Anti–LAMP-2 Autoantibodies in ANCA-Associated Pauci-Immune Glomerulonephritis

Flint, Shaun; Savage, Caroline O.S.

doi:10.1681/asn.2012010065

Cited by 16 publications

(11 citation statements)

References 10 publications

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“…Kain et al were able, very recently, to repeat their findings in different European patient cohorts [36]. The conflicting data have no obvious explanation, but may be related to methodological and population differences as discussed by Flint et al [37]. Major findings with respect to ANCA antigens are summarized in Fig.…”

Section: Anti-neutrophil Cytoplasmic Autoantibodies (Anca) and The Exmentioning

confidence: 94%

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How anti-neutrophil cytoplasmic autoantibodies activate neutrophils

Kettritz

2012

Clinical and Experimental Immunology

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SummaryNeutrophils are pivotal to host defence during infectious diseases. However, activated neutrophils may also cause undesired tissue damage. Ample examples include small-vessel inflammatory diseases (vasculitis) that are associated with anti-neutrophil cytoplasmic autoantibodies (ANCA) residing in the patients' plasma. In addition to being an important diagnostic tool, convincing evidence shows that ANCA are pathogenic. ANCA-neutrophil interactions induce important cellular responses that result in highly inflammatory necrotizing vascular damage. The interaction begins with ANCA binding to their target antigens on primed neutrophils, proceeds by recruiting transmembrane molecules to initiate intracellular signal transduction and culminates in activation of effector functions that ultimately mediate the tissue damage.

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Section: Anti-neutrophil Cytoplasmic Autoantibodies (Anca) and The Exmentioning

confidence: 94%

“…The conflicting data have no obvious explanation, but may be related to methodological and population differences as discussed by Flint et al . [37]. Major findings with respect to ANCA antigens are summarized in Fig.…”

Section: Anti‐neutrophil Cytoplasmic Autoantibodies (Anca) and The Exmentioning

confidence: 98%

How anti-neutrophil cytoplasmic autoantibodies activate neutrophils

Kettritz

2012

Clinical and Experimental Immunology

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“…Вместе с тем сведения о значении антител к ЛАМП2 при рauci-иммунном ГН противоречивы [63,[65][66][67], что может объясняться неоднородностью групп пациентов. Так, уже через месяц от начала терапии результаты опреде-ления антител к ЛАМП2 становились отрицательными у 36 из 37 больных АНЦА-СВ [65], а в исследовании, не вы-явившем различий с контрольной группой в частоте гипер-продукции антител к ЛАМП2, доля случаев дебюта АНЦА-ГН не превышала 15% [66].…”

Section: таблицаunclassified

Problems in the Diagnosis and Treatment of Anca-Associated Systemic Vasculitis: In the Focus of Anca-Negative Pauci-Immune Glomerulonephritis

Бекетова¹,

Frolova²,

Столяревич³

et al. 2016

rsp

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“…However, another study found the same frequency of anti-LAMP-2 ANCA in patients with pauci-immune glomerulonephritis and those with other types of glomerulonephritis and failed to show that anti-LAMP-2 ANCA causes vasculitic lesions or glomerulonephritis in experimental animals [192]. Thus, although the LAMP-2 pathway remains promising, more studies are needed to clarify its role as a mechanism in ANCA-associated disease and as a link between infection and pathogenic ANCA formation [193]. …”

Section: Role Of Infections In the Pathogenesis Of Anca-mediated Dmentioning

confidence: 99%

Glomerular Disease in Patients with Infectious Processes Developing Antineutrophil Cytoplasmic Antibodies

et al. 2013

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To identify differences in treatment and outcome of various types of glomerulonephritis developing in the course of infections triggering antineutrophil cytoplasmic antibody (ANCA) formation, we analyzed published reports of 50 patients. Immunosuppressives were added to antibiotics in 22 of 23 patients with pauci-immune glomerulonephritis. Improvement was noted in 85% of 20 patients with information on outcomes. Death rate was 13%. Corticosteroids were added to antibiotics in about 50% of 19 patients with postinfectious glomerulonephritis. Improvement rate was 74%, and death rate was 26%. Two patients with mixed histological features were analyzed under both pauci-immune and post-infectious glomerulonephritis categories. In 9 patients with other renal histology, treatment consisted of antibiotics alone (7 patients), antibiotics plus immunosuppressives (1 patient), or immunosuppressives alone (1 patient). Improvement rate was 67%, permanent renal failure rate was 22%, and death rate was 11%. One patient with antiglomerular basement disease glomerulonephritis required maintenance hemodialysis. Glomerulonephritis developing in patients who became ANCA-positive during the course of an infection is associated with significant mortality. The histological type of the glomerulonephritis guides the choice of treatment. Pauci-immune glomerulonephritis is usually treated with addition of immunosuppressives to antibiotics.

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Anti–LAMP-2 Autoantibodies in ANCA-Associated Pauci-Immune Glomerulonephritis

Cited by 16 publications

References 10 publications

How anti-neutrophil cytoplasmic autoantibodies activate neutrophils

How anti-neutrophil cytoplasmic autoantibodies activate neutrophils

Problems in the Diagnosis and Treatment of Anca-Associated Systemic Vasculitis: In the Focus of Anca-Negative Pauci-Immune Glomerulonephritis

Glomerular Disease in Patients with Infectious Processes Developing Antineutrophil Cytoplasmic Antibodies

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