Department of Intensive Care, Austin Hospital, Melbourne, Victoria, Australia.
Semin Respir Crit Care Med. 2011 Oct;32(5):639-50. doi: 10.1055/s-0031-1287872. Epub 2011 Oct 11.
Acute renal failure (now acute kidney injury) is a common complication of critical illness affecting between 30 and 60% of critically ill patients. The development of a consensus definition (RIFLE--risk, injury, failure, loss, end-stage system) has allowed standardization of reporting and epidemiological work. Multicenter multinational epidemiological studies indicate that sepsis is now the most common cause of acute renal failure in the intensive care unit (ICU) followed by cardiac surgery-associated acute kidney injury. Unfortunately, our understanding of the pathogenesis of acute renal failure in these settings remains limited. Because of such limited understanding, no reproducibly effective therapies have been developed. In addition the diagnosis of acute renal failure still rests upon the detection of changes in serum creatinine, which only occur if more than 50% of glomerular filtration is lost and are often delayed by more than 24 hours. Such diagnostic delays make the implementation of early therapy nearly impossible. In response to these difficulties, there has been a concerted effort to use proteomics to identify novel early biomarkers of acute renal failure. The identification and study of neutrophil gelatinase- associated lipocalin has been an important step in this field. Another area of active interest and investigation relates to the role of intravenous fluid resuscitation and fluid balance. Data from large observational studies and randomized, controlled trials consistently indicate that a positive fluid balance in patients with acute renal failure represents a major independent risk factor for mortality and provides no protection of renal function. The pendulum is clearly swinging away from a fluid-liberal approach to a fluid-conservative approach in these patients. Finally, there is a growing appreciation that acute renal failure may identify patients who are at increased risk of subsequent chronic renal dysfunction and mortality, opening the way to post-ICU interventional trials.
急性肾衰竭（现称急性肾损伤）是危重病的常见并发症，影响 30%至 60%的危重病患者。制定共识定义（RIFLE-风险、损伤、衰竭、丧失和终末期器官系统）使报告和流行病学工作标准化。多中心多国流行病学研究表明，脓毒症是目前 ICU 中急性肾衰竭的最常见原因，其次是心脏手术后相关性急性肾损伤。不幸的是，我们对这些情况下急性肾衰竭的发病机制的理解仍然有限。由于这种有限的理解，尚未开发出可重复有效的治疗方法。此外，急性肾衰竭的诊断仍然依赖于血清肌酐的检测，只有当肾小球滤过率丧失超过 50%时才会发生这种情况，而且通常会延迟超过 24 小时。这种诊断延迟使得早期治疗几乎不可能实现。为了应对这些困难，人们一直在协同努力，利用蛋白质组学来识别急性肾衰竭的新的早期生物标志物。中性粒细胞明胶酶相关脂质运载蛋白的鉴定和研究是该领域的重要一步。另一个活跃的研究领域涉及静脉补液复苏和液体平衡的作用。来自大型观察性研究和随机对照试验的数据一致表明，急性肾衰竭患者的正液体平衡是死亡率的一个主要独立危险因素，并且不能保护肾功能。显然，在这些患者中，从液体自由的方法向液体保守的方法转变。最后，人们越来越认识到急性肾衰竭可能会识别出那些随后发生慢性肾功能障碍和死亡风险增加的患者，为 ICU 后干预试验开辟了道路。
