性明显相关.     

IgA肾病患者补体经典途径在血液及尿液中的活化及与肾损伤的关系

目的 研究循环系统中经典途径补体活化及调节方式在IgA肾病（IgAN）中的致病作用及与肾损伤的关系.方法 IgA肾病组30例,10例狼疮性肾炎（LN）患者作阳性对照,30例健康体检者作对照组.采用ELISA试剂盒检测IgA肾病患者和对照组血及尿液中经典途径补体激活标志物C1q、经典途径调节因子（sCR）1,分析补体浓度与肾组织病理结果及临床生化指标的相关性.将IgA肾病组患者按照病理Lee氏结果进行分组,Lee氏Ⅰ～Ⅲ级定为轻度损伤组,Lee氏Ⅳ～Ⅴ级定为重度损伤组,比较两组间的补体浓度差异.分析血C1q与sCR1间相关性.结果 IgA肾病组患者血清C1q及sCR1水平均高于对照组（P＜0.05）,而IgA肾病组与LN组间比较差异无统计学意义（P ＞0.05）;LN组患者尿液C1q浓度明显高于另外2组（P＜0.01）.当血清肌酐＞ 133μmol/L时,血C1q与肌酐水平呈显著负相关（P＜0.05）.尿C1q与肌酐水平呈显著正相关（P＜0.05）.Lee氏Ⅳ～Ⅴ级组患者血液及尿液C1q均明显低于Lee氏Ⅰ～Ⅲ级组（P＜0.05）.血sCR1与血C1q间呈显著正相关（P＜0.05）.结论 IgA肾病患者循环系统中可能存在补体经典途径激活通路,尤其是在肾损伤严重组,且与疾病的严重程度相关.IgA肾病中可溶型CR1对C1q存在介导调节作用.     

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。     

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.     

肾病范围蛋白尿在判断IgA肾病预后中的意义

目的：研究ＩｇＡ肾病进展为慢性肾功能不全（ＣＲＩ）的临床危险因素。方法：对８４５例经肾活检确诊的ＩｇＡ肾病患者进行追踪观察。用病例对照研究方法研究血肌酐水平、高血压、肾病范围蛋白尿、年龄、性别与ＩｇＡ肾病预后的关系。结果：血肌酐≥１２０μｍｏｌ／Ｌ、高血压、男性、年龄＞４０岁、肾病范围蛋白尿的比值比（ＯＲ）分别为１１４，４７，２８，２１，１９８。比较发病时血肌酐＜１２０μｍｏｌ／Ｌ，５年后发展为ＣＲＩ及５年后肾功能仍正常的病例，发现肾病范围蛋白尿的ＯＲ值为１８（Ｐ＜００１）。结论：血肌酐≥１２０μｍｏｌ／Ｌ、高血压、肾病范围蛋白尿、年龄＞４０岁、男性均为ＩｇＡ肾病进展为ＣＲＩ的临床危险因素。其中肾病范围蛋白尿判断预后的意义更大。     

新月体IgA肾病的临床和病理

目的　了解新月体IgA肾病的临床、病理和免疫病理特征。方法　选择新月体IgA肾病 2 0例 ,男性 13例 ,女性 7例 ,平均发病年龄为 2 8 5± 12 6岁 ,平均病程为 5 1± 5 3个月 ;占IgA肾病 3 1%及新月体肾炎 16 4% ;并与总体IgA肾病患者的临床及免疫病理进行比较。结果　本组患者临床多数表现为急进性肾炎综合征 (90 % ) ,肉眼血尿发生率高达 75 % ,有高血压者占 6 5 % ,有肾病综合征者占 45 %。病理上肾小球病变除表现为新月体 (平均 6 5 % )外 ,还有节段性袢坏死 (6 0 % )、内皮增生 (30 % )、炎细胞浸润 (40 % )等急性病变 ,以及肾小球全球硬化、节段硬化、包囊壁断裂等慢性病变 ;小管间质病变较重 ,中重度小管萎缩、间质纤维化及间质炎细胞浸润分别为 70 %、80 %及 85 % ;间质血管炎和 (或 )纤维素样坏死的发生率为 40 % ;免疫病理表现为IgA、IgA G、IgA M及IgA G M沉积四种类型。此外 ,肾组织CD 4、CD 8、CD 68及PCNA 细胞浸润数均明显高于正常供肾组织。结论新月体IgA肾病患者临床上主要表现为急进性肾炎综合征 ,肉眼血尿发生率高 ;病理上具有小球、小管、间质及血管等多部位及多种多样病理改变。尽管多数患者病情急 ,病程短 ,然而小管间质病变仍较重 ;免疫病理也多样化 ,IgA M和IgA M     

原发性肾小球肾炎外周血细胞粘附分子浓度变化及其临床意义

目的 探讨原发性肾小球闰变患者外周血粘附分子Ｐ选择素（ＣＤ６２Ｐ）细胞表面糖蛋白（ＣＤ４４）的表达特征及其临床意义。方法 采用流式细胞术对９０例原发性肾炎患者外周血ＣＤ６２Ｐ和ＣＤ４４进行了检测分析,以３０例正常人作为对照。结果 原发笥肾小球肾炎患乾ＣＤ６２Ｐ和ＣＤ４４表达均较正常组显著增高（Ｐ〈０．０１）,其中尿毒症组Ｃ生细胞数增高极为显著,ＩgＡ肾病组ＣＤ６２Ｐ和ＣＤ４４表达均较其它肾脏疾病组     

Relationship between urinary angiotensinogen and salt sensitivity of blood pressure in patients with IgA nephropathy

We demonstrated previously that the blood pressure of patients with IgA nephropathy becomes salt sensitive as renal damage progresses. We also showed that increased urinary angiotensinogen levels in such patients closely correlate with augmented renal tissue angiotensinogen gene expression and angiotensin II levels. Here, we investigated the relationship between urinary angiotensinogen and salt sensitivity of blood pressure in patients with IgA nephropathy. Forty-one patients with IgA nephropathy consumed an ordinary salt diet (12 g/d of NaCl) for 1 week and a low-salt diet (5 g/d of NaCl) for 1 week in random order. The salt-sensitivity index was calculated as the reciprocal of the slope of the pressure-natriuresis curve drawn by linking 2 data points obtained during consumption of each diet. The urinary angiotensinogen:creatinine ratio was significantly higher in patients who consumed the ordinary salt diet compared with the low-salt diet (17.5 μg/g [range: 7.3 to 35.6 μg/g] versus 7.9 μg/g [range: 3.1 to 14.2 μg/g] of creatinine, respectively; P<0.001). The sodium sensitivity index in our patients positively correlated with the glomerulosclerosis score (r=0.43; P=0.008) and changes in logarithmic urinary angiotensinogen:creatinine ratio (r=0.37; P=0.017) but not with changes in urinary protein excretion (r=0.18; P=0.49). In contrast, changes in sodium intake did not alter the urinary angiotensinogen:creatinine ratio in patients with Ménière disease and normal renal function (n=9). These data suggest that the inappropriate augmentation of intrarenal angiotensinogen induced by salt and associated renal damage contribute to the development of salt-sensitive hypertension in patients with IgA nephropathy.     

CD40/CD40L在肾小管上皮细胞转分化中的作用及其可能机制

目的 探讨CD40/CD40L在肾小管上皮细胞转分化中的作用及其可能机制.方法 将74例IgA肾病患者肾穿活检组织分为轻度系膜增生组27例、局灶增生组28例和增生硬化组19例,采用免疫组化及Masson方法观察各组肾小管间质内CD40、CD40L、TGF-β、α-SMA、Vimentin和胶原纤维的表达.结果 IgA肾病组织中小管上皮细胞高表达CD40和CD40L,肾小管间质中TGF-β、α-SMA、Vimentin及胶原纤维表达随分级变化而变化,三组间以上指标比较有统计学差异（P＜0.05或＜0.01）.结论 IgA肾病中,CD40和CD40L可能通过TGF-β启动并调节肾小管上皮细胞转分化,参与肾小管间质纤维化.     

Cellular crescents and segmental glomerular necrosis in IgA nephropathy are indicative of the beneficial effects of corticosteroid therapy

OBJECTIVE: Recent reports have revealed that corticosteroid (PSL) therapy has a long-term beneficial effect for stabilization of renal function in progressive IgA nephropathy. PATIENTS AND METHODS: We analyzed serum creatinine (Cr), daily proteinuria and the results of other routine laboratory examinations during a short-term course of PSL therapy in 28 cases of progressive IgA nephropathy. The cases were divided into two groups according to changes in renal function during the PSL treatment period: group I (15 cases), improved renal function; group II (13 cases), no significant change in renal function. RESULTS: In group I, serum Cr and proteinuria were significantly decreased, with maximum effects observed at 3 months of PSL therapy, and remained low during the period of treatment. In contrast, group II showed no significant changes in serum Cr levels during the period of therapy, although proteinuria was transiently decreased after 3 months of therapy. Histologically, cellular/fibrocellular (C/F) crescents and/or segmental glomerular necrosis (SGN) occurred with a significantly higher incidence in group I (87%) than in group II (46%) (p < 0.05). CONCLUSIONS: These results suggested that the early response to PSL in reducing serum Cr and proteinuria by 3 months of treatment may be clinically useful to predict the prognosis of IgA nephropathy and that C/F crescents and/ or SGN may be histologically indicative of the beneficial effects of PSL therapy in IgA nephropathy.     

Immunohistologic analysis of renal CD40 and CD40L expression in lupus nephritis and other glomerulonephritides

Objective. To investigate potential mechanisms by which CD40L-mediated signals may be involved in the pathogenesis of lupus glomerulonephritis (GN). Methods. Renal in situ CD40L and CD40 expression was examined in patient biopsy specimens. Immuno-histochemical studies were performed on frozen sections utilizing anti-CD40L monoclonal antibody (MAb), anti-CD40 MAb, or control MAb. As controls, we analyzed normal kidney specimens and specimens obtained from patients with IgA nephropathy, focal segmental glomerulosclerosis, minimal change disease, idiopathic membranous GN, and antineutrophil cytoplasmic antibody-positive pauci-immune GN. Staining distribution was noted and staining intensity scored on a semiquantitative scale of 0 (no staining) to 3+ (intense staining). Results. In normal kidney, CD40 was expressed on parietal epithelial cells, mesangial cells, endothelial cells, and distal tubules but not proximal tubules. Glomerular and tubular CD40 expression was markedly up-regulated in class III and class IV lupus GN, where there was intense staining of crescents, proximal and distal tubules, and interstitial mononuclear cells. In contrast, CD40 expression in class V lupus GN was similar to that in normal kidney. Interstitial mono-nuclear cells expressing CD40L were present in class IV lupus GN. However, these findings were not unique to lupus GN: up-regulation of CD40 and CD40L expression was similarly observed in other inflammatory renal diseases. Conclusion. This study shows that CD40 is expressed on a variety of renal parenchymal and non-parenchymal cells in normal kidney. Renal CD40 expression is up-regulated in class III and class IV lupus nephritis, as well as in other inflammatory renal diseases, and is associated with the presence of CD40L+ mononuclear cells.     

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.     

Gremlin在原发性肾小球疾病患者肾小管间质中的表达及其意义

目的探讨原发性肾小球疾病患者肾小管间质中Gremlin的表达及其意义。方法采用免疫组化法检测63例原发性肾小球疾病患者及9例正常肾组织穿刺标本中Gremlin、转化生长因子（TGF）-β1,及a-平滑肌肌动蛋白的表达,并用计算机图像分析软件检测肾小管间质Gremlin、TGF—β1及a-SMA阳性染色相对面积,同时检测原发性肾小球疾病患者血肌酐和尿素氮。结果与对照组比较,原发性肾小球疾病患者肾小管间质Gremlin、TGF-β1。及a-SMA表达均明显增加（P〈0．05）;原发性肾小球疾病患者小管间质Gremlin表达阳性率随小管间质纤维化损害程度增高而增加（P〈0．05）,并与TGF-β1,及a—SMA表达呈正相关（r=0．583、0．596,P均〈0．05）;肾小管间质Gremlin表达阳性率与患者血肌酐、尿素氮水平呈正相关（r=0．802、0．708,P均〈0．05）。结论Gremlin表达与原发性肾小球疾病肾间质纤维化程度密切相关,它可以作为原发性肾小球疾病肾间质纤维化程度的一个标志。     

Preliminary study on specificity of IgA released from lymphocytes by EB virus transformation in patients with IgA nephropathy

A study on the specificity of IgA in the supernatant of Epstein-Barr Virus (EBV) transformed lymphocytes obtained from patients with IgA nephropathy is described. Renal biopsy specimens were obtained from nine patients with IgA nephropathy and nine patients with other glomerular diseases. Mononuclear cells obtained from two patients with IgA nephropathy and two healthy adults were transformed with EBV and the supernatant of such transformed cell culture was applied to acid (pH 3.2)-treated renal sections obtained from the same and other patients with IgA nephropathy, as well as to those with other glomerular diseases. The sections were stained with FITC-labeled heavy chain-specific anti-human IgA antiserum and then examined with a fluorescent microscope. It was demonstrated that IgA in the supernatant specifically bound with the glomerular mesangial areas in patients with IgA nephropathy, while it did not bind with such areas in patients with other glomerular diseases. Although IgA in such samples bound with autologous renal tissues, about 50% bound with allogeneic renal specimens of IgA nephropathy. IgA in the supernatant of transformed lymphocytes from healthy adults was not bound with the glomerular mesangial areas of patients with IgA nephropathy and other glomerular diseases. It is concluded that IgA in the supernatant of lymphocytes by EB virus transformation is specific to the mesangial areas of IgA nephropathy and that some heterogeneity is seen among patients with this disease.     

Apelin和APJ在IgA肾病中的表达及与肾间质纤维化相关性研究

目的探讨多肽Apelin及其受体APJ在IgA肾病(IgAN)患者血浆及肾组织中的表达情况,分析其与患者临床指标及肾间质纤维化程度之间的相关关系。方法选取2018年1月至2018年12月在北京友谊医院经肾活检确诊的原发性IgAN患者56例,按2009年IgAN牛津病理分型中的肾小管萎缩/肾间质纤维化程度标准,将患者分为3组:T0组(20例)、Tl组(17例)和T2组(19例);选取同期该院肾活检确诊的微小病变性肾病(MCD)患者20例作为对照。收集患者一般资料和常规临床指标,留取血浆和肾组织标本,采用酶联免疫吸附法检测血浆Apelin-12水平,免疫组织化学法观察肾脏APJ受体的表达。对各组指标进行比较,Pearson和Spearman相关分析明确IgAN患者肾组织APJ的表达量与血浆Apelin-12、肾间质纤维化面积及常规临床指标的相关性;多元线性回归分析影响IgAN患者肾组织APJ表达的相关因素。结果 T0组、T1组和T2组血浆Apelin-12和肾组织APJ表达量的差异有统计学意义(均P<0.05),随着肾间质纤维化程度的加重,血浆Apelin-12的浓度逐渐降低,肾脏APJ的表达逐渐增加(均P<0.05)。相关分析显示:IgAN患者肾脏APJ的表达量与肾间质纤维化面积(r=0.930, P<0.001)、血肌酐(r=0.739, P<0.001)、尿素氮水平(r=0.659, P<0.001)呈正相关,与血浆Apelin-12水平(r=-0.712, P<0.001)和估算肾小球滤过率(eGFR)(r=-0.882, P<0.001)呈负相关。多元线性回归分析显示:IgAN患者肾脏APJ的表达量与肾间质纤维化面积呈正相关(β=0.749, P<0.001)。结论 IgAN患者血浆Apelin水平降低,机体上调肾组织APJ受体表达,且APJ的表达量与肾间质纤维化程度呈正相关。提示在IgAN肾间质纤维化的病理过程中,内源性Apelin/APJ系统发挥一定的自身调节作用。