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Genetically distinct subsets within ANCA-associated vasculitis.
TLDR
This study confirms that the pathogenesis of ANCA-associated vasculitis has a genetic component, shows genetic distinctions between granulomatosis with polyang iitis and microscopic polyangiitis that are associated with ANCA specificity, and suggests that the response against the autoantigen proteinase 3 is a central pathogenic feature ofproteinase 3 ANCA -associated vasulitis. Expand
Ciliopathies with skeletal anomalies and renal insufficiency due to mutations in the IFT-A gene WDR19.
TLDR
The results suggest that isolated nephronophthisis, Jeune, and Sensenbrenner syndromes are clinically overlapping disorders that can result from a similar molecular cause. Expand
Plasma levels of soluble interleukin 2 receptor, soluble CD30, interleukin 10 and B cell activator of the tumour necrosis factor family during follow-up in vasculitis associated with proteinase
TLDR
Increased T cell activation in patients with ANCA-associated vasculitis in remission during and after immunosuppressive treatment is associated with persistent or renewed ANCA positivity. Expand
Renal survival in proteinase 3 and myeloperoxidase ANCA-associated systemic vasculitis.
TLDR
AAV patients with renal involvement who needed RRT had the worst survival probability and the only major determinants for long-term renal survival were renal function at 6 months and renal relapses. Expand
Early Conversion From Calcineurin Inhibitor‐ to Everolimus‐Based Therapy Following Kidney Transplantation: Results of the Randomized ELEVATE Trial
TLDR
Conversion to everolimus at 10–14 weeks posttransplant was associated with renal function similar to that with standard therapy overall, and reporting on de novo donor‐specific antibodies (DSA) was limited but suggested more frequent anti‐HLA Class I DSA underEverolimus. Expand
Accelerated atherosclerosis in patients with Wegener's granulomatosis.
TLDR
Although endothelial activation markers in WG patients with inactive disease were not increased, the raised levels of hsCRP, MMPs, and TIMP-1 suggest that enhanced inflammation and excessive vascular remodelling are contributing factors in the development of accelerated atherosclerosis in Wg. Expand
Prediction of relapses in PR3-ANCA-associated vasculitis by assessing responses of ANCA titres to treatment.
TLDR
Positive c-ANCA (immunofluorescence) and PR3-AN CA (ELISA) titres during early follow-up identify patients at increased risk of relapse. Expand
Urinary Soluble CD163 in Active Renal Vasculitis.
TLDR
Data indicate that urinary sCD163 level associates very tightly with active renal vasculitis, and assessing this level may be a noninvasive method for diagnosing renal flare in the setting of a known diagnosis of SVV. Expand
Renal expression of matrix metalloproteinases in human ANCA-associated glomerulonephritis.
TLDR
Ren renal expression of MMPs, tissue inhibitor of metalloproteinase-1 (TIMP-1) and markers of neutrophil and monocyte infiltration in renal biopsies of patients with active anti-neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis is analysed. Expand
Urinary matrix metalloproteinases reflect renal damage in anti-neutrophil cytoplasm autoantibody-associated vasculitis.
TLDR
Urinary Mmp-2, MMP-9, and TIMP-1 are elevated in AAV but do not reflect renal MMP expression and glomerular inflammation, however, urinary M MP-2 activity and TIMp-1 levels reflect tubulointerstitial damage and correlate negatively with creatinine clearance at biopsy. Expand
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