Report of a patient with rheumatoid arthritis developing rapidly progressive glomerulonephritis associated with anti-glomerular basement membrane antibody and antineutrophil cytoplasmic antibody

1997 ◽  
Vol 1 (1) ◽  
pp. 62-66 ◽  
Author(s):  
Kinya Hiroshige ◽  
Masasuke Soejima ◽  
Kougi Yuu ◽  
Toshiyuki Muta ◽  
Masayuki Takasugi ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Rapidly Progressive Glomerulonephritis ◽  
Antineutrophil Cytoplasmic Antibody

Acute renal failure in systemic sclerosis revealing Goodpasture syndrome: “All that glitters is not scleroderma renal crisis”

2019 ◽  
Vol 5 (1) ◽  
pp. NP1-NP5 ◽  
Author(s):  
Renaud Felten ◽  
Benoît Nespola ◽  
Emmanuel Chatelus ◽  
Laurent Arnaud ◽  
Jacques-Eric Gottenberg ◽  
...  
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Systemic Sclerosis ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Rapidly Progressive Glomerulonephritis ◽  
Antineutrophil Cytoplasmic Antibody ◽  
Scleroderma Renal Crisis ◽  
Goodpasture Syndrome ◽  
Renal Crisis

The most common cause of acute renal failure in systemic sclerosis patients is scleroderma renal crisis but other etiologies have to be considered such as another autoimmune disease. We report the case of a 60-year-old male admitted to our hospital with a renal failure. His medical history included a diagnosis of systemic sclerosis 6 months ago. Antinuclear antibodies were positive at a titer of 1:1280 with positive anti-Scl-70 and anti-myeloperoxidase (34 U/mL) antibodies. Scleroderma renal crisis was suspected. However, antineutrophil cytoplasmic antibody–associated vasculitis could not be excluded and a renal biopsy was performed. Histopathology revealed crescentic glomerulonephritis and rupture of Bowman’s capsule. Anti-glomerular basement membrane antibodies were detected in serum and the diagnosis of Goodpasture syndrome was confirmed by kidney’s immunofluorescence analysis showing typical deposits. Only three other cases of systemic sclerosis associated with Goodpasture syndrome have been reported in the literature. Also, rapidly progressive glomerulonephritis with positivity of both antineutrophil cytoplasmic antibody and anti-glomerular basement membrane antibodies has been described. Several studies have suggested that antineutrophil cytoplasmic antibody positivity occurs first leading to damages of the glomerular basement membrane, to the release of alpha-3 NC1 antigen, and ultimately to anti-glomerular basement membrane antibody production. Although rare, antineutrophil cytoplasmic antibody–associated vasculitis and Goodpasture syndrome should be searched for in systemic sclerosis patients with acute renal failure.

scholarly journals The development of rapidly progressive glomerulonephritis associated with both antineutrophil cytoplasmic antibody-associated vasculitis and anti-glomerular basement membrane nephritis in the course of nontuberculous mycobacterium infection: a case report

2020 ◽  
Vol 4 (1) ◽  
Author(s):  
Mikiya Kato ◽  
Risa Wakiya ◽  
Tomohiro Kameda ◽  
Kousuke Inoue ◽  
Tadashi Sofue ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Rapidly Progressive Glomerulonephritis ◽  
Mycobacterial Infection ◽  
Antineutrophil Cytoplasmic Antibody ◽  
Antineutrophil Cytoplasmic Antibodies ◽  
Nontuberculous Mycobacterium ◽  
Case Presentation ◽  
One Year ◽  
Sequential Appearance

Abstract Background Antineutrophil cytoplasmic antibodies (ANCA) and Anti-glomerular basement membrane (GBM) antibodies often induce rapidly progressive glomerulonephritis (RPGN). Some reports have demonstrated RPGN with the sequential appearance of ANCA then anti-GBM antibodies, suggesting that ANCA may induce the development of anti-GBM antibodies. Whereas, many reports have shown that the development of ANCA is associated with various infectious diseases, such as non-tuberculous mycobacterial infection. Case presentation A 65-year-old woman with pulmonary non-tuberculous mycobacterial (NTM) infection was monitored without treatment. One year later, serum myeloperoxidase (MPO)- ANCA were elevated (14.1 U/mL (normal value < 3.0 U/ml)). A high fever and RPGN appeared 1 year later, and serum MPO-ANCAs were 94.1 U/mL. Anti-GBM antibodies were also detected. A renal biopsy revealed crescentic glomerulonephritis with linear deposits of IgG and C3c along the GBM and interstitial inflammation with endarteritis of arterioles. The diagnosis was RPGN associated with anti-GBM nephritis and ANCA-associated vasculitis. Conclusion This report shows that preceding NTM infection may have induced ANCA and anti-GBM antibodies and caused the development of RPGN.

scholarly journals SARS-CoV-2 infection and recurrence of anti-glomerular basement disease: a case report

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Alexander Winkler ◽  
Emanuel Zitt ◽  
Hannelore Sprenger-Mähr ◽  
Afschin Soleiman ◽  
Manfred Cejna ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Plasma Cells ◽  
Rapidly Progressive Glomerulonephritis ◽  
Kidney Injury ◽  
Pulmonary Involvement ◽  
Pulmonary Haemorrhage ◽  
Basement Membranes ◽  
High Avidity ◽  
History Of

Abstract Background Anti-glomerular basement membrane disease (GBM) disease is a rare autoimmune disease causing rapidly progressive glomerulonephritis and pulmonary haemorrhage. Recently, an association between COVID-19 and anti-glomerular basement membrane (anti-GBM) disease has been proposed. We report on a patient with recurrence of anti-GBM disease after SARS-CoV-2 infection. Case presentation The 31-year-old woman had a past medical history of anti-GBM disease, first diagnosed 11 years ago, and a first relapse 5 years ago. She was admitted with severe dyspnoea, haemoptysis, pulmonary infiltrates and acute on chronic kidney injury. A SARS-CoV-2 PCR was positive with a high cycle threshold. Anti-GBM autoantibodies were undetectable. A kidney biopsy revealed necrotising crescentic glomerulonephritis with linear deposits of IgG, IgM and C3 along the glomerular basement membrane, confirming a recurrence of anti-GBM disease. She was treated with steroids, plasma exchange and two doses of rituximab. Pulmonary disease resolved, but the patient remained dialysis-dependent. We propose that pulmonary involvement of COVID-19 caused exposure of alveolar basement membranes leading to the production of high avidity autoantibodies by long-lived plasma cells, resulting in severe pulmonary renal syndrome. Conclusion Our case supports the assumption of a possible association between COVID-19 and anti-GBM disease.

scholarly journals Etanercept-Induced Anti-Glomerular Basement Membrane Disease

2021 ◽  
pp. 292-300
Author(s):  
Saif Al-Chalabi ◽  
Henry H.L. Wu ◽  
Rajkumar Chinnadurai ◽  
Arvind Ponnusamy
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Rapidly Progressive Glomerulonephritis ◽  
Alveolar Haemorrhage ◽  
Small Vessel Vasculitis ◽  
Drug Induced ◽  
Psoriatic Arthropathy ◽  
Tnf Α ◽  
Life Threatening ◽  
Factor Α

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.

scholarly journals Anti-glomerular basement membrane disease: an update on subgroups, pathogenesis and therapies

2018 ◽  
Vol 34 (11) ◽  
pp. 1826-1832 ◽  
Author(s):  
Mårten Segelmark ◽  
Thomas Hellmark
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
De Novo ◽  
Correct Diagnosis ◽  
Rapidly Progressive Glomerulonephritis ◽  
Human Leukocyte ◽  
Pulmonary Haemorrhage ◽  
Leukocyte Antigen ◽  
Type Iv

Abstract Most patients with anti-glomerular basement membrane (anti-GBM) disease present with rapidly progressive glomerulonephritis with or without pulmonary haemorrhage; however, there are several variants and vigilance is necessary to make a correct diagnosis. Such variants include overlap with anti-neutrophil cytoplasm antibodies-associated vasculitis and membranous nephropathy as well as anti-GBM occurring de novo after renal transplantation. Moreover, patients can present with isolated pulmonary haemorrhage as well as with negative tests for circulating anti-GBM. Virtually all patients with anti-GBM disease have autoantibodies that react with two discrete epitopes on the α3 chain of type IV collagen. Recent evidence suggests that healthy persons have low-affinity natural antibodies reacting with the same epitopes, but most people are protected from developing disease-causing high-affinity autoantibodies by human leukocyte antigen-dependent regulatory T-cells (Tregs). The α3 chain-derived peptides presented by the HLA-DR15 antigen lack the ability to promote the development of such Tregs. The detection of anti-GBM in circulation using the rapid assay test has led to early diagnosis and improved prognosis. However, our present tools to curb the inflammation and to eliminate the assaulting antibodies are insufficient. Only about one-third of all patients survive with functioning native kidneys. More effective therapies need to be developed; agents that inhibit neutrophil recruitment, deplete B cells and cleave immunoglobulin G (IgG) in vivo may become new weapons in the arsenal to combat anti-GBM disease.

scholarly journals Voltage-gated potassium channel Kv1.3 blocker as a potential treatment for rat anti-glomerular basement membrane glomerulonephritis

2010 ◽  
Vol 299 (6) ◽  
pp. F1258-F1269 ◽  
Author(s):  
Toshitake Hyodo ◽  
Takashi Oda ◽  
Yuichi Kikuchi ◽  
Keishi Higashi ◽  
Taketoshi Kushiyama ◽  
...  
Keyword(s):  
T Cells ◽  
Basement Membrane ◽  
Potassium Channel ◽  
Glomerular Basement Membrane ◽  
Memory T Cells ◽  
Critical Role ◽  
Rapidly Progressive Glomerulonephritis ◽  
Effector Memory ◽  
Voltage Gated ◽  
Effector Memory T Cells

The voltage-gated potassium channel Kv1.3 has been recently identified as a molecular target that allows the selective pharmacological suppression of effector memory T cells (TEM) without affecting the function of naïve T cells (TN) and central memory T cells (TCM). We found that Kv1.3 was expressed on glomeruli and some tubules in rats with anti-glomerular basement membrane glomerulonephritis (anti-GBM GN). A flow cytometry analysis using kidney cells revealed that most of the CD4+ T cells and some of the CD8+ T cells had the TEM phenotype (CD45RC−CD62L−). Double immunofluorescence staining using mononuclear cell suspensions isolated from anti-GBM GN kidney showed that Kv1.3 was expressed on T cells and some macrophages. We therefore investigated whether the Kv1.3 blocker Psora-4 can be used to treat anti-GBM GN. Rats that had been given an injection of rabbit anti-rat GBM antibody were also injected with Psora-4 or the vehicle intraperitoneally. Rats given Psora-4 showed less proteinuria and fewer crescentic glomeruli than rats given the vehicle. These results suggest that TEM and some macrophages expressing Kv1.3 channels play a critical role in the pathogenesis of crescentic GN and that Psora-4 will be useful for the treatment of rapidly progressive glomerulonephritis.

scholarly journals Membranous nephropathy followed by anti-glomerular basement disease: A case report and review of clinical presentation and treatment

2018 ◽  
Vol 6 ◽  
pp. 2050313X1880762
Author(s):  
Claudius Speer ◽  
Matthias Martin Gaida ◽  
Rüdiger Waldherr ◽  
Christian Nusshag ◽  
Florian Kälble ◽  
...  
Keyword(s):  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Membranous Nephropathy ◽  
Clinical Presentation ◽  
Rapidly Progressive Glomerulonephritis ◽  
Renal Vein Thrombosis ◽  
Simultaneous Occurrence ◽  
Rapid Decline ◽  
Crescent Formation ◽  
Vein Thrombosis

Membranous nephropathy is a common cause of nephrotic syndrome in adults and can be primary or secondary through autoimmune disease, medication, infection, or malignancy. Rapidly progressive glomerulonephritis with crescent formation is rare in patients with membranous nephropathy. Thus, in cases with rapid decline in renal function, after excluding complications such as malignant hypertension, acute hypersensitivity interstitial nephritis, and bilateral renal vein thrombosis, the simultaneous occurrence of a superimposed glomerulonephritis should be considered. We report a 55-year-old man suffering from a biopsy-confirmed primary membranous nephropathy, who developed rapidly progressive glomerulonephritis with anti-glomerular basement membrane antibodies after being affected with membranous nephropathy for 8 years. The kidney biopsy revealed a concurrence of membranous nephropathy and anti-glomerular basement membrane disease. Clinical presentation and treatment of membranous nephropathy followed by anti-glomerular basement membrane disease are discussed based on our observation with promising follow-up.

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