tailieunhanh - Báo cáo khoa học: "Circulating pro-apoptotic mediators in burn septic acute renal failure"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về ngành y học đề tài: Circulating pro-apoptotic mediators in burn septic acute renal failure. | Available online http content 12 2 126 Commentary Circulating pro-apoptotic mediators in burn septic acute renal failure Heleen M Oudemans-van Straaten Department of Intensive Care Onze Lieve Vrouwe Gasthuis Oosterpark 1091 AC Amsterdam Netherlands Corresponding author HM Oudemans-van Straaten Published 31 March 2008 This article is online at http content 12 2 126 2008 BioMed Central Ltd Critical Care 2008 12 126 doi cc6798 See related research by Mariano et al. http content 12 2 R42 Abstract The pathogenesis of septic acute kidney injury AKI is not well understood. In the present issue of Critical Care the combined clinical and experimental study from Mariano s group provides new insight into the disease. The study shows that plasma from septic burn patients with acute renal failure initiated pro-apoptotic effects and functional alterations in renal tubular cells and podocytes in vitro that correlated with the degree of proteinuria and renal dysfunction. Pro-apoptotic effects were not attributable to antibiotic or uremic toxicity but were partially attributable to endotoxin. Sepsis and burn had additive effects. Apart from increasing our understanding of the pathogenesis of septic AKI the study justifies further research on therapeutic interventions in several directions. These include the binding and elimination of the source of endotoxin by selective decontamination of the digestive tract the blocking of apoptotic pathways or the extracorporeal removal of circulating toxic mediators using high permeability hemofiltration or coupled plasma filtration and absorption. We still have no uniform concept of the pathogenesis of septic acute kidney injury AKI . While renal hypoperfusion is the predominant factor in hypodynamic states neither systemic nor intrarenal vasomotor changes seem to be the sole contributor to AKI in sepsis. Inflammatory and procoagulatory mediators likely play an .