Septic acute kidney injury hemodynamic syndrome, inflammatory disorder, or both 英文参考文献.docVIP

Lipcsey and Bellomo Critical Care 2011,15:1008 /content/15/6/1008 COMMENTARY Septic acute kidney injury: hemodynamic syndrome, in? ammatory disorder, or both? Miklos Lipcsey and Rinaldo Bellomo * 1,2 3 For related research see Benes et al., /content/15/5/R256 support them is weak is is especially true because renal perfusion (renal blood ? ow (RBF)) cannot be reliably measured in man. Importantly, changes in intra- RBF distribution and glomerular hemodynamics may account for loss of function, even in the presence of maintained or increased RBF [5,6]. In addition, con ven- tional views of the pathophysiology of S-AKI have been derived from models of acute kidney injury with limited relevance to human disease and, when di? erent models are studied, they deliver di? erent changes in RBF and function [6]. Finally, the role of nitric oxide [7] and the role of nonhemodynamic mechanisms such as apoptosis and the innate immune response remain poorly under- stood. It is in this context that one should assess the experiments from Matejovic’s group [1]. Abstract Septic acute kidney injury (S-AKI) is the most common cause of kidney injury in the ICU. Decreased renal blood ?ow and in?ammation have both been suggested as mechanisms of S-AKI. Benes and colleagues present a study of S-AKI in which sepsis is induced by fecal peritonitis and bacterial infusion. In this study, although decreased renal blood ?ow and increased renal vascular resistance were present in some of the animals that developed S-AKI, in?ammatory activation without decreased renal blood ?ow and increased renal vascular resistance was seen in other animals. Systemic hemodynamic ?ndings provided little information on renal hemodynamics or risk of S-AKI. The study highlights the extraordinary complexity of S-AKI and the need for clinicians to recognize our limited understanding o