Recurrence of anti-glomerular basement membrane antibody mediated glomerulonephritis in an isograft

Almkuist, R.D.; Buckalew, Vardaman M.; Hirszel, Przemyslaw; Maher, John F.; James, Paul M.; Wilson, Curtis B.

doi:10.1016/0090-1229(81)90007-6

Cited by 58 publications

(15 citation statements)

References 11 publications

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“…10 Consistent with this, the vast majority of reported cases of recurrent disease had recrudescence of detectable anti-GBM antibodies at clinical recurrence, despite prior immunosuppressive therapy. [10][11][12][13][14][15] Furthermore, there is no evidence that prior immunosuppressive therapy alters the ability to detect anti-GBM antibodies by changing the epitopes recognised by the antibodies or otherwise interfering with the assays used.…”

Section: Discussionmentioning

confidence: 99%

“…Others have reported similar patients with isolated pulmonary haemorrhage and no evidence of anti-GBM disease diagnosed initially as idiopathic pulmonary haemosiderosis who subsequently developed renal involvement with positive anti-GBM antibodies. 4 15 Donald et al 23 actually described ''idiopathic pulmonary haemosiderosis'' in a small series of subjects with isolated pulmonary haemorrhage and negative antibodies, despite one subject having linear IgG staining of glomerular capillary loops on renal biopsy.…”

Section: Discussionmentioning

confidence: 99%

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Alveolar haemorrhage in anti-glomerular basement membrane disease without detectable antibodies by conventional assays

Serisier

Wong²,

Armstrong³

2006

Thorax

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Alveolar haemorrhage in anti-glomerular basement membrane disease without detectable antibodies by conventional assays

Serisier

Wong²,

Armstrong³

2006

Thorax

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“…The central role of anti-GBM antibodies in the pathogenesis of GP has been demonstrated by their ability to transfer the disease to monkeys and by the recurrence of disease in human kidney allografts (1,2). The target autoantigen has been identified as the noncollagen domain 1 of the ␣3 chain of type IV collagen [␣3(IV)NC1] (3).…”

mentioning

confidence: 99%

Antigen and Epitope Specificity of Anti–Glomerular Basement Membrane Antibodies in Patients with Goodpasture Disease with or without Anti-Neutrophil Cytoplasmic Antibodies

Yang¹,

Hellmark²,

Zhao³

et al. 2007

Journal of the American Society of Nephrology

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Goodpasture disease (GP) is defined by the presence of anti-glomerular basement membrane (anti-GBM) antibodies and rapidly progressive glomerulonephritis. Besides anti-GBM, many patients with GP produce anti-neutrophil cytoplasmic antibodies (ANCA). For elucidation of the pathophysiologic significance of ANCA in this setting, epitope and antigen specificity of the anti-GBM antibodies and antigen specificity of ANCA were studied. Bovine testis ␣(IV)NC1 (tNC1); recombinant human ␣1, ␣3, ␣4, and ␣5(IV)NC1 (r␣1 through r␣5); and three chimeric proteins that contain previously defined epitope regions designated E A , E B , and S2 were used to examine the anti-GBM antibodies by ELISA in 205 Chinese patients with GP with or without ANCA. In the 205 anti-GBM antibody-positive sera, 63 (30.7%) were also ANCA positive (61 myeloperoxidase-ANCA and six proteinase 3-ANCA, four being triple positive). All 205 sera recognized tNC1 and r␣3(IV)NC1. In the double-positive group, 54.0, 66.7, 71.4% of the sera could recognize r␣1, r␣4, and r␣5, respectively, compared with 49.3, 60.6, and 55.6% for patients with anti-GBM antibodies alone. The levels of the antibodies to r␣3, tNC1, and the ␣3/␣1 ratio were lower in the double-positive group than that in patients with anti-GBM antibody alone (P < 0.05). Most of the sera could recognize the epitope regions E A , E B , and S2, but the absorbance values to E A , E B , and S2 were lower in double-positive group (P < 0.05). Double-positive patients had a broader spectrum of anti-GBM antibodies and lower levels of antibodies against ␣3(IV)NC1 compared with that of patients with anti-GBM antibodies alone.

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“…Human anti-glomerular basement membrane antibodies can initiate glomerulonephritis when infused into primates (Lerner et al 1976) or when human allografts are transplanted into patients with active GPS (Almkuist 1981).…”

Section: Pathogenesismentioning

confidence: 99%

Goodpasture’s Disease

El-Diasty

El-Ghar

2011

Systemic Vasculitis

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Recurrence of anti-glomerular basement membrane antibody mediated glomerulonephritis in an isograft

Cited by 58 publications

References 11 publications

Alveolar haemorrhage in anti-glomerular basement membrane disease without detectable antibodies by conventional assays

Alveolar haemorrhage in anti-glomerular basement membrane disease without detectable antibodies by conventional assays

Antigen and Epitope Specificity of Anti–Glomerular Basement Membrane Antibodies in Patients with Goodpasture Disease with or without Anti-Neutrophil Cytoplasmic Antibodies

Goodpasture’s Disease

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