ArticleKidney international2015
Renal participation of myeloperoxidase in antineutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis.
Article in Kidney international, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers, 1 of them a synthesis that pooled it.
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Who cites it
94 citing papers in PubMed, 1 synthesis or guideline pooled it, 154 citations in OpenAlex.
- Neutrophil Extracellular Traps (NETs) and Vasculitis.International journal of medical sciences · 2021Pooled it
- Urinary UDP-sugars provide actionable prediction of acute kidney injury in cardiac surgery patients.American journal of physiology. Heart and circulatory physiology · 2026Article
- Anti-neutrophil cytoplasmic antibody-associated vasculitis: biological insights and biomarker-guided disease management.Nature reviews. Nephrology · 2026Review
- Review
- A neutrophil-mesangial cell axis promotes glomerular injury in lupus nephritis.Annals of the rheumatic diseases · 2026Article
- Renal Tubular Epithelial Cells as Central Hubs of Kidney Disease.Diagnostics (Basel, Switzerland) · 2026Review
- Neutrophil extracellular traps in the animal model of adenine-induced chronic kidney disease.PloS one · 2026Article
- Identification of Renal Transcripts Associated with Kidney Function and Prognosis in ANCA-Associated Vasculitis.Journal of the American Society of Nephrology : JASN · 2026Article
- Gene therapy enhances deoxyribonuclease I treatment in antimyeloperoxidase glomerulonephritis.JCI insight · 2025Article
- NLRP3 inflammasome activity and pyroptosis are involved in CD206Acta biochimica et biophysica Sinica · 2025Article
- Advances in the treatment of ANCA-associated vasculitis.Nature reviews. Rheumatology · 2025Review
- Neutrophils and NETs in kidney disease.Nature reviews. Nephrology · 2025Review
- The Utility of Myeloperoxidase Immunostaining to Characterize Immune Deposits in Patients With Crescentic Glomerulonephritis.Kidney international reports · 2025Article
- Immune Landscape Variation in Antineutrophil Cytoplasmic Antibody-Associated Vasculitis Circulation Before and After Plasmapheresis by Single-Cell Transcriptome.Mediators of inflammation · 2025Article
- Tissue-resident memory T cells in urinary tract diseases.Frontiers in immunology · 2025Review
- Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis in China: Epidemiology, Management, Prognosis, and Outlook.Kidney diseases (Basel, Switzerland) · 2024Review
- Cathepsin C inhibition reduces neutrophil serine protease activity and improves activated neutrophil-mediated disorders.Nature communications · 2024Article
- Slowly Progressive ANCA-associated Glomerulonephritis with Strong Mesangial MPO Deposits Following a Diagnosis of Interstitial Lung Disease.Internal medicine (Tokyo, Japan) · 2024Article
- Top Five Stories of the Cellular Landscape and Therapies of Atherosclerosis: Current Knowledge and Future Perspectives.Current medical science · 2024Review
- Farnesoid X receptor prevents neutrophil extracellular traps via reduced sphingosine-1-phosphate in chronic kidney disease.American journal of physiology. Renal physiology · 2023Article
34 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Myeloperoxidase (MPO) is an important neutrophil lysosomal enzyme, a major autoantigen, and a potential mediator of tissue injury in MPO-ANCA-associated vasculitis (MPO-AAV) and glomerulonephritis. Here we examined MPO deposition in kidney biopsies from 47 patients with MPO-AAV. Leukocyte accumulation and fibrin deposition consistent with cell-mediated immunity was a major feature. Tubulointerstitial macrophage, CD4+ and CD8+ T-cell, and neutrophil numbers correlated with low presenting eGFR. MPO was not detected in kidneys from patients with minimal change or thin basement membrane disease, but was prominent in glomerular, periglomerular, and tubulointerstitial regions in MPO-AAV. Extracellular MPO released from leukocytes was pronounced in all MPO-AAV patients. Similar numbers of neutrophils and macrophages expressed MPO in the kidneys, but colocalization studies identified neutrophils as the major source of extracellular MPO. Extraleukocyte MPO was prominent in neutrophil extracellular traps in the majority of patients; most of which had traps in half or more glomeruli. These traps were associated with more neutrophils and more MPO within glomeruli. Glomerular MPO-containing macrophages generated extracellular trap-like structures. MPO also localized to endothelial cells and podocytes. The presence of the most active glomerular lesions (both segmental necrosis and cellular crescents) correlated with intraglomerular CD4+ cells and MPO+ macrophages. Thus, cellular and extracellular MPO may cause glomerular and interstitial injury.
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