Evolution of antiglomerular basement membrane glomerulonephritis into membranous glomerulonephritis

Hecht, Natalie; Omoloja, Abiodun Aderogba; Witte, DP; Canessa, Leonardo

doi:10.1007/s00467-007-0639-3

Cited by 6 publications

(2 citation statements)

References 17 publications

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“…[113][114][115][116] The occurrence of ANCA antibodies and signs of vasculitis in up to 20% of anti-GBM patients, and examples of anti-GBM disease occurring with membranous nephropathy, suggest that some of the proposed etiologic factors in these diseases are operative in anti-GBM disease as well (Table 1). 111,117,118 ANCA-Associated GN Necrotizing crescentic GN without immune deposits, later called pauci-immune GN, was described in 1979, 119 and a decade later linked to ANCA directed against myeloperoxidase (MPO) and proteinase 3 (PR3). 120 It is characterized by a focal necrotizing and crescentic GN with large gaps in the capillary wall associated with a smoldering, nephritic clinical course, usually in older individuals who may also exhibit extrarenal vasculitic disease.…”

Section: T Cellsmentioning

confidence: 99%

Basic and Translational Concepts of Immune-Mediated Glomerular Diseases

Couser

2012

Journal of the American Society of Nephrology

172

155

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Genetically modified immune responses to infections and self-antigens initiate most forms of GN by generating pathogen-and danger-associated molecular patterns that stimulate Toll-like receptors and complement. These innate immune responses activate circulating monocytes and resident glomerular cells to release inflammatory mediators and initiate adaptive, antigen-specific immune responses that collectively damage glomerular structures. CD4 T cells are needed for B cell-driven antibody production that leads to immune complex formation in glomeruli, complement activation, and injury induced by both circulating inflammatory and resident glomerular effector cells. Th17 cells can also induce glomerular injury directly. In this review, information derived from studies in vitro, well characterized experimental models, and humans summarize and update likely pathogenic mechanisms involved in human diseases presenting as nephritis (postinfectious GN, IgA nephropathy, antiglomerular basement membrane and antineutrophil cytoplasmic antibodymediated crescentic GN, lupus nephritis, type I membranoproliferative GN), and nephrotic syndrome (minimal change/FSGS, membranous nephropathy, and C3 glomerulopathies). Advances in understanding the immunopathogenesis of each of these entities offer many opportunities for future therapeutic interventions.

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Section: T Cellsmentioning

confidence: 99%

Basic and Translational Concepts of Immune-Mediated Glomerular Diseases

Couser

2012

Journal of the American Society of Nephrology

172

155

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“…It has been proposed in analogy to the model of Heymann nephritis that membranoustype deposits may subsequently arise from in situ immune complex formation in the setting of anti-GBM disease in association with increased antigen synthesis by injured podocytes, facilitated by the capping and shedding of antigen-antibody complexes into the subepithelial space [24,27,29,30,49]. Also, anti-GBM antibodies might alter the permeability of GBM, allowing circulating immune complexes to access otherwise inaccessible parts of the GBM [12][13][14]28].…”

Section: Discussionmentioning

confidence: 99%

A case of anti-GBM glomerulonephritis superimposed on HBV-associated membranous nephropathy

et al. 2013

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In September 2010, a 75-year-old hepatitis B virus (HBV)-positive man was admitted to our hospital because of fever, persistent cough, general fatigue, and leg edema. The patient was a hepatitis B surface antigen carrier with detectable HBV DNA level. On admission, laboratory examination revealed severe inflammatory signs, decreased serum albumin, and renal insufficiency with proteinuria. The patient had rapidly progressive renal insufficiency without pulmonary involvement over the few days after admission. Renal biopsy showed membranous nephropathy (MN) with crescent formation. Further serological study revealed a high titer of anti-glomerular basement membrane (GBM) antibody, suggestive of anti-GBM glomerulonephritis superimposed on HBV-associated MN. For both preventing HBV reactivation during immunosuppressive therapy and treating HBV-associated MN, the administration of entecavir was immediately initiated, and then treatment with plasma exchange (PE) and intravenous methylprednisolone administration was performed. Both HBV DNA level and an anti-GBM titer became undetectable, and clinical remission of MN was subsequently achieved. This was a rare case of an elderly patient with anti-GBM glomerulonephritis superimposed on HBVassociated MN, who was successfully treated with PE, corticosteroid, and entecavir combination therapy.

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Urinary tract

Rosaí¹

2011

Rosai and Ackerman's Surgical Pathology

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Evolution of antiglomerular basement membrane glomerulonephritis into membranous glomerulonephritis

Cited by 6 publications

References 17 publications

Basic and Translational Concepts of Immune-Mediated Glomerular Diseases

Basic and Translational Concepts of Immune-Mediated Glomerular Diseases

A case of anti-GBM glomerulonephritis superimposed on HBV-associated membranous nephropathy

Urinary tract

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