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5 "Crescentic glomerulonephritis"
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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
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  • 163 Download
  • 9 Web of Science
  • 10 Crossref
AbstractAbstract PDFSupplementary 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.

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
  • 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
Original Articles
Podocyte Expression of Osteopontin and FSP-1/S100A4 in Human Crescentic Glomerulonephritis.
Ghil Suk Yoon, Tae Sook Kim
Korean J Pathol. 2011;45(3):237-246.
DOI: https://doi.org/10.4132/KoreanJPathol.2011.45.3.237
  • 3,030 View
  • 23 Download
AbstractAbstract PDF
BACKGROUND
Osteopontin (OPN) is a cytokine associated with a cell-matrix via integrins. Fibroblast specific protein-1 (FSP-1), known as S100A4, has been implicated in cell migration by non-muscle myosin. We investigated whether the role of OPN and FSP-1/S100A4 expression in their contribution to the podocyte phenotype change to form podocyte bridge and cellular crescent.
METHODS
Glomerular expression of OPN and FSP-1/S100A4 in renal biopsies of 16 patients with crescentic glomerulonephritis (CrGN) and 13 normal renal biopsies were studied by immunohistochemistry.
RESULTS
The expression of OPN and FSP-1/S100A4 was increased in the podocytes of glomeruli, with and without crescents, in patients with CrGN. Neither OPN nor FSP-1/S100A4 was expressed in glomeruli from the normal controls (p<0.01). A significant positive correlation was found between the expression of OPN in glomerular tufts and cellular crescents, and the expression of OPN and FSP-1/S100A4 in glomerular tufts (p<0.05).
CONCLUSIONS
The results suggest that OPN plays a role in early podocyte attachment to Bowman's capsule, and FSP-1/S100A4 potentiate podocyte contribution to cellular crescent formation by inducing cellular migration and growth.
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.
  • 1,544 View
  • 12 Download
AbstractAbstract PDF
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.
Expression of Adhesion Molecules in IgA Nephropathy, Diffuse Crescentic Glomerulonephritis, and Minimal Change Disease.
Kyoung Cheol Moon, So Yeon Park, Hwal Woong Kim, Hyun Soon Lee
Korean J Pathol. 2000;34(5):331-340.
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AbstractAbstract PDF
Accumulation of leukocytes within the glomerulus is a key event in the pathogenesis of glomerulonephritis. This process is mediated by pairs of adhesion molecules. We have examined the expression pattern of selectins (E and P), intercellular adhesion molecule-1 (ICAM-1), and vascular cell adhesion molecule-1 (VCAM-1) in 30 renal biopsies with IgA nephropathy, diffuse crescentic glomerulonephritis, and minimal change disease. Normal controls were obtained from four nephrectomy specimens with renal cell carcinoma. ICAM-1 expression was significantly increased in the glomerular endothelial and mesangial cells in cases with IgA nephropathy compared with normal controls. VCAM-1 was expressed in glomerular mesangial cells in all cases with IgA nephropathy and diffuse crescentic glomerulonephritis, but faintly expressed in 3 cases with minimal change disease and not expressed in normal controls. P-selectin was faintly expressed in the glomeruli in cases with IgA nephropathy and diffuse crescentic glomerulonephritis. E-selectin was only expressed in the vascular endothelium in one case with IgA nephropathy and in the other with diffuse crescentic glomerulonephritis. ICAM-1 and VCAM-1 were strongly expressed in the crescents. However, selectin was not expressed in the crescent. These results suggest that adhesion molecules, particularly ICAM-1 and VCAM-1, play an important role in the pathogenesis of glomerular damage and crescent formation in primary glomerular diseases.
Case Report
Crescentic Glomerulonephritis in a Patient with Rheumatoid Arthritis: A case report.
Ki Ouk Min, Yeong Jin Choi, Byoung Kee Kim, Sun Moo Kim, Sang In Shim
Korean J Pathol. 1995;29(1):116-118.
  • 1,479 View
  • 20 Download
AbstractAbstract PDF
Crescentic glomerulonephritis in rheumatoid arthritis is described recently with increasing frequency. It can occur directly as a manifestation of rheumatoid arthritis or may be a reaction to drugs such as D-penicillamine and bucillamine. We report a case of crescentic glomerulonephritis in a 46-year-old woman with rheumatoid arthritis for 20 years who had been treated intermittently with herb medicine or nonsteroidal anti-inflammatory drugs (NSAIDS). Light microscopic examination showed severe focal segmental and global necrotizing glomerulonephritis with crescent formation in 50% of the glomeruli. Immunofluorescent study revealed scanty amount of mesangial granular deposits of IgA, IgM, C3 and fibrinogen in a diffuse pattern.

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