Protective effect of astaxanthin on ANCA-associated vasculitis.

Objective: Anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a systemic autoimmune disease characterized by inflammation and fibrinoid necrosis of medium and small vessels, and its pathogenesis is closely related to inflammation and oxidative stress. Astaxanthin (ATX) is a carotenoid with anti-inflammatory, antioxidant, and immunomodulatory effects. We hypothesized that ATX could play a role in AAV treatment.

Pathogenesis of antimicrobial peptides LL-37 and CpG-ODN in ANCA associated vasculitis.

Objectives: Anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitides (AAV) are a group of systemic autoimmune disorders characterized by necrotizing inflammation of small- to medium-sized blood vessels. The pathogenesis of patients with AAV are still in investigation. In this study, we explored the involvement of LL-37 and nucleic acids in AAV.

Significance of serum peptidylarginine deiminase type 4 in ANCA-associated vasculitis.

Objective: To investigate the clinical significance of peptidylarginine deiminase type 4 (PAD4) in the pathogenesis of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). To make a primary observation on the relationship of chronic bronchitis and bronchiectasis (CB) with the pathogenesis of AAV by PAD4.

Methods: The sera from 13 patients with AAV, 13 patients with CB, 11 patients with rheumatoid arthritis (RA), 11 patients with primary chronic kidney disease (CKD) and 12 normal controls were collected.

Renal neutrophils infiltration in antineutrophil cytoplasmic antibodies-negative pauci-immune crescentic glomerulonephritis.

Introduction: This study aims to investigate the evidence of neutrophil infiltration in renal tissue from patients with antineutrophil cytoplasmic antibodies (ANCA)-negative pauci-immune crescentic glomerulonephritis (CrGN), and a comparison with their ANCA-positive counterparts was performed.

Methods: Renal biopsy specimens from 31 patients with pauci-immune CrGN were collected. Twelve patients were ANCA negative, and 19 patients were ANCA positive.

Modified C-reactive protein might be a target autoantigen of TINU syndrome.

Background And Objectives: The cross-reactive antigen(s) of tubulointerstitial nephritis and uveitis (TINU) syndrome from renal tubulointerstitia and ocular tissue remain unidentified. The authors' recent study demonstrated that the presence of serum IgG autoantibodies against modified C-reactive protein (mCRP) was closely associated with the intensity of tubulointerstitial lesions in lupus nephritis. The study presented here investigates the possible role of IgG autoantibodies against mCRP in patients with TINU syndrome.

Differential deposition of C4d and MBL in glomeruli of patients with ANCA-negative pauci-immune crescentic glomerulonephritis.

Objective: Our previous study suggested involvement of alternative pathway activation of complement in ANCA-positive pauci-immune crescentic glomerulonephritis (CrGN). This study was to investigate the evidence of complement activation in renal biopsy specimens of patients with ANCA-negative pauci-immune CrGN.

Methods: Renal biopsy specimens from 12 patients with ANCA-negative pauci-immune CrGN were used to detect the staining of membrane attack complex (MAC), C3d, C4d, mannose-binding lectin (MBL), factor B by immunohistochemistry, and/or immunofluorescence.

Complement activation is involved in renal damage in human antineutrophil cytoplasmic autoantibody associated pauci-immune vasculitis.

Objective: This study was to investigate the evidence for complement activation in renal biopsy specimens of patients with myeloperoxidase (MPO)-antineutrophil cytoplasmic autoantibody (ANCA)-associated pauci-immune vasculitis.

Methods: Renal biopsy specimens from seven patients with MPO-ANCA positive pauci-immune necrotizing crescentic glomerulonephritis (NCGN) were used to detect the staining of membrane attack complex (MAC), C3d, C4d, mannose-binding lectin (MBL), factor B and factor P using immunohistochemistry and immunofluorescence. Renal tissue from seven patients with minimal change disease (MCD) and two normal renal tissue were used as controls.

Complement deposition in renal histopathology of patients with ANCA-associated pauci-immune glomerulonephritis.

Background: The pathogenesis of ANCA-associated pauci-immune glomerulonephritis has not been fully elucidated. Several studies had suggested that complement deposition could be detected in renal histopathology. The current study investigated the clinical and pathological significance of complement deposition in renal histopathology of patients with ANCA-associated pauci-immune glomerulonephritis.