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Case Study
- Concurrent Anti-glomerular Basement Membrane Nephritis and IgA Nephropathy
- Kwang-Sun Suh, Song-Yi Choi, Go Eun Bae, Dae Eun Choi, Min-kyung Yeo
- J Pathol Transl Med. 2019;53(6):399-402. Published online September 16, 2019
- DOI: https://doi.org/10.4132/jptm.2019.08.05
- 5,476 View
- 178 Download
- 10 Web of Science
- 11 Crossref
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Abstract
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Supplementary Material - Anti–glomerular basement membrane (GBM) nephritis is characterized by circulating anti-GBM antibodies and crescentic glomerulonephritis (GN) with deposition of IgG along the GBM. In a limited number of cases, glomerular immune complexes have been identified in anti-GBM nephritis. A 38-year-old female presented azotemia, hematuria, and proteinuria without any pulmonary symptoms. A renal biopsy showed crescentic GN with linear IgG deposition along the GBM and mesangial IgA deposition. The patient was diagnosed as concurrent anti-GBM nephritis and IgA nephropathy. Therapies with pulse methylprednisolone and cyclophosphamide administration were effective. Concurrent cases of both anti-GBM nephritis and IgA nephropathy are rare among cases of anti-GBM diseases with deposition of immune complexes. This rare case of concurrent anti-GBM nephritis and IgA nephropathy with literature review is noteworthy.
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Citations
Citations to this article as recorded by
- Coexistence of anti-glomerular basement membrane disease and IgA nephropathy: an illustrative case and comprehensive literature review
Zewei Chen, Dechao Xu, Fangzheng Cui, Huihui Hou, Zhiguo Mao, Xiang Gao
Renal Failure.2024;[Epub] CrossRef - Clinical features and prognosis of patients with anti-GBM disease combined with mesangial IgA deposition
Wei Ning, Ya-fei Zhao, Ya-ru Liu, Yuan-yuan Qi, Zhan-zheng Zhao
Frontiers in Immunology.2024;[Epub] CrossRef - Anti-glomerular basement membrane vasculitis
Claudio Ponticelli, Marta Calatroni, Gabriella Moroni
Autoimmunity Reviews.2023; 22(1): 103212. CrossRef - High-frequency plasma exchange therapy for immunocompromised, type I crescentic glomerulonephritis complicated with IgA nephropathy: A case report and literature review
Huihui Chen, Jingjing Jin, Mei Juan Cheng, Lei He, Wei Zhou, Liping Guo, Zhe Zhe Niu, Xiang Nan Liang, Rong Fang Zhu, Yaling Bai, Jin Sheng Xu
Medicine.2023; 102(3): e32698. CrossRef - Clinical and immunological characteristics of patients with combined anti-glomerular basement membrane disease and IgA nephropathy
Cong-rong Shen, Xiao-yu Jia, Zhao Cui, Xiao-juan Yu, Ming-hui Zhao
Clinical Kidney Journal.2023; 16(9): 1480. CrossRef - Anti-glomerular basement membrane disease with IgA nephropathy: A case report
Chuan Guo, Ming Ye, Shen Li, Ting-Ting Zhu, Xiang-Rong Rao
World Journal of Clinical Cases.2022; 10(12): 3916. CrossRef - Case Report: Coexistence of Anti-Glomerular Basement Membrane Disease, Membranous Nephropathy, and IgA Nephropathy in a Female PatientWith Preserved Renal Function
Wei Qu, Nan Liu, Tianhua Xu, Binyao Tian, Meng Wang, Yanqiu Li, Jianfei Ma, Li Yao
Frontiers in Pharmacology.2022;[Epub] CrossRef - Great prognosis of concurrent anti-GBM disease and IgA nephropathy in a young woman: A case report
Fu Shaojie, Su Sensen, Huang Jingda, Wang Luyu, Zhang Fei, Yu Jinyu, Xu Zhonggao, Wu Hao
Medicine.2022; 101(37): e30686. CrossRef - Serodiagnosis of Anti-glomerular Basement Membrane Disease Using a Newly Developed Chemiluminescence Immunoassay
Alexander Kühnl, Lea Hartwig, Cornelia Dähnrich, Wolfgang Schlumberger
Frontiers in Medicine.2022;[Epub] CrossRef - PATHOLOGY AND RENAL OUTCOME OF THREE UNCOMMON FACES OF CRESCENTRIC GLOMERULONEPHRITIS
Keya Basu, Dipankar Sircar, Manimoy Bandopadhyay
INDIAN JOURNAL OF APPLIED RESEARCH.2021; : 7. CrossRef - Pneumocystis pneumonia secondary to intensive immunosuppression treatment for anti-GBM disease complicated with IgA nephropathy
Manyu Zhang, Dingwei Yang, Weixiu Wang, Fuhao Zhao, Xiaoxiao Zhang, Xue Li
Medicine.2021; 100(45): e27728. CrossRef
- Coexistence of anti-glomerular basement membrane disease and IgA nephropathy: an illustrative case and comprehensive literature review
Original Article
- The Role of MIB-1 Expression and Apoptosis in Experimental Crescentic Glomerulonephritis.
- Nam Hoon Kim, Wan Seop Kim, Jung Woo Noh, Moon Hyang Park
- Korean J Pathol. 1999;33(4):231-242.
- 1,660 View
- 14 Download
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Abstract
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- It has been postulated that programmed cell death via apoptosis may be critical for remodelling of glomeruli after inflammatory injury. To understand the regulatory mechanism of apoptosis in experimental crescentic glomerulonephritis (CGN), we examined the MIB-1 score (proliferation index, PI) and apoptotic index during the progression of experimental CGN to end-stage renal failure. CGN was induced in New Zealand White rabbits by administration of guinea pig anti-GBM IgG after sensitization with guinea pig IgG and their kidneys were analyzed for the development of crescents through sequential renal biopsies. Serum creatinine levels progressively increased in a time course until day 45. The PI in glomeruli, tubular epithelial cells, and interstitium progressively increased during the progression of experimental CGN. The mean numbers of MIB-1 positive intraglomerular nuclei (PI) were significantly correlated with degrees of crescent formation and the numbers of apoptotic cells in the glomeruli, tubules, and interstitium. Significant apoptosis was present from day 1 (15.8 10.16 cells/glomerular cross section) and increased in number with the proliferative lesions as glomerular inflammation continued. Moreover, apoptosis increased during the resolution of the glomerular inflammation, and many apoptotic cells were present in the sclerotic lesions in day 17 (18.6 12.99 cells/glomerular cross section). As glomerular inflammation subsided, cellular crescents progressed to fibrous crescents with a reduction of cellularity by day 45. On day 45, the glomerular PI and the numbers of apoptotic cells were markedly decreased. The correlations found in CGN between the creatinine level and the percentage of crescents, between the percentage of crescent and PI, and between the PI and number of apoptotic cells support the hypothesis that there is a change in the glomerular and tubulo-interstitial apoptosis under pathologic conditions. These findings indicate that apoptosis plays an essential role in the resolution of intra- and extraglomerular inflammation and in the elimination of glomerular cells within the sclerotic regions for progressive CGN. The regulation of the apoptotic phenomenon and increased PI during CGN may be important in the progression of glomerular inflammation and the development of pathologic glomerular sclerosis.
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