title: Update on crescentic glomerulonephritis.
abstract: The recent years have seen a number of major progresses in the field of extracapillary glomerulonephritis. This entity is the final damage caused by unrelated immunological disorders such as immune complexes glomerular deposits or microvascular injury caused by proinflammatory cytokines, neutrophil extracellular traps (NET), and cell adhesion molecules in the context of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV). This review provides a summary of recent advances in the understanding of crescentic glomerulonephritis, focusing on interplays of local immune cells and on local mediators participating to crescent formation especially in anti-glomerular basement membrane (anti-GBM) antibody disease. The recent advances about AAV and lupus nephritis are covered by other chapters of this issue. Nevertheless, these considerations may apply to the general case of crescentic glomerulonephritis of all causes.
authors.affiliation: Paris Cardiovascular Centre - PARCC, Institut National de la Santé et de la Recherche Médicale (INSERM), Paris, France.
authors.forename: Carole
authors.initials: C
authors.lastname: Hénique
authors.forename: Christina
authors.initials: C
authors.lastname: Papista
authors.forename: Léa
authors.initials: L
authors.lastname: Guyonnet
authors.forename: Olivia
authors.initials: O
authors.lastname: Lenoir
authors.forename: Pierre-Louis
authors.initials: PL
authors.lastname: Tharaux
mesh_terms: D056648:Anti-Neutrophil Cytoplasmic Antibody-Associated Vasculitis / Q000276:immunology / Q000473:pathology; D016207:Cytokines / Q000276:immunology*; D005921:Glomerulonephritis / Q000145:classification / Q000276:immunology* / Q000473:pathology*; D006801:Humans; D009504:Neutrophils / Q000276:immunology* / Q000473:pathology
chemical_list: D016207:Cytokines