No hay notas en la diapositiva.
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