Anti-MPO-ANCA-Positive Microscopic Polyangiitis following Subacute Bacterial Endocarditis

Hellmich, Bernhard; Ehren, Marianne; Lindstaedt, Michael; Meyer, Martin; Pfohl, Martin; Schatz, H.

doi:10.1007/pl00011214

Cited by 42 publications

(37 citation statements)

References 12 publications

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“…[53][54][55][56] It is known that PR3-ANCApositive patients who carry nasal Staphylococcus aureus chronically are at higher risk for disease relapse. 54 While MPO-AAV in association with S. aureus infection has been mentioned, 57,58 so far no studies on the role of nasal S. aureus carriage in MPO-AAV have been performed. A sequence homology between PR3 and parts of the S. aureus genome has been suggested, but evidence that such interaction is operative in vivo is lacking.…”

Section: Etiologymentioning

confidence: 99%

Proteinase 3-ANCA Vasculitis versus Myeloperoxidase-ANCA Vasculitis

Hilhorst

Paassen

Tervaert

2015

Journal of the American Society of Nephrology

177

137

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In patients with GN or vasculitis, ANCAs are directed against proteinase 3 (PR3) or myeloperoxidase (MPO). The differences between PR3-ANCA-associated vasculitis (AAV) and MPO-AAV described in the past have been supplemented during the last decade. In this review, we discuss the differences between these two small-vessel vasculitides, focusing especially on possible etiologic and pathophysiologic differences. PR3-AAV is more common in northern parts of the world, whereas MPO-AAV is more common in southern regions of Europe, Asia, and the Pacific, with the exception of New Zealand and Australia. A genetic contribution has been extensively studied, and there is a high prevalence of the HLA-DPB1*04:01 allele in patients with PR3-AAV as opposed to patients with MPO-AAV and/or healthy controls. Histologically, MPO-AAV and PR3-AAV are similar but show qualitative differences when analyzed carefully. Clinically, both serotypes are difficult to distinguish, but quantitative differences are present. More organs are affected in PR3-AAV, whereas renal limited vasculitis occurs more often in patients with MPO-AAV. For future clinical trials, we advocate classifying patients by ANCA serotype as opposed to the traditional disease type classification.

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Section: Etiologymentioning

confidence: 99%

Proteinase 3-ANCA Vasculitis versus Myeloperoxidase-ANCA Vasculitis

Hilhorst

Paassen

Tervaert

2015

Journal of the American Society of Nephrology

177

137

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“…In particular, S. aureus is often cultured in these cases (103,104). Furthermore, several patients developed ANCA-associated systemic vasculitis during subacute bacterial endocarditis (105,106). Of note, in all cocaine users with cocaine-induced midline destructive lesions, S. aureus nasal colonization was present, and some of these patients were ANCA positive (107).…”

Section: Introductionmentioning

confidence: 99%

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Wijngaarden¹,

Rijn²,

Hagen³

et al. 2008

Clinical Journal of the American Society of Nephrology

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The first description of what is now known as antineutrophil cytoplasmic autoantibody-associated necrotizing vasculitis appeared more than 140 yr ago. Since then, many aspects of the pathogenic pathway have been elucidated, indicating the involvement of antineutrophil cytoplasmic autoantibodies, but why antineutrophil cytoplasmic autoantibodies are produced in the first place remains unknown. Over the years, many hypotheses have emerged addressing the etiology of antineutrophil cytoplasmic antibody production, but no exclusive factor or set of factors can so far be held responsible. Herein is reviewed the most influential hypotheses regarding the causes of antineutrophil cytoplasmic antibody-associated vasculitis with the aim of placing in an epidemiologic background the different hypotheses that are centered on environmental and genetic influences.Clin J Am Soc Nephrol 3: 237-252, 2008237-252, . doi: 10.2215 A ntineutrophil cytoplasmic autoantibody (ANCA)-associated necrotizing vasculitis was probably first described in 1866 by Kussmaul and Maier (1) as "polyarteritis nodosa." It was not until the early 1930s when the first case of what was later named Wegener's granulomatosis (WG) was described (2). The disease was named after Friedrich Wegener, who described it as an entity in 1939 (3). In 1985, antibodies associated with the disease were detected and later became known as ANCA (4). WG is a systemic autoimmune disease that can cause damage in various organs. Later, microscopic polyangiitis (MPA) was distinguished as a separate ANCA-associated vasculitis. The disease-or its immunosuppressive treatment-can cause high levels of morbidity and death, especially in patients with renal involvement. Animal experiments have shown that ANCA directed against myeloperoxidase (MPO) can cause vasculitis that resembles human vasculitic disease (5,6); however, the cause of ANCA production remains unresolved.Theories have been developed to explain how ANCA could interact with neutrophils, along with monocytes and most probably T lymphocytes, to form the lesions that are characteristic of ANCA-associated vasculitis, such as fibrinoid necrosis and granulomas (7). A recent theory of interest has been postulated by Pendergraft et al. (8), stating that an antibody against the complementary peptide of proteinase-3 (PR3) in an idiotypic/anti-idiotypic network is essential to the development of ANCA and to the development of clinical vasculitis, but why and how these ANCA are produced in the first place remains unanswered. Nonetheless, many hypotheses have been developed about the initiating factor for ANCA production. Many factors, either directly or indirectly, have been considered important in the development of ANCA: Silica exposure (9); genetic predisposition (10); bacterial infection by Staphylococcus aureus (11); viral infection by, for instance, parvovirus B19 (12); and thyroid drugs (13) all have been correlated with and held to contribute to the incidence of ANCA-associated vasculitis. Some of these hypotheses are still th...

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“…Hierdurch lässt sich bei einer Sensitivität von 67-96% (in Abhän-gigkeit des verwendeten ELISAs) die Spezifität auf 99% erhöhen [7,10]. Sowohl cANCA als auch pANCA kann bei infektiösen Endokarditiden auftreten [11], sodass stets eine Diagnosesicherung mittels Histologie angestrebt werden sollte. ANCA sind nicht nur als Krankheitsmarker, sondern auch als pathogen anzusehen, da beobachtet wurde, dass durch passiven Transfer von ANCA von der Mutter auf den Fetus eine generalisierte Vaskulitis ausgelöst werden kann [25].…”

Section: Autoantikörperunclassified

Diagnostik der Glomerulonephritiden

2009

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Glomerulonephritis occurs frequently in patients with multisystemic rheumatic disease, especially in collagen vascular disorders and vasculitides. From a clinical point of view nephrotic syndrome has to be distinguished from nephritic syndrome. Rapid deterioration of renal function is referred to as rapid progressive glomerulonephritis. The differential diagnosis of glomerulonephritis can be narrowed by the findings on urine sediment, amount of proteinuria, degree of renal insufficiency and serological findings. In particular, the presence of urine acanthocytes and cellular casts are diagnostic for glomerulonephritis or vasculitis. Renal biopsy is necessary to establish the final diagnosis in most cases; however, some histological pattern such as membranous glomerulonephritis may occur in several different etiopathogenetic diseases and one disease process may lead to different histomorphologic pictures. Rapid progressive glomerulonephritis is a nephrological emergency and should be diagnosed and treated early to prevent dialysis-dependent renal insufficiency.

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Anti-MPO-ANCA-Positive Microscopic Polyangiitis following Subacute Bacterial Endocarditis

Cited by 42 publications

References 12 publications

Proteinase 3-ANCA Vasculitis versus Myeloperoxidase-ANCA Vasculitis

Proteinase 3-ANCA Vasculitis versus Myeloperoxidase-ANCA Vasculitis

Hypotheses on the Etiology of Antineutrophil Cytoplasmic Autoantibody–Associated Vasculitis

Diagnostik der Glomerulonephritiden

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