Innate immunity components analysis in renal tissues of rats with glomerular hypertension

Abstract

Innate immunity components analysis in renal tissue of rats with glomerular hypertension Chronic kidney disease (CKD) can be initiated by mechanical action as a consequence of glomerular hypertension and hyperflow, immune, toxic or a decrease in the glomerular permeability. Subsequently, we observed an intense cell proliferation, excessive extracellular matrix production, cytokines, growth factors and intense recruitment of inflammatory cells. In the late stage, we observe glomerular scarring process and irreversible interstitial injury. In the 80's, Brenner et al. showed that glomerular capillary hydraulic pressure (PGC) was elevated in CKD models and glomerular injury was limited when PGC was reduced by protein restriction in the diet or pharmacological approaching. In vitro observations indicated that glomerular cells subjected to mechanical stretching increase their proliferation rate and synthesizing inflammatory mediators such as TGF-beta derived from cyclooxygenase and adhesion molecules. The found of this effect with the three major cell types in the glomeruli - endothelial cells, mesangial cells and podocytes - helped shed light on the intriguing connection between mechanical aggression to the glomerulus and the development of CKD. However, several key aspects of this relationship remain unclear. (AU)