Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học quốc tế cung cấp cho các bạn kiến thức về ngành y đề tài: Protective effect of resin adsorption on septic plasma-induced tubular injury. | Cantaluppi et al. Critical Care 2010 14 R4 http content 14 1 R4 c CRITICAL CARE RESEARCH Open Access Protective effect of resin adsorption on septic plasma-induced tubular injury 3 1 1 1 Vincenzo Cantaluppi Viktoria Weber Carola Lauritano Federico Figliolini Silvia Beltramo Luigi Biancone h I r r I m l 2 I4 l 2 I f KI I 74 f I I I i - D r KS r r 4 í 11 I ỉ J K K k D I c J z t I K 12 I r I 4 4 s5 I z Ĩ KS KS I f s m I I I- r I 1 2 6 Massimo De Cal Dinna Cruz Claudio Ronco Giuseppe Paolo Segoloni Ciro Tetta Giovanni Camussi Abstract Introduction A pro-apoptotic effect of circulating mediators on renal tubular epithelial cells has been involved in the pathogenesis of sepsis-associated acute kidney injury AKI . Adsorption techniques have been showed to efficiently remove inflammatory cytokines from plasma. The aim of this study was to evaluate the efficiency of the hydrophobic resin Amberchrom CG161 M to adsorb from septic plasma soluble mediators involved in tubular injury. Methods We enrolled in the study 10 critically ill patients with sepsis-associated AKI and we evaluated the effects of their plasma on granulocyte adhesion apoptosis and functional alterations of cultured human kidney tubular epithelial cells. We established an in v fro model of plasma adsorption and we studied the protective effect of unselective removal of soluble mediators by the Amberchrom CG161 M resin on septic plasma-induced tubular cell injury. Results Plasma from septic patients induced granulocyte adhesion apoptosis and altered polarity in tubular cells. Plasma adsorption significantly decreased these effects and abated the concentrations of several soluble mediators. The inhibition of granulocyte adhesion to tubular cells was associated with the down-regulation of ICAM-1 and CD40. Resin adsorption inhibited tubular cell apoptosis induced by septic plasma by down-regulating the activation of caspase-3 8 9 and of Fas death receptor-mediated signalling pathways. The .
