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1 pondents for SLE, and 64% of respondents for ANCA-associated vasculitis.
2 gain access to PMN granule components during ANCA-associated vasculitis.
3 ion in most patients 75 years and older with ANCA-associated vasculitis.
4 ing CLU and C3, predicting kidney failure in ANCA-associated vasculitis.
5 erapy among patients 75 years and older with ANCA-associated vasculitis.
6 sive renal failure and is commonly linked to ANCA-associated vasculitis.
7 rophil cytoplasmic antibodies (ANCAs) in PR3-ANCA-associated vasculitis.
8 mark of crescentic GN (cGN), often caused by ANCA-associated vasculitis.
9 nged disease control in patients with severe ANCA-associated vasculitis.
10 e neutrophil activation in patients with PR3-ANCA-associated vasculitis.
11 idase (MPO) is a well defined autoantigen in ANCA-associated vasculitis.
12 ted endothelial cell damage in patients with ANCA-associated vasculitis.
13 8(+) T cells mediate disease in experimental ANCA-associated vasculitis.
14 ctivation is involved in the pathogenesis of ANCA-associated vasculitis.
15 ipheral granulocytes of patients with active ANCA-associated vasculitis.
16 ents with biopsy-proven renal involvement of ANCA-associated vasculitis.
17 ibitor of metalloproteinase-1, and CXCL13 in ANCA-associated vasculitis.
18 n be detected in most European patients with ANCA-associated vasculitis.
19 a central pathogenic feature of proteinase 3 ANCA-associated vasculitis.
20 o cyclophosphamide for inducing remission in ANCA-associated vasculitis.
21 m the development of focal necrotizing GN in ANCA-associated vasculitis.
22 ith cyclophosphamide as induction therapy in ANCA-associated vasculitis.
23 dard intravenous cyclophosphamide for severe ANCA-associated vasculitis.
24 other autoimmune diseases, including classic ANCA-associated vasculitis.
25 ESR or ANCA levels to monitor patients with ANCA-associated vasculitis.
26 minocycline as agents capable of inducing an ANCA-associated vasculitis.
27 clinical antineutrophil cytoplasm antibody (ANCA) associated vasculitis.
28 ment of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.
29 ment of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.
30 E), and antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.
32 ies for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) are limited by partial
40 from anti-neutrophil cytoplasmic antibodies (ANCA)-associated vasculitis (AAV) showed increased level
41 seases, antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), a chronic, severe dis
42 s with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), avacopan received reg
43 In anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), hematuria and protein
44 causes anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), with rapidly progress
54 in experimental murine myeloperoxidase (MPO)-ANCA-associated vasculitis (AAV) show mast cells degranu
55 key driver of the vascular injury process in ANCA-associated vasculitis (AAV), and neutrophil serine
56 rine (AZA) for remission-induction in severe ANCA-associated vasculitis (AAV), but renal outcomes are
57 i-Neutrophil Cytoplasmic Antibody (ANCA) and ANCA-Associated vasculitis (AAV), systemic autoimmune di
60 severe antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, ANCA positivity, and resist
62 s with anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis and myasthenia gravis were r
63 discovery cohort of 1233 U.K. patients with ANCA-associated vasculitis and 5884 controls and was rep
64 -complex (MHC) and non-MHC associations with ANCA-associated vasculitis and also that granulomatosis
66 eloperoxidase concentration in patients with ANCA-associated vasculitis and controls, and assessed ne
67 eroxidase (MPO) underlies the development of ANCA-associated vasculitis and GN, but the mechanisms un
69 of 80 to 90% among patients with refractory ANCA-associated vasculitis and may be safer than cycloph
70 eatment for induction of remission in severe ANCA-associated vasculitis and may be superior in relaps
72 ry support for the concept that proteinase 3 ANCA-associated vasculitis and myeloperoxidase ANCA-asso
73 ivation of these cells by ANCA is central to ANCA-associated vasculitis and necrotizing crescentic gl
74 and guidelines addressing the management of ANCA-associated vasculitis and not specifically develope
75 ffective and safe new treatment modality for ANCA-associated vasculitis and possibly other autoimmune
76 3:1 ratio, 44 patients with newly diagnosed ANCA-associated vasculitis and renal involvement to a st
77 immunodominant epitopes in the pathology of ANCA-associated vasculitis and suggest that autoantibody
78 ed focus to long-term morbidities related to ANCA-associated vasculitis and their treatments, such as
79 free in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis, and a pair of urinary prote
80 hat CD8(+) cells are a therapeutic target in ANCA-associated vasculitis, and suggest that a molecular
81 ens for antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis are effective in 70 to 90% o
82 CA-associated vasculitis and myeloperoxidase ANCA-associated vasculitis are distinct autoimmune syndr
84 patients receiving rituximab for refractory ANCA-associated vasculitis at 4 centers in the UK was us
85 + T-cell counts could identify patients with ANCA-associated vasculitis at a substantial risk of rena
87 350 patients who received a new diagnosis of ANCA-associated vasculitis between 1985 and 2003 and wer
88 cheme with which to categorize patients with ANCA-associated vasculitis, but adding the percentage of
89 to differentiate active GN from remission in ANCA-associated vasculitis, but their predictive value f
92 a rare anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, characterized by asthma, eo
93 elial growth factor, in patients with active ANCA-associated vasculitis compared with patients during
94 icroparticles in the plasma of children with ANCA-associated vasculitis compared with that in healthy
96 tudinal analysis revealed that patients with ANCA-associated vasculitis could be divided into two gro
97 tosus, anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis, Crohn's disease, Behcet's d
103 involved 93 patients 75 years and older with ANCA-associated vasculitis from 36 university and nonuni
104 ctively, among three groups of patients with ANCA-associated vasculitis from Vienna, Austria (n=19);
105 Data surrounding sex-specific differences in ANCA-associated vasculitis glomerulonephritis (ANCA-GN)
106 This study confirms that the pathogenesis of ANCA-associated vasculitis has a genetic component, show
107 be controlled with immunosuppressive drugs, ANCA-associated vasculitis has become a chronic and rela
108 neutrophil cytoplasmic antibodies (ANCAs) in ANCA-associated vasculitis has been debated for some tim
109 During the 21st century, the management of ANCA-associated vasculitis has moved away from reliance
110 peroxidase (MPO) ANCA and proteinase 3 (PR3) ANCA associated vasculitis have been developed, which ha
112 controlled trial, we assigned patients with ANCA-associated vasculitis in a 1:1 ratio to receive ora
113 ine the efficacy and safety of rituximab for ANCA-associated vasculitis in a larger multicenter cohor
114 , microscopic polyangiitis, or renal-limited ANCA-associated vasculitis in complete remission after a
115 omarker study including 102 individuals with ANCA-associated vasculitis in remission aimed to predict
118 ltured neutrophils from patients with active ANCA-associated vasculitis, indicating that increased tr
121 -2) in anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis is controversial because of
127 s demonstrated that the renal risk score for ANCA-associated vasculitis is transferable to anti-GBM d
129 -MPO antibodies, increase sFlt1 during acute ANCA-associated vasculitis, leading to an antiangiogenic
130 omerular myeloperoxidase deposition, seen in ANCA-associated vasculitis, may enhance crescentic GN th
132 ase 3 (PRTN3) in leukocytes of patients with ANCA-associated vasculitis observed longitudinally (n=82
134 in anti-neutrophil cytoplasmic autoantibody (ANCA) associated vasculitis poses a significant clinical
135 hundred sixty-six consecutive patients with ANCA-associated vasculitis, positive for either proteina
136 rophil microparticles in the pathogenesis of ANCA-associated vasculitis, potentially providing a targ
138 is of patients enrolled in the Rituximab for ANCA-Associated Vasculitis (RAVE) Trial who had renal in
139 copic polyangiitis, and 5 with renal-limited ANCA-associated vasculitis) received azathioprine (58 pa
143 V: 163 subjects enrolled in the Rituximab in ANCA-Associated Vasculitis trial were screened for the p
145 histopathological classification system for ANCA-associated vasculitis was recently published, but w
146 The benefit of infliximab (a mAb to TNF) in ANCA-associated vasculitis was recently reported in a pr
147 ntigen gene expression and disease status in ANCA-associated vasculitis, we measured gene-specific DN
148 features and an HLA-DQ association with MPO+ ANCA-associated vasculitis, while ANCA-negative EGPA may