The evolution of crescentic nephritis and alveolar haemorrhage following induction of autoimmunity to glomerular basement membrane in an experimental model of Goodpasture's disease

2003 ◽  
Vol 200 (1) ◽  
pp. 118-129 ◽  
Author(s):  
John Reynolds ◽  
Jill Moss ◽  
Mark A Duda ◽  
Jennifer Smith ◽  
Ayman M Karkar ◽  
...  
2002 ◽  
Vol 39 (6) ◽  
pp. 1162-1167 ◽  
Author(s):  
Alan D. Salama ◽  
Tammy Dougan ◽  
Jeremy B. Levy ◽  
H.Terry Cook ◽  
Steve H. Morgan ◽  
...  

2018 ◽  
Vol 6 (2) ◽  
Author(s):  
Elena V Zakharova ◽  
Tatyana A Makarova ◽  
Zhanna V Sheikh ◽  
Hadyja M Emirova ◽  
Ekaterina S Stolyarevich

2018 ◽  
Vol 90 (6) ◽  
pp. 130-136 ◽  
Author(s):  
M L Bulanova ◽  
D V Potapov ◽  
N M Bulanov ◽  
L V Lysenko(Kozlovskaya)

Goodpasture’s disease (anti-GBM disease) is a rare small vessels vasculitis characterized by the presence of autoantibodies directed against the glomerular basement membrane (GBM) and alveolar basement membrane. Common feature of anti-GBM disease is a combination of rapidly progressive glomerulonephritis and alveolar hemorrhage (pulmonary-renal syndrome). We present a case of atypical disease course in a young male patient who developed alveolar hemorrhage without renal failure. The only symptom of renal involvement was isolated hematuria. Plasmapheresis combined with immunosuppression (cyclophosphamide and corticosteroids) was effective. We present a review of state-of-art data on the pathogenesis and disease course of anti-GBM disease.


Author(s):  
Jeremy Levy ◽  
Charles Pusey

Antiglomerular basement membrane disease (anti-GBM disease, also known as Goodpasture’s disease) is a rare autoimmune disease caused by pathogenic autoantibodies directed against the noncollagenous, C-terminal domain of the α‎-3 chain of type IV collagen (α‎3(IV)NC1). Immunohistology is characteristic, with linear deposition of IgG (sometimes with IgA or IgM) and complement C3 along the GBMs....


2021 ◽  
pp. 292-300
Author(s):  
Saif Al-Chalabi ◽  
Henry H.L. Wu ◽  
Rajkumar Chinnadurai ◽  
Arvind Ponnusamy

Anti-glomerular basement membrane (anti-GBM) disease is a rare form of small-vessel vasculitis that typically causes rapidly progressive glomerulonephritis with or without alveolar haemorrhage. Previously, there has only been one reported case of tumour necrosis factor-α (TNF-α) antagonist-induced anti-GBM disease. Here, we describe the first reported case of etanercept-induced anti-GBM disease. A 55-year-old Caucasian man was referred to our tertiary specialist renal centre with a history of painless macroscopic haematuria. The patient has been receiving weekly etanercept injections over the past 12 months for psoriatic arthropathy. The serum immunology panel results highlighted a significantly raised anti-GBM titre (370.1 U). Etanercept was stopped, and the patient was empirically commenced on pulsed methylprednisolone, cyclophosphamide, and plasma exchange. A renal biopsy showed crescentic glomerulonephritis. Few days after admission, he tested positive for coronavirus disease 2019 (COVID-19), and a decision was made to withhold cyclophosphamide. There was further decline in renal function with hyperkalaemia for which he received 2 sessions of haemodialysis. He was restarted on cyclophosphamide upon discharge. The patient was switched to rituximab treatment afterwards as he developed leucopenia 2 weeks following the commencement of cyclophosphamide. The serum creatinine level continued to improve and remained dialysis-independent. In conclusion, with the increased use of etanercept and other TNF-α antagonists, the prescribing clinician must be aware of the rare but life-threatening drug-induced vasculitis. We recommend careful monitoring of renal indices with the use of this class of medications.


Nephrology ◽  
2004 ◽  
Vol 9 (2) ◽  
pp. 49-51 ◽  
Author(s):  
JONATHAN H ERLICH ◽  
JACOB SEVASTOS ◽  
BRUCE A PUSSELL

Sign in / Sign up

Export Citation Format

Share Document