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Journal of Southern Medical University logoLink to Journal of Southern Medical University
. 2017 Mar 20;37(3):308–311. [Article in Chinese] doi: 10.3969/j.issn.1673-4254.2017.03.05

系膜区IgG沉积对IgA肾病临床及病理影响

Clinical and pathological features in IgA nephropathy with IgG deposition in the glomerular mesangial area

Xiaomeng XU 1, Shuangshuang ZHU 2, Xiaohong WANG 1, Xiaofei SHAO 1, Bin LI 1, Ying ZHANG 1, Qin LIU 1, Jiamin LI 1, Honglei WANG 1, Yongqiang LI 1, Hequn ZOU 1,*
PMCID: PMC6780451  PMID: 28377344

Abstract

Objective

To investigate the relationship between the clinical and pathological findings in IgA nephropathy with or without IgG deposition in the glomerular mesangial area.

Methods

The data were collected from 122 patients with a diagnosis of IgA nephropathy by renal biopsy in the Third Affiliated Hospital of Southern Medical University between November, 2009 and February, 2016. All the samples were examined by light microscopy, immunofluorescence and electron microscopy. According to the results of immunofluorescence assay, the patients were divided into IgA group (n=63) and IgA-IgG group (n= 59). The pathological classification of IgA nephropathy was analyzed according to Oxford classification and Lee's classification. The clinical and pathological findings were compared between the two groups.

Results

Compared with the patients with IgA nephropathy but without IgG deposition, patients with IgA nephropathy with IgG deposition had higher serum creatinine, higher 24-h urine protein, higher blood uric acid, higher triglyceride levels (P<0.05) and lower eGFR (P<0.05); more of these patients were in Lee's grade IV-V, had renal tubular atrophy and/or interstitial fibrosis, and had MEST scores more than 3 (P<0.05).

Conclusion

Patients with IgA nephropathy with IgG deposition in the glomerular mesangial have severer clinical symptoms and more serious pathological changes. Measures should be taken to control IgG deposition in patients with IgA nephropathy to delay the progress of the disease.

Keywords: IgA nephropathy, mesangial IgG deposition, Lee's classification, Oxford classification

IgA肾病是世界范围内最常见的原发性肾小球疾病[1-3] 。根据侯凡凡等[4] 7万余例肾活检资料报道，在我国IgA肾病约占肾活检患者的28.1%，是我国最常见的肾小球肾炎。IgA肾病临床、病理及预后差异较大，临床可表现为单纯镜检血尿至终末期肾脏病，病理可从单纯系膜细胞增生至慢性硬化性肾病，并且大约1/3的患者进展至终末期肾脏病（ESRD）需要行肾脏替代治疗[5-8] 。

IgA肾病是一种病理诊断，免疫病理以肾小球系膜区IgA沉积伴补体C3沉积为特征，常伴IgG于系膜区沉积[7, 9] 。然而，系膜区IgG沉积并不会改变IgA肾病的诊断，很少有关注其在IgA 肾病的意义[10-11] 。另外，关于IgA肾病单纯IgA沉积与IgA-IgG沉积的临床及病理差异尚未完全被认识[12] 。本研究拟利用本中心肾活检证实的IgA肾病进行探讨两者间区别。

1. 资料和方法

1.1. 研究对象

收集从2009年11月~2016年2月份在南方医科大学第三附属医院肾活检诊断为IgA 肾病患者138 例。并且排除下列疾病：（1）系统性红斑狼疮、紫癜肾炎、肿瘤、血液病等系统性疾病所致继发性IgA肾病；（2）患者肾活检光镜下肾小球数目小于8 个；（3）肾活检时eGFR＜10 mL/min·1.73 m2；（4）IgA肾病合并膜性肾病。

IgA 肾病诊断依靠组织病理学免疫荧光分析，以IgA（荧光强度大于等于++）和补体C3为主沉积于肾小球系膜区，伴或者不伴IgG和IgM沉积。所有肾活检样本均行光镜、免疫荧光和电镜检查。根据患者免疫应该系膜区有无IgG沉积于系膜区，将IgA肾病患者分为单纯IgA沉积组与IgA-IgG沉积组。根据上述纳入及排除标准总计122例患者符合上述标准被纳入研究，其中单纯IgA沉积组63例，IgA-IgG沉积组59例。所有患者在肾活检时均未长期服用糖皮质激素和/或免疫抑制剂。所有参与者获得知情同意。

1.2. 临床指标

收集患者的年龄、性别、收缩压、舒张压、血肌酐（Scr）、24 h尿蛋白、血清白蛋白（ALB）、尿酸、高密度脂蛋白（HDL）、胆固醇、甘油三酯（TG）、低密度脂蛋白（LDL-C）。eGFR使用适合中国人的MDRD公式计算，eGFR = [175×（血肌酐）-1.234 ×（年龄）-0.179×（女性，×0.79）][13] 。

1.3. 病理分级

除了对IgA肾病进行Lee氏[14] 分级外，我们还对其进行牛津分级[15] ：（1）系膜细胞增生(M)：M1和M0；（2）内皮细胞增生E1、E0；（3）节段性肾小球硬化S1或S0；（4）肾小管萎缩或/和间质纤维化（T）T0：0~50%，T1：>50%。MEST得分=M+E+S+T，范围从0~4。肾活检的诊断是经两位病理医生独立的诊断，有争议的病例经所有作者参与临床病理讨论后决定诊断。

1.4. 统计分析

统计分析均使用SPSS19.0软件。正态分布计量资料使用均数±标准差表示。偏态分别计量资料使用中位数与四分位数间距表示。计数资料使用率来表示。对于分类变量使用χ2检验。双侧P值小于0.05认为差异有统计学意义。

2. 结果

2.1. 两组间临床资料对比

IgA-IgG 沉积组患者的血肌酐、24 h尿蛋白、血尿酸、甘油三酯水平明显高于单纯IgA 沉积组；eGFR低于单纯IgA 沉积组（P＜0.05）。两组在血清白蛋白、总胆固醇、血清低密度脂蛋白、高密度脂蛋白、收缩压、舒张压等资料差异无统计学意义（表 1）。

1.

IgA肾病系膜区IgA沉积组与IgA-IgG沉积组患者临床资料对比

Comparison of clinical characteristics between IgA group and IgA-IgG group

Characteristics IgA group (n=63) IgA-IgG group (n=59) P
Scr: Serum creatinine; ALB: Albumin; eGFR: Estimated glomerular filtration rate; LDL: Low-density lipoprotein; HDL: High density lipoprotein; SBP: Systolic pressure; DBP: Diastolic pressure.
Age (year) 42.19±11.08 43.55±14.33 0.978
Number of Male (%) 32（51.6） 30（48.4） 0.995
Scr (μmol/L) 80.22±31.10 106.18±41.46 ＜0.001
ALB (g/L) 39.19±4.17 37.33±5.44 0.657
Proteinuria (g/24 h) 1.23±3.19 3.02±4.11 ＜0.001
eGFR (mL/min·1.73m2) 119.80±19.82 81.13±33.60 ＜0.001
Uric acid (μmol/L) 378.79±124.16 398.12±118.11 0.012
Cholesterol (mmol/L) 4.47±1.06 4.59± 1.46 0.897
Triglyceride 1.43 (0.65-2.21) 1.93 (1.16-2.98) 0.001
LDL (mmol/L) 3.53±0.87 3.56±1.45 0.897
HDL (mmol/L) 1.10±0.56 1.05±0.41 0.879
SBP (mmHg) 133.53±27.29 131.04±20.02 0.612
DBP (mmHg) 81.75±15.11 81.18±13.85 0.529
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2.2. 两组间病理资料对比

本研究进一步对比两组间Lee氏分级及牛津分级的差异。IgA肾病患者单纯IgA 沉积组有15 例为Lee氏分级Ⅳ~Ⅴ级，IgA-IgG 沉积组有25例为Lee氏分级Ⅳ~Ⅴ级，两组比较差异有统计学意义（P＜0.05）。与单纯IgA 沉积组对比，IgA-IgG 沉积组肾小管萎缩或/和间质纤维化评分及MEST评分≥3比例较高（P＜0.05）。两组在系膜细胞增生、内皮细胞增生以及节段性肾小球硬化评分中差异无统计学意义（P＞0.05，表 2）。

2.

IgA肾病系膜区IgA沉积组与IgA-IgG沉积组患者病理资料对比

Comparison of pathological characteristics between IgA group and IgA-IgG group [n(%)]

Characteristics IgA group (n=63) IgA-IgG group (n=59) P
T/I fibrosis: Tubular atrophy and interstitial fibrosis.
Lee's grade IV-V 15 (23.8) 25 (42.4) 0.029
Oxford classification
Mesangial proliferation (M1) 44 (69.8) 50 (84.7) 0.051
Endothelial hypercellularity 18 (28.6) 20 (33.9) 0.525
Segmental glomerulosclerosis (S1) 17 (27.0) 20 (33.9) 0.406
T/I fibrosis ≥25% 20 (31.7) 33 (55.9) 0.007
MEST score ≥3 21 (33.3) 36 (61.0) 0.002
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3. 讨论

本研究收集并分析了经肾活检确诊的122例IgAN患者，根据免疫荧光是否伴IgG于系膜区沉积分为单纯IgA沉积组与IgA-IgG 组，探讨IgG沉积与IgA肾病临床及病理联系。结果显示IgA-IgG 沉积组患者的血肌酐、24 h 尿蛋白、血尿酸、甘油三酯水平明显高于单纯IgA 沉积组；eGFR低于单纯IgA 沉积组（P＜0.05）；病理中有更多的患者处于Lee氏分级Ⅳ~Ⅴ级、肾小管萎缩或/和间质纤维化评分及MEST评分≥3 比例多。研究表明24 h尿蛋白及肾小管萎缩或/和间质纤维化是IgA肾病预后不良的指标。本研究结果提示系膜区伴IgG沉积的IgA肾病患者临床及病理较重，可能临床预后较差。Berger等[16] 首次提出IgA肾病，并且该病可伴IgG沉积。Hass 等[13] 结果提示IgG 沉积率约45%。Okada等[17] 在日本人群中的研究结果提示IgG 沉积率约50%。本研究对我国人群122例IgA肾病的研究结果提示IgG沉积率为48.4%。

IgA肾病IgA1铰链区O-糖链糖基化缺陷是IgA肾病发生发展的重要原因[18-19] 。IgA肾病患者循环中IgA1分子铰链区可结合IgG或IgA1[18, 20] 。另外，IgA肾病循环免疫复合物包含异常IgA1分子结合系膜细胞[21] 。蛋白尿与IgA肾病预后较差密切相关[22-24] ，本研究结果也提示伴IgG沉积的IgA肾病患者24 h尿蛋白量大于不伴IgG沉积者（P＜0.001）。我们推测由免疫复合物组成的异常IgA1分子，和抗糖基化特异性IgG抗体结合决定了系膜区是否有IgG的沉积。这也可能是伴IgG沉积的患者临床及病理较重的原因。另外，研究表明系膜区IgG沉积及IgA沉积受肾活检时机及治疗的影响[21] ，本研究所选病例肾活检时均未予以激素或免疫抑制剂治疗，可排除药物对系膜区IgG沉积及IgA肾病病理诊断的影响。Wada等[12] 对57例IgA肾病随访33.3个月资料表明，伴IgG沉积者达到完全缓解者少、是持续尿检异常的独立危险因素。此外，研究表明IgA肾病伴IgG沉积是进展至终末期肾脏病的危险因素。本研究结果提示伴IgG沉积的IgA肾病患者临床及病理较重。

研究表明与其他IgA肾病病理分级相比，牛津分级及MEST评分可以早期预测IgA肾病预后[25] 。本研究使用Lee氏及牛津分级两种病理分级，分别探讨系膜区IgG沉积与IgA肾病的关系。该病理分型对肾小球、肾小管均有评分，可克服Hass分级着重强调肾小球病变的不足[26] 。IgA 肾病牛津分级四个指标（系膜细胞增生、内皮细胞增生、节段性肾小球硬化、肾小管萎缩或/和间质纤维化）是临床预后的预测因子[27] 。本研究首次探讨IgA肾病系膜区IgG沉积与IgA肾病牛津分级的关系，结果提示伴IgG沉积的IgA肾病患者病理较重，肾小管萎缩或/和间质纤维化评分及MEST评分≥3 比例较高（P＜0.05）。

综上所述，IgA肾病系膜区伴IgG沉积患者临床及病理较重，应加强对IgA 肾病系膜区伴IgG 沉积的认识，延缓IgA肾病的进展。

Biographies

徐小蒙，在读博士研究生，E-mail: xuxiaomeng@foxmail.com

祝爽爽，医师，E-mail: zhushuang101@126.com

Funding Statement

国家自然科学基金（81270840）；欧盟第七框架计划资助项 目（UroSense-286386）；中国南方智谷引进创新团队和项目 （CXTD-001）；广东省科技计划项目(2014A020212196)；广东省医学 科研基金项目（B2013260）

Supported by National Natural Science Foundation of China (81270840)

Contributor Information

祝 爽爽 (Shuangshuang ZHU), Email: zhushuang101@126.com.

邹 和群 (Hequn ZOU), Email: hequnzou@hotmail.com.

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