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酒精性肝硬化相关继发性IgA肾病中肾小球半乳糖缺乏IgA1及巨噬细胞凋亡抑制因子染色

Glomerular galactose-deficient IgA1 and apoptosis inhibitor of macrophage staining in secondary IgA nephropathy associated with alcoholic cirrhosis.

作者信息

Umezawa Yukako, Aoki Ryosuke, Ichikawa Daisuke, Suzuki Yusuke, Suzuki Tomo

机构信息

Department of Nephrology, Kameda Medical Center, 929, Higashicho, Kamogawa, Chiba, 296-8602, Japan.

Department of Nephrology, Faculty of Medicine, Juntendo University, Tokyo, Japan.

出版信息

J Nephrol. 2025 Feb 13. doi: 10.1007/s40620-025-02213-9.

DOI:10.1007/s40620-025-02213-9
PMID:39946052
Abstract

Immunoglobulin A nephropathy (IgAN) is associated with liver diseases, including alcoholic cirrhosis. When IgAN occurs in patients with liver disease, it is referred to as secondary IgAN; however, the mechanisms underlying secondary IgAN remain unclear. Herein, we present a case report of IgAN in a patient with a history of alcoholic liver cirrhosis, who presented with hematuria and proteinuria. A kidney biopsy revealed diffuse subendothelial deposition and mild mesangial proliferation. Immunofluorescence showed strong positive signals for IgA and IgM in the glomerular capillaries. There were no restrictions between the kappa and lambda staining. Electron microscopy revealed electron-dense deposits in the mesangial and subendothelial kidney regions. Histological diagnosis confirmed IgAN, typically associated with alcoholism. Further examination revealed that galactose-deficient IgA1 antibodies had merged with IgA, and a positive staining for the apoptosis inhibitor of macrophage antibodies along the glomerular capillaries was observed. These findings suggest that primary IgAN and alcoholic cirrhosis-related IgAN may share a common underlying mechanism.

摘要

免疫球蛋白A肾病(IgAN)与包括酒精性肝硬化在内的肝脏疾病有关。当IgAN发生在肝病患者中时,被称为继发性IgAN;然而,继发性IgAN的潜在机制仍不清楚。在此,我们报告一例有酒精性肝硬化病史的IgAN患者,该患者表现为血尿和蛋白尿。肾活检显示弥漫性内皮下沉积和轻度系膜增生。免疫荧光显示肾小球毛细血管中IgA和IgM呈强阳性信号。κ和λ染色之间没有限制。电子显微镜显示系膜和肾内皮下区域有电子致密沉积物。组织学诊断证实为IgAN,通常与酗酒有关。进一步检查发现,缺乏半乳糖的IgA1抗体与IgA合并,并观察到沿肾小球毛细血管的巨噬细胞凋亡抑制抗体呈阳性染色。这些发现表明,原发性IgAN和酒精性肝硬化相关的IgAN可能有共同的潜在机制。

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本文引用的文献

1
Clinical Presentation, Pathological Spectrum, and Outcomes of Alcoholic Cirrhosis-Related Immunoglobulin A Nephropathy.酒精性肝硬化相关免疫球蛋白A肾病的临床表现、病理谱及预后
Kidney Int Rep. 2024 Feb 16;9(5):1369-1378. doi: 10.1016/j.ekir.2024.02.1397. eCollection 2024 May.
2
Efficacy of SGLT2 inhibitors in IgA nephropathy associated with alcoholic liver cirrhosis accompanied by nephrotic syndrome: a case report.钠-葡萄糖协同转运蛋白2抑制剂对酒精性肝硬化伴肾病综合征相关IgA肾病的疗效:一例报告
Front Nephrol. 2024 Jan 22;3:1331757. doi: 10.3389/fneph.2023.1331757. eCollection 2023.
3
IgA glycosylation and immune complex formation in IgAN.
IgA 糖基化与 IgAN 中的免疫复合物形成。
Semin Immunopathol. 2021 Oct;43(5):669-678. doi: 10.1007/s00281-021-00883-8. Epub 2021 Sep 27.
4
IgA Nephropathy: Core Curriculum 2021.IgA 肾病:2021 年核心课程。
Am J Kidney Dis. 2021 Sep;78(3):429-441. doi: 10.1053/j.ajkd.2021.01.024. Epub 2021 Jul 9.
5
Crucial Role of AIM/CD5L in the Development of Glomerular Inflammation in IgA Nephropathy.AIM/CD5L 在 IgA 肾病肾小球炎症发展中的关键作用。
J Am Soc Nephrol. 2020 Sep;31(9):2013-2024. doi: 10.1681/ASN.2019100987. Epub 2020 Jul 1.
6
Secondary IgA Nephropathy Shares the Same Immune Features With Primary IgA Nephropathy.继发性IgA肾病与原发性IgA肾病具有相同的免疫特征。
Kidney Int Rep. 2019 Nov 6;5(2):165-172. doi: 10.1016/j.ekir.2019.10.012. eCollection 2020 Feb.
7
Immunostaining for galactose-deficient immunoglobulin A is not specific for primary immunoglobulin A nephropathy.免疫染色法检测半乳糖缺乏免疫球蛋白 A 对于原发性免疫球蛋白 A 肾病不具有特异性。
Nephrol Dial Transplant. 2020 Dec 4;35(12):2123-2129. doi: 10.1093/ndt/gfz152.
8
IgA nephropathy and IgA vasculitis with nephritis have a shared feature involving galactose-deficient IgA1-oriented pathogenesis.IgA 肾病和伴有肾炎的 IgA 血管炎具有涉及半乳糖缺乏 IgA1 定向发病机制的共同特征。
Kidney Int. 2018 Mar;93(3):700-705. doi: 10.1016/j.kint.2017.10.019. Epub 2018 Jan 10.
9
IgA nephropathy featuring massive wire loop-like deposits in two patients with alcoholic cirrhosis.两名酒精性肝硬化患者出现以大量线圈样沉积物为特征的IgA肾病。
BMC Nephrol. 2017 Dec 13;18(1):362. doi: 10.1186/s12882-017-0769-1.
10
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Transplant Direct. 2017 Jul 11;3(8):e193. doi: 10.1097/TXD.0000000000000708. eCollection 2017 Aug.