Henoch–Schönlein purpura nephritis associated with human parvovirus B19 infection

Watanabe, Toru; Oda, Y.

doi:10.1046/j.1442-200x.2000.01161.x

Cited by 27 publications

(12 citation statements)

References 10 publications

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“…Specifically, Kawasaki disease is reported in children expressing B19‐specific antibodies and DNA in peripheral blood 12,13 . Small vessel vasculitic syndromes associated with B19 infection include cases of WG, microscopic PAN, 2,5 , 7,14 , 15 and HSP, 15–17 where B19 DNA has been isolated from the peripheral blood and skeletal muscle. Such cases have shown a poor response to cyclophosphamide and other immunosuppressant agents, the conventional standard therapy.…”

Section: Discussionmentioning

confidence: 99%

Parvoviral infection of endothelial cells and stromal fibroblasts: a possible pathogenetic role in scleroderma

et al. 2003

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Parasitism of endothelia and fibroblasts by B19 with resultant enhanced TNF-alpha expression may be of pathogenetic importance in SSc even in the absence of demonstrable viremia. The vascular deposition of C5b-9 suggests a role for humoral immunity possibly induced by a state of endothelial neoantigenicity evoked by virally mediated cell injury. Treatment strategies include anti-viral therapy, including in the context of intravenous gamma-globulin and anti-TNF therapy.

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Section: Discussionmentioning

confidence: 99%

Parvoviral infection of endothelial cells and stromal fibroblasts: a possible pathogenetic role in scleroderma

et al. 2003

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“…Follow-up biopsy done 1 yr later because of persistence of the nephrotic syndrome showed FSGS, and B19 DNA remained detectable by PCR. Thrombotic microangiopathy (49,56), hemolytic uremic syndrome (62), and renal involvement in association with systemic vasculitides such as Henoch Schö nlein purpura (54,63), polyarteritis nodosa (64) and Wegener's granulomatosis (64) have also been associated with B19 infection.…”

Section: Glomerular Diseases Associated With Parvovirusmentioning

confidence: 99%

Parvovirus B19 and the Kidney

Waldman¹,

Kopp²

2007

Clinical Journal of the American Society of Nephrology

113

105

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“…It was described in association with viral and other infectious agents [6][7][8] or otherwise reported to be drug-induced [9,10]. Antigenic stimuli causing elevation of circulating immunoglobulin A (IgA), complement activation leading to systemic inflammation of small vessels and the involvement of proinflammatory cytokines have all been implicated [11][12][13].…”

Section: Introductionmentioning

confidence: 99%

Henoch–Schonlein purpura: polymorphisms in thrombophilia genes

et al. 2006

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Henoch-Schonlein purpura (HSP) is a small-sized vasculitis affecting mainly children. Based on the hypothesis that an inherited predilection to hypercoagulability may predispose to HSP or may mark those who develop acute clinical manifestations, we evaluated the possible roles of methylenetetrahydrofolate reductase (MTHFR) gene C677T, factor V (FV) gene G1691A (Leiden), and prothrombin gene G20210A polymorphisms in patients with HSP. Fifty-two HSP patients (32 boys and 20 girls) from different ethnic groups (22 Jews and 30 Arabs) and 104 ethnically matched controls were studied for these three polymorphisms. The frequencies of these mutations for each group, separately and in combinations, are described. The mutation frequencies in the MTHFR, prothrombin and FV genes in HSP patients did not differ from those in controls. In a small number of individuals (n=5) homozygosity for the 677T thermolabile variant of MTHFR was associated with hematuria. To summarise, hypercoagulability does not seem to play a role in HSP. Studies in larger cohorts and possibly inclusion of additional factors may be needed to ascertain whether homozygoty for MTHFR 677T polymorphism can influence disease severity.

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Henoch–Schönlein purpura nephritis associated with human parvovirus B19 infection

Cited by 27 publications

References 10 publications

Parvoviral infection of endothelial cells and stromal fibroblasts: a possible pathogenetic role in scleroderma

Parvoviral infection of endothelial cells and stromal fibroblasts: a possible pathogenetic role in scleroderma

Parvovirus B19 and the Kidney

Henoch–Schonlein purpura: polymorphisms in thrombophilia genes

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