肝肾综合征是肝硬化合并腹水时的常见并发症，绝大多数都是由于血容量不足所致，是功能性的，并无肾脏形态学的异常，有较高的发病率和死亡率，其发病率在住院肝硬化患者中为20%。临床上常用血肌酐作为评价肝硬化患者肾功能的指标，但其具有一定局限性，有可能会遗漏很多潜在的具有临床意义的肾功能不全，特别是当血肌酐升高，但又没有达到肝肾综合征（HRS）诊断标准时。曾有研究报道，轻度急性肾损害即Acute kidney injury，AKI（血肌酐增高超过26.4umol/l（0.3mg/dl））会降低开放性心脏手术患者的生存率。那么轻度的急性肾损害（血肌酐增高超过26.4umol/l（0.3mg/dl）或者比基础值升高50%）是否会影响肝硬化合并有腹水患者的预后呢。为此，来自多伦多大学的Cynthia等人进行了一项研究，研究结果发表在2013年1月的《GUT》上。研究结果表明，轻度急性肾损害会影响肝硬化腹水患者的预后。

　　纳入该研究血的标准是：血肌酐基础值小于110umol/l，且无器质性肾脏疾病的证据的肝硬化合并腹水的患者。每4-6周进行一次血液检查包括血常规、生化、肝功能，每4个月评估一次。最后共有90名患者（平均年龄55.8±0.8岁）完成研究，中位数随访时间为14.05±1.07月。研究结果表明，49名患者AKI至少发作1次，剩下41名从未发生过。这49名患者共发作82次AKI，大多数是因为细菌感染（包括自发性腹膜炎），其次是大量放腹水后未补充适量的白蛋白、大量利尿导致的血流动力学紊乱。这些AKI事件中血肌酐平均高峰值在正常范围内。在随访结束后，有73次AKI治愈，仍有9名患者AKI持续存在，其中2个达到肝肾综合征的诊断标准。研究发现虽然大多数轻度AKI患者都能治愈，随着血肌酐逐渐并且显著的升高，平均动脉压逐渐降低，与非AKI的患者相比，生存率也显著降低。

　　研究结果认为，肝硬化腹水患者AKI与生存率存在临床相关性，并能产生不利的影响。所以我们需要尽所能避免肝硬化腹水患者AKI的发生，并积极的治疗。

　　Acute kidney injury in decompensated cirrhosis

　　Cynthia D Tsien, Rania Rabie, Florence Wong

　　Background Hepatorenal syndrome in cirrhosis with ascites is a well-defined entity with significant morbidity and mortality. It is unclear whether milder degrees of acute kidney injury (AKI), defined as a serum creatinine increase of over 26.4 μmol/l (0.3 mg/dl) or by 50% from baseline, also has a negative impact on patient outcomes. Objectives To determine the prevalence of AKI in cirrhosis with ascites and the impact of AKI on patient outcomes. Design Patients with cirrhosis with ascites and baseline serum creatinine less than 110 μmol/l, and no evidence of structural renal disease, prospectively underwent 4–6-weekly blood work-up for full blood count, biochemistry and liver function. Clinical assessments occurred every 4 months for the development of AKI and other complications. Results 90 patients (mean age 55.8±0.8 years) with a mean follow-up of 14.05±1.07 months were enrolled. 82 episodes of AKI occurred in 49 patients, with the majority of episodes precipitated by a disturbance in systemic haemodynamics. The mean peak serum creatinine of the AKI episodes was within the laboratory's normal range. 73 episodes of AKI resolved; nine did not. There was no clear clinical predictor for the development or resolution of AKI. Despite resolution of most AKI episodes, a gradual and significant increase in serum creatinine and a gradual reduction in mean arterial pressure were observed during follow-up, associated with a significant reduction in survival compared with non-AKI patients. Conclusion Minor increases in serum creatinine are clinically relevant and can adversely affect survival. Every effort should be made to avoid precipitation of AKI in cirrhosis and ascites.