Immunoelectron microscopic localization of membrane attack complex and hepatitis B e antigen in membranous nephropathy

Akano, Norihisa; Yoshioka, Kazuo; Aya, Naofumi; Miyamoto, Hiroyuki; Takemura, Tamiko; Tohda, Machi; Maki, Sunao

doi:10.1007/bf00734087

Cited by 10 publications

(10 citation statements)

References 17 publications

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“…Further more, vitronectin and C5b-9 deposits were frequently ob served as ring-shaped structures. As previously reported [5,7,[27][28][29], these ring-shaped structures were apparently associated with the striated membranous structures. Stri ated membranous structures are very common in both normal and pathological human glomeruli; their origin is still obscure, but they may be a remnant produced by lysis of cellular elements [5,27].…”

Section: Discussionsupporting

confidence: 65%

Immunohistochemical Studies of Vitronectin, C5b-9, and Vitronectin Receptor in Membranous Nephropathy

Ogawa

Yorioka²,

Yamakido³

1994

Nephron

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To investigate the involvement of vitronectin, the terminal complement complex (C5b-9), and the vitronectin receptor in the pathogenesis of membranous nephropathy, the immunohistochemical localization of these antigens in the kidney was determined using the immunoperoxidase method and monoclonal antibodies: antivitronectin, anti-SC5b-9 (neoantigen), and antivitronectin receptor (specific for α_vβ₃ and α_v). The subjects were 6 patients with membranous nephropathy, and the controls were 2 patients with minimal-change nephrotic syndrome. In membranous nephropathy, vitronectin was localized in subepithelial deposits and in epithelial cell foot processes and was intensely positive in the foot processes adjacent to subepithelial deposits. C5b-9 showed a similar pattern of localization to vitronectin. Both α_vβ₃ and α_v were localized in the basal portions of the foot processes of visceral epithelial cells as well as along the borders of these cells adjacent to the urinary space. Deposition at the former site was heavier than at the latter, and localization was especially prominent adjacent to the subepithelial deposits. In addition, α_v was localized around and within some of the electron-lucent subepithelial deposits in the basement membrane. In contrast, the deposition of vitronectin, C5b-9, α_vβ₃ and α_v was always less intense in minimal-change nephrotic syndrome than in membranous nephropathy. Vitronectin and C5b-9 were localized to small parts of mesangium and glomerular basement membrane, while α_vβ₃ and α_v deposits showed no difference in intensity between the basal portions of the foot processes and the urinary border of the visceral epithelial cells. Thus, membranous nephropathy featured increased localization of vitronectin, C5b-9, and vitronectin receptors both within and around the subepithelial deposits, suggesting that the mechanism of immune complex disposal via the vitronectin receptor and the vitronectin-C5b-9 complex, associated with complement activation due to subepithelial immune complex formation, may also be active.

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Section: Discussionsupporting

confidence: 65%

Immunohistochemical Studies of Vitronectin, C5b-9, and Vitronectin Receptor in Membranous Nephropathy

Ogawa

Yorioka²,

Yamakido³

1994

Nephron

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“…C5b-9 colocalized with immune deposits containing IgG, C3, and sometimes C1q and C4 in the capillary wall in all stages of primary membranous nephropathy ( 44 , 67 , 70 , 72 , 75 , 77 , 81 , 82 , 87 , 96 , 112 , 139 , 143 , 147 – 149 , 152 , 154 – 156 ), except for stage I according to one report ( 72 ). It colocalized with causative autoantibodies in subepithelial immune deposits ( 150 , 155 , 156 ).…”

Section: Kidney Diseases Due To Immune Complex Depositionmentioning

confidence: 96%

“…In line with this, staining of C5b-9 was more intense and extensive in membranous nephropathy than in healthy kidneys ( 18 , 44 , 67 , 72 , 75 , 82 , 96 , 123 , 139 ), also when recurring in a transplant ( 147 ). It was intense in the glomerulus ( 57 , 81 , 82 , 139 , 143 , 148 – 151 ), always along the capillary wall, but not or hardly in the mesangium ( 18 , 44 , 67 , 72 , 75 , 77 , 79 , 87 , 98 , 112 , 123 , 141 , 147 , 152 – 155 ), in a granular ( 77 , 82 , 112 , 154 ), linear ( 123 ), or mixed pattern ( 79 ). It was furthermore focally found along Bowman’s capsule ( 79 , 152 ), as coarse granules along the tubular basement membrane ( 18 , 44 , 57 , 67 , 70 , 72 , 75 , 79 , 96 , 112 , 142 ), occasionally on tubular cells ( 79 , 112 ), in the vascular wall ( 18 , 57 , 67 , 72 , 96 , 112 ), in capsular adhesions, crescents, and glomerular and vascular areas of hyalinosis and sclerosis ( 44 , 57 , 67 ...…”

Section: Kidney Diseases Due To Immune Complex Depositionmentioning

confidence: 99%

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Deposition of the Membrane Attack Complex in Healthy and Diseased Human Kidneys

et al. 2021

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The membrane attack complex—also known as C5b-9—is the end-product of the classical, lectin, and alternative complement pathways. It is thought to play an important role in the pathogenesis of various kidney diseases by causing cellular injury and tissue inflammation, resulting in sclerosis and fibrosis. These deleterious effects are, consequently, targeted in the development of novel therapies that inhibit the formation of C5b-9, such as eculizumab. To clarify how C5b-9 contributes to kidney disease and to predict which patients benefit from such therapy, knowledge on deposition of C5b-9 in the kidney is essential. Because immunohistochemical staining of C5b-9 has not been routinely conducted and never been compared across studies, we provide a review of studies on deposition of C5b-9 in healthy and diseased human kidneys. We describe techniques to stain deposits and compare the occurrence of deposits in healthy kidneys and in a wide spectrum of kidney diseases, including hypertensive nephropathy, diabetic nephropathy, membranous nephropathy, IgA nephropathy, lupus nephritis, C3 glomerulopathy, and thrombotic microangiopathies such as the atypical hemolytic uremic syndrome, vasculitis, interstitial nephritis, acute tubular necrosis, kidney tumors, and rejection of kidney transplants. We summarize how these deposits are related with other histological lesions and clinical characteristics. We evaluate the prognostic relevance of these deposits in the light of possible treatment with complement inhibitors.

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“…C3 positivity of glomeruli, vessels and tubuli is frequently observed in human ne phropathies (NP). The presence of C3b/C3c indicates an ongoing complement activation, which results in the de position of membrane attack complex (MAC) capable of producing cell lysis [8], MAC is known to be an important mediator of glomerular injury in human GN as well as in experimental nephritis [9][10][11], In glomeruli, the presence of C3 and immunoglobulins is accompanied by compara ble deposits of MAC in many cases [12][13][14][15], In contrast, the tubular and vascular MAC deposits do not correlate with the presence of immunoglobulins and C3 positivity in the tubulointerstitium [16,17]. Although a systematic study has not been performed, few studies have attempted to relate the tubular MAC deposition to interstitial leuko-cyte infiltration.…”

Section: Introductionmentioning

confidence: 99%

Membrane Attack Complex and Membrane Cofactor Protein Are Related to Tubulointerstitial Inflammation in Various Human Glomerulopathies

Mosolits¹,

Magyarlaki²,

Nagy

1997

Nephron

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Immunohistochemical analysis of the membrane attack complex (MAC) and the membrane cofactor protein (MCP) was performed on the tubuli and cortical vessels of 46 kidney biopsies with various types of human glomerulopathies. Irrespective of the type of glomerulopathy, significant correlations between tubular MAC and interstitial lymphomonocyte infiltration (p < 0.001) and interstitial volume (p < 0.02) were found. Tubular MCP was significantly overexpressed at the site of MAC deposition (p < 0.002). There was no correlation between the vascular MAC and MCP and tubulointerstitial lesions. Since tubular MAC is deposited in inflamed areas of tubulointerstitium, we propose that MAC might contribute to the development of tubulointerstitial inflammatory processes in human glomerulopathies. MCP as a regulatory factor in the tubulointerstitium might abrogate further tissue damage and cell-stimulatory effects of the MAC.

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Immunoelectron microscopic localization of membrane attack complex and hepatitis B e antigen in membranous nephropathy

Cited by 10 publications

References 17 publications

Immunohistochemical Studies of Vitronectin, C5b-9, and Vitronectin Receptor in Membranous Nephropathy

Immunohistochemical Studies of Vitronectin, C5b-9, and Vitronectin Receptor in Membranous Nephropathy

Deposition of the Membrane Attack Complex in Healthy and Diseased Human Kidneys

Membrane Attack Complex and Membrane Cofactor Protein Are Related to Tubulointerstitial Inflammation in Various Human Glomerulopathies

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