Acute Kidney Injury
Acute Kidney Injury
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DOI：
10.1007/978-3-319-11020-2_41
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发表时间：
2015
期刊：
影响因子：
--
通讯作者：
P. Marik
中科院分区：
文献类型：
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作者：
P. Marik
急性肾损伤（正式名称为急性肾衰竭）是ICU中常见的问题。阿基是一种以肾脏排泄功能快速丧失为特征的综合征，通常通过氮代谢终产物（尿素和肌酐）的蓄积或尿量减少或两者兼而有之来诊断[1，2]。虽然血清肌酐（Scr）不是GFR的完美标志物，但它经常被用作估计GFR的替代品。目前，正在研究其他生物标志物作为阿基的更敏感指标（半胱氨酸蛋白酶抑制剂C、IL-18、中性粒细胞明胶酶相关脂质运载蛋白、肾损伤分子1等）。[2，3]。阿基的定义是Scr增加两倍或以上、GFR下降> 50%或尿量<0 mls/kg/h持续12小时[2]。阿基代表了从肾损伤到肾衰竭到肾功能完全丧失的风险范围。步枪标准已用于定义和分类阿基（见表41.1）[4]。在危重患者中阿基通常是肾外损伤的结果，最常见的是败血症、创伤、低血容量性“休克”和横纹肌溶解。脓毒症患者阿基的病理生理学复杂且知之甚少;然而，肾血流量减少似乎不起作用[2]。多达三分之二的ICU患者发生阿基，阿基严重程度的增加与死亡率的增加相关[5]。即使是不需要透析治疗的中度阿基，死亡风险也会增加约5倍[6]。Coca及其同事证明，Scr升高低于步枪分类中使用的水平与短期死亡的两倍风险相关[7]。在这项研究中，Scr增加10- 24%的患者的相对死亡风险为1.8（95% CI，1.3-2.5）。尽管肾脏替代治疗和积极的支持性护理有所改善，但需要透析的患者的死亡率仍超过50%[8]。因此，必须尽一切努力避免这种并发症;即适当的液体复苏和避免使用潜在的肾毒性药物。血管内容量不足和少尿患者的治疗干预选择是液体复苏，而不是呋塞米/Lasix™。然而，正如第一章所讨论的那样。如图9所示，高中心静脉压的过量容量复苏会“矛盾地”损害肾功能（见第10章）。8）。因此，合理的循证液体复苏方法对于降低危重患者肾功能不全的风险至关重要。
Acute kidney injury (formally known as acute renal failure) is a common problem in the ICU. AKI is a syndrome characterized by the rapid loss of the kidney’s excretory function and is typically diagnosed by the accumulation of the end products of nitrogen metabolism (urea and creatinine) or decreased urine output or both [1, 2]. Although serum creatinine (Scr) is not a perfect marker of GFR, it is frequently used as a surrogate to estimate GFR. Currently, additional biomarkers are undergoing investigation as more sensitive indicators of AKI (cystatin C, IL-18, neutrophil gelatinase-associated lipocalin, kidney injury molecule 1, etc.) [2, 3]. AKI is defined as a twofold or greater increase in Scr, a GFR decrease of >50 % or urine output of <0 mls/kg/h for 12 h [2]. AKI represents a spectrum from risk to kidney injury to kidney failure to complete loss of kidney function. The RIFLE criteria have been used to define and classify AKI (see Table 41.1) [4]. In critically ill patients AKI is usually the result of extrarenal insults, most commonly sepsis, trauma, hypovolemic “shock”, and rhabdomyolysis. The pathophysiology of AKI in patients with sepsis is complex and poorly understood; however decreased renal blood flow does not appear to play a role [2]. AKI occurs in up to two-thirds of ICU patients and that increasing severity of AKI is associated with increasing mortality [5]. Even modest degrees of AKI not resulting in dialysis treatment increase the risk of death approximately fivefold [6]. Coca and colleagues demonstrated that elevations of the Scr less than used in the RIFLE classification are associated with a twofold risk of short-term death [7]. In this study patients with a 10–24 % increase in Scr had a relative risk of death of 1.8 (95 % CI, 1.3–2.5). The mortality of patients who require dialysis has remained in excess of 50 % despite improvements in renal-replacement therapy and aggressive supportive care [8]. It is therefore essential that all efforts be made to avoid this complication; i.e. appropriate fluid resuscitation and avoidance of potentially nephrotoxic drugs. The therapeutic intervention of choice in patients with intravascular volume depletion and oliguria is fluid resuscitation and not furosemide/Lasix™. However, as discussed in Chap. 9, excessive volume resuscitation with a high central venous pressure will “paradoxically” impair renal function (see Chap. 8). A rational evidence-based approach to fluid resuscitation is therefore essential to reduce the risk of renal dysfunction in critically ill patients.