What stuff is this! A historical perspective on fibrinoid necrosis

Bajema, Ingeborg M.; Bruijn, Jan A.

doi:10.1002/(sici)1096-9896(0000)9999:9999<n/a::aid-path610>3.0.co;2-i

Cited by 30 publications

(10 citation statements)

References 21 publications

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“…Although fibrinoid necrosis is a ubiquitous feature of ANCA-associated vascular injury, 19 little is known about its pathogenesis. 20 Meanwhile, there are striking parallels in composition between fibrinoid necrosis and the fibrin clot in vascular repair. Both lesions consist primarily of fibrin, platelets, leukocytes, and extracellular matrix molecules such as fibronectin.…”

Section: Discussionmentioning

confidence: 99%

Anti-Plasminogen Antibodies Compromise Fibrinolysis and Associate with Renal Histology in ANCA-Associated Vasculitis

Berden

Nolan

Morris

et al. 2010

Journal of the American Society of Nephrology

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Antibodies recognizing plasminogen, a key component of the fibrinolytic system, associate with venous thrombotic events in PR3-ANCA vasculitis. Here, we investigated the prevalence and function of anti-plasminogen antibodies in independent UK and Dutch cohorts of patients with ANCA-associated vasculitis (AAV). We screened Ig isolated from patients (AAV-IgG) and healthy controls by ELISA. Eighteen of 74 (24%) UK and 10/38 (26%) Dutch patients with AAV had anti-plasminogen antibodies compared with 0/50 and 1/61 (2%) of controls. We detected anti-plasminogen antibodies in both PR3-ANCA-and MPO-ANCA-positive patients. In addition, we identified anti-tissue plasminogen activator (tPA) antibodies in 13/74 (18%) patients, and these antibodies were more common among patients with anti-plasminogen antibodies (P ϭ 0.011). Eighteen of 74 AAV-IgG (but no control IgG) retarded fibrinolysis in vitro, and this associated with anti-plasminogen and/or anti-tPA antibody positivity. Only 4/18 AAV-IgG retarded fibrinolysis without harboring these antibodies; dual-positive samples retarded fibrinolysis to the greatest extent. Patients with anti-plasminogen antibodies had significantly higher percentages of glomeruli with fibrinoid necrosis (P Ͻ 0.05) and cellular crescents (P Ͻ 0.001) and had more severely reduced renal function than patients without these antibodies. In conclusion, anti-plasminogen and anti-tPA antibodies occur in AAV and associate with functional inhibition of fibrinolysis in vitro. Seropositivity for anti-plasminogen antibodies correlates with hallmark renal histologic lesions and reduced renal function. Conceivably, therapies that enhance fibrinolysis might benefit a subset of AAV patients.

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Section: Discussionmentioning

confidence: 99%

Anti-Plasminogen Antibodies Compromise Fibrinolysis and Associate with Renal Histology in ANCA-Associated Vasculitis

Berden

Nolan

Morris

et al. 2010

Journal of the American Society of Nephrology

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“…Most observers will agree that the term vasculitis should reflect conditions in which inflammatory cells significantly damage vessels and not merely transverse them to enter the surrounding tissue. 40 Histologic Evidence of Vessel Wall Injury (Vasculitis) 2).…”

Section: Histologic Diagnostic Criteriamentioning

confidence: 99%

“…40,41 These changes commonly coexist with signs of endothelial damage in the form of endothelial swelling, shrinkage (apoptosis), or sloughing. Not only fibrin, but its precursors and metabolites (fibrinogen fibrinopeptides), necrotic endothelial and inflammatory cells, and immunoreactants are present in zones of fibrinoid necrosis.…”

Section: Histologic Diagnostic Criteriamentioning

confidence: 99%

Cutaneous Vasculitis Update: Diagnostic Criteria, Classification, Epidemiology, Etiology, Pathogenesis, Evaluation and Prognosis

Carlson

Ng²,

Chen³

2005

The American Journal of Dermatopathology

204

238

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Vasculitis, inflammation of the vessel wall, can result in mural destruction with hemorrhage, aneurysm formation, and infarction, or intimal-medial hyperplasia and subsequent stenosis leading to tissue ischemia. The skin, in part due to its large vascular bed, exposure to cold temperatures, and frequent presence of stasis, is involved in many distinct as well as un-named vasculitic syndromes that vary from localized and self-limited to generalized and life-threatening with multi-organ disease. To exclude mimics of vasculitis, diagnosis of cutaneous vasculitis requires biopsy confirmation where its acute signs (fibrinoid necrosis), chronic signs (endarteritis obliterans), or past signs (acellular scar of healed arteritis) must be recognized and presence of extravascular findings such as patterned fibrosis or collagenolytic granulomas noted. Although vasculitis can be classified by etiology, many cases have no identifiable cause, and a single etiologic agent can elicit several distinct clinicopathologic expressions of vasculitis. Therefore, the classification of cutaneous vasculitis is best approached morphologically by determining vessel size and principal inflammatory response. These histologic patterns roughly correlate with pathogenic mechanisms that, when coupled with direct immunofluorescent examination, anti-neutrophil cytoplasmic antibody (ANCA) status, and findings from work-up for systemic disease, allow for specific diagnosis, and ultimately, more effective therapy. Herein, we review cutaneous vasculitis focusing on diagnostic criteria, classification, epidemiology, etiology, pathogenesis, and evaluation of the cutaneous vasculitis patient.

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“…It is the classic vessel lesion in accelerated or malignant hypertension, and brain vessels may be particularly vulnerable to its development. It is also a not uncommon vessel response to other insults, and thus may be seen in vasculitis, particularly anti neutrophil cytoplasmic antibody (ANCA)-associated, 72 irradiation damage, some tumours and in Duret brain stem haemorrhages. 73 It has been suggested to represent, in many of these contexts, the result of abnormal physical forces on the arterial wall, either ''forced dilatation'' or vasospasm.…”

Section: Necrotisingmentioning

confidence: 99%