Soluble thrombomodulin and antibodies to bovine glomerular endothelial cells in patients with Henoch-Schonlein purpura

Fujieda, Mikiya; Oishi, Naobumi; Naruse, Keishi; Hashizume, Minoru; Nishiya, Koji; Kurashige, Takanobu; Ito, Katsuhiko

doi:10.1136/adc.78.3.240

Cited by 35 publications

(29 citation statements)

References 23 publications

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“…On the other hand, there have been several reports on endothelial cell dysfunction in HSPN [22]. Fujieda et al showed that endothelial cells are damaged in HSPN, and high titers of IgA anti-endothelial cell antibodies and elevated serum thrombomodulin values may be clinically useful markers of renal involvement in patients with HSPN [22].…”

Section: Discussionmentioning

confidence: 96%

The role of serum myeloid-related protein 8/14 complex in Henoch–Schönlein purpura nephritis

et al. 2011

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Myeloid-related protein (MRP) 8/14 complex is a marker of monocyte and neutrophil activation. We evaluated whether serum MRP8/14 complex is associated with clinical manifestations and pathological findings of Henoch-Schönlein purpura nephritis (HSPN). Patients were divided into two groups based on serum MRP8/14 complex levels at renal biopsy. Group 1 consisted of 18 HSPN patients with less than median (670 ng/ml) MRP8/14 complex levels, and Group 2 of 12 HSPN patients with greater than median levels. Clinical manifestations, laboratory findings and serum E-selectin levels, as a marker of vascular endothelial cell dysfunction, as well as histological and immunohistochemical findings were investigated for both groups. We also measured MRP8/14 complex levels in disease control and healthy control children. Urinary protein excretions, serum MRP8/14 complex levels, and serum E-selectin levels were all higher in Group 2 than in Group 1 patients. Serum MRP8/14 complex levels were higher in HSPN patients than in controls. Serum MRP8/14 complex levels were strongly associated with serum E-selectin levels. Pathological findings revealed that the proportions of patients with ISKDC grades III, IV and V in Group 2 were higher than in Group 1. Our findings suggest that serum MRP8/14 complex levels might be associated with the severity of renal injury and endothelial cell dysfunction in HSPN patients.

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Section: Discussionmentioning

confidence: 96%

The role of serum myeloid-related protein 8/14 complex in Henoch–Schönlein purpura nephritis

et al. 2011

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“…Recent in vitro studies [1,2,3,4,5,6] demonstrated that circulating serum growth factor, adhesion molecules, or other markers of endothelial cell damage were elevated in the acute phase of HSP, especially in severe forms developing anaphylactoid nephritis. These vascular abnormalities reduce the availability of nitric oxide, which induces structural and mechanical changes, and may offer important insights into the development and progression of vascular-initiated end-organ damage.…”

Section: Discussionmentioning

confidence: 99%

“…Although the precise etiology remains unclear, it has been reported that vascular endothelial function plays a major role in the pathogenesis of HSP. Recent in vitro studies have demonstrated that circulating serum growth factor [1,2], adhesion molecules [3,4], or other markers of endothelial cell damage [5,6] were elevated in the acute phase of HSP. However, there have been few clinical studies of vascular endothelium and/or smooth muscle in HSP.…”

Section: Introductionmentioning

confidence: 99%

Impaired vascular endothelium-dependent relaxation in Henoch-Sch�nlein purpura

Kurotobi

Kawakami

Honda

et al. 2004

Pediatric Nephrology

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Few reports have focused on vascular endothelial function in children with Henoch-Schönlein purpura (HSP). The purpose of the present study was to assess endothelial function and to follow serial changes from the acute to convalescent phases in children with HSP. Forearm flow-mediated vasodilation was evaluated in 21 patients with HSP, aged 4.0-10.3 years (median 6.2 years), and in 14 control subjects. Vascular dimension, mean velocity, and flow volume were measured by ultrasonography in brachial artery before and after hyperemia, and during incremental infusions of nitroglycerin (0.5, 1.0 microg/kg per min). In the controls, significant increases in dimension, mean velocity, and flow volume were observed in reactive hyperemia ( P<0.01). In contrast, patients in the acute phase of HSP showed a flow velocity profile indicating a highly resistant forearm circulation, and significantly attenuated responses after hyperemia ( P<0.01 vs. control), whereas the responses to nitroglycerin were well preserved. In addition, the impaired hyperemic responses recovered in the convalescent phase, with no significant differences compared with controls. These results clearly suggest that forearm vascular endothelium-dependent relaxation was attenuated in patients with acute HSP.

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“…Kawasaki et al reported that the accumulation of macrophages in the glomeruli was a predictor of poor prognosis in HSPN patients 27) . On the other hand, there have been several reports on endothelial cell dysfunction in HSPN 28,29) . Fujieda et al showed that endothelial cells are damaged in cases of HSPN, and high IgA antiendothelial cell antibody titers and elevated serum thrombomodulin levels may be clinically useful markers of renal involvement in patients with HSPN 28) .…”

Section: Pathogenesismentioning

confidence: 99%

“…On the other hand, there have been several reports on endothelial cell dysfunction in HSPN 28,29) . Fujieda et al showed that endothelial cells are damaged in cases of HSPN, and high IgA antiendothelial cell antibody titers and elevated serum thrombomodulin levels may be clinically useful markers of renal involvement in patients with HSPN 28) . Kawasaki et al reported that serum E -selectin concentrations at the time of the first biopsy in patients with HSPN were higher than those at the time of the second biopsy and could be used to evaluate glomerular endothelial dysfunction in HSPN 29) .…”

Section: Pathogenesismentioning

confidence: 99%

HENOCH-SCH^|^Ouml;NLEIN PURPURA NEPHRITIS IN CHILDHOOD: PATHOGENESIS, PROGNOSTIC FACTORS AND TREATMENT

Kawasaki

Ono

Ohara

et al. 2013

FJMS

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: Henoch -Schönlein purpura (HSP) is a systemic disorder characterized by leukocytoclastic vasculitis involving the capillaries and the deposition of IgA immune complexes. Renal involvement is the principal cause of morbidity and mortality in children with HSP. Thus, it is important to clarify the onset mechanism as well as the prognostic factors of Henoch -Schönlein purpura nephritis (HSPN) and to identify the most appropriate treatment. We herein review the pathogenesis, the prognostic factors and treatment of HSPN. As to the pathogenesis, several studies suggest that galactose -deficient IgA1 (Gd -IgA1) is recognized by anti -glycan antibodies, leading to the formation of circulating immune complexes and their mesangial deposition, thereby inducing renal injury. With regard to the prognostic factors, a number of factors have been suggested including nephrotic syndrome, decreased factor XIII activity, hypertension, severe renal injury, high renal accumulation of activated macrophage, alpha -smooth muscle actin, and high serum myeloid -related protein levels. For the treatment of severe HSPN, aggressive therapies including multiple drug combination therapy and plasmapheresis have been shown to be effective in ameliorating proteinuria and histological severity. Nevertheless, detailed investigation into the pathogenesis of HSPN and double -blind randomized control studies on children with HSPN are still necessary.

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Soluble thrombomodulin and antibodies to bovine glomerular endothelial cells in patients with Henoch-Schonlein purpura

Abstract: (Arch Dis Child 1998;78:240-244)

Cited by 35 publications

References 23 publications

The role of serum myeloid-related protein 8/14 complex in Henoch–Schönlein purpura nephritis

The role of serum myeloid-related protein 8/14 complex in Henoch–Schönlein purpura nephritis

Impaired vascular endothelium-dependent relaxation in Henoch-Sch�nlein purpura

HENOCH-SCH^|^Ouml;NLEIN PURPURA NEPHRITIS IN CHILDHOOD: PATHOGENESIS, PROGNOSTIC FACTORS AND TREATMENT

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