NEFRITIS LUPICA: CLASIFICACIONES Y MODELOS ANIMALES
•Transferir como PPS, PDF•
1 gostou•828 visualizações
NEFRITIS LUPICA 1er Congreso de Nefrología en la Práctica Clínica DR JUAN VICENTE CUELLAR GONZALEZ . El lupus eritematoso sistémico (LES) es una enfermedad autoinmune multisistémica. Producción de autoanticuerpos (Anticuerpos contra Ag nucleares, DNA de doble cadena, histonas y ribonucleoproteínas). Parte 2 de 4
Recomendados
Mais conteúdo relacionado
Mais de Nefrologia Integral de Celaya
Mais de Nefrologia Integral de Celaya (9)
Último
Último (20)
NEFRITIS LUPICA: CLASIFICACIONES Y MODELOS ANIMALES
- 1. NEFRITIS LUPICA 1er Congreso de Nefrología en la Práctica Clínica DR JUAN VICENTE CUELLAR GONZALEZ Parte 2 de 4 Nefrología Integral de Celaya @neficelaya nefrologiaintegral
- 2. PATOGENESIS Nature Reviews Rheumatology 6, 13-20 (January 2010)
- 3. MODELOS ANIMALES EN NEFRITIS LUPICA NZB B/W F1 y MRL-1pr Defectos primarios que condicionan Proliferación de linfos B, incluyendo Defectos en la apoptosis que condicionan Una delección clonal defectuosa
- 4. N Engl J Med 2010; 363(11):1080-1082
Notas do Editor
- Renal deposition of autoantibodies, exposure to circulating inflammatory mediators and activation of the complement cascade initiate an inflammatory program that involves upregulation of adhesion molecules on endothelial cells, activation of intrinsic renal cells, induction of chemokines and recruitment of inflammatory cells that release cytokines and other molecules. Podocyte injury results in proteinuria and decreased glomerular basement membrane production, which compromises the vasculature. Microvascular thromboses and endothelial cell death contribute to renal hypoxia which, in turn, causes tubular atrophy. Progressive inflammation recruits an increasingly diverse set of inflammatory mediators that amplify injury. Endothelial cell activation and renal dendritic cell activation are reversible in early-stage nephritis, but activation of fibrotic pathways and smooth-muscle myofibroblast cells, and progressive podocyte loss eventually result in irreversible renal damage. These pathways could all be amenable to therapeutic intervention