Bellomo Rinaldo, Wan Li, Langenberg Christoph, Ishikawa Ken, May Clive N
Contrib Nephrol. 2011;174:98-107. doi: 10.1159/000329246. Epub 2011 Sep 9.
Acute kidney injury (AKI) is a serious condition that affects many intensive care unit (ICU) patients. The most common causes of AKI in the ICU are severe sepsis and septic shock. The mortality of AKI in septic critically ill patients remains high despite our increasing ability to support vital organs. This is partly due to our poor understanding of the pathogenesis of sepsis-induced renal dysfunction. However, new concepts are emerging to explain the pathogenesis of septic AKI, which challenge previously held dogma. Throughout the past half century, septic AKI has essentially been considered secondary to tubular injury, which, in turn, has been considered secondary to renal ischemia. This belief is curious because the hallmark of septic AKI and AKI in general is the loss of glomerular filtration rate (GFR). It would seem logical, therefore, to focus on the glomerulus in trying to understand why such loss of GFR occurs. Recent experimental observations suggest that, at least in the initial phases of septic AKI, profound changes occur which involve glomerular hemodynamics and lead to loss of GFR. These observations imply that changes in the vasoconstrictor tone of both the afferent and efferent arterioles are an important component of the pathogenesis of septic AKI.
急性肾损伤（AKI）是一种严重病症，影响着众多重症监护病房（ICU）患者。ICU中AKI最常见的病因是严重脓毒症和脓毒性休克。尽管我们维持重要器官功能的能力不断提高，但脓毒症危重患者中AKI的死亡率仍然很高。部分原因在于我们对脓毒症诱导的肾功能障碍发病机制了解不足。然而，新的概念正在涌现，以解释脓毒症相关性急性肾损伤的发病机制，这些概念挑战了之前的教条。在过去的半个世纪里，脓毒症相关性急性肾损伤基本上被认为继发于肾小管损伤，而肾小管损伤又被认为继发于肾缺血。这种观点令人费解，因为脓毒症相关性急性肾损伤以及一般急性肾损伤的标志是肾小球滤过率（GFR）的丧失。因此，在试图理解为何会出现这种GFR丧失时，将重点放在肾小球上似乎是合乎逻辑的。最近的实验观察表明，至少在脓毒症相关性急性肾损伤的初始阶段，会发生深刻的变化，这些变化涉及肾小球血流动力学并导致GFR丧失。这些观察结果表明，入球小动脉和出球小动脉血管收缩张力的变化是脓毒症相关性急性肾损伤发病机制的重要组成部分。
