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　　肝腎綜合征是肝硬化合并腹水時的常見并發(fā)癥，絕大多數(shù)都是由于血容量不足所致，是功能性的，并無腎臟形態(tài)學的異常，有較高的發(fā)病率和死亡率，其發(fā)病率在住院肝硬化患者中為20%。臨床上常用血肌酐作為評價肝硬化患者腎功能的指標，但其具有一定局限性，有可能會遺漏很多潛在的具有臨床意義的腎功能不全，特別是當血肌酐升高，但又沒有達到肝腎綜合征（HRS）診斷標準時。曾有研究報道，輕度急性腎損害即Acute kidney injury，AKI（血肌酐增高超過26.4umol/l（0.3mg/dl））會降低開放性心臟手術患者的生存率。那么輕度的急性腎損害（血肌酐增高超過26.4umol/l（0.3mg/dl）或者比基礎值升高50%）是否會影響肝硬化合并有腹水患者的預后呢。為此，來自多倫多大學的Cynthia等人進行了一項研究，研究結果發(fā)表在2013年1月的《GUT》上。研究結果表明，輕度急性腎損害會影響肝硬化腹水患者的預后。

　　納入該研究血的標準是：血肌酐基礎值小于110umol/l，且無器質性腎臟疾病的證據(jù)的肝硬化合并腹水的患者。每4-6周進行一次血液檢查包括血常規(guī)、生化、肝功能，每4個月評估一次。最后共有90名患者（平均年齡55.8±0.8歲）完成研究，中位數(shù)隨訪時間為14.05±1.07月。研究結果表明，49名患者AKI至少發(fā)作1次，剩下41名從未發(fā)生過。這49名患者共發(fā)作82次AKI，大多數(shù)是因為細菌感染（包括自發(fā)性腹膜炎），其次是大量放腹水后未補充適量的白蛋白、大量利尿導致的血流動力學紊亂。這些AKI事件中血肌酐平均高峰值在正常范圍內。在隨訪結束后，有73次AKI治愈，仍有9名患者AKI持續(xù)存在，其中2個達到肝腎綜合征的診斷標準。研究發(fā)現(xiàn)雖然大多數(shù)輕度AKI患者都能治愈，隨著血肌酐逐漸并且顯著的升高，平均動脈壓逐漸降低，與非AKI的患者相比，生存率也顯著降低。

　　研究結果認為，肝硬化腹水患者AKI與生存率存在臨床相關性，并能產生不利的影響。所以我們需要盡所能避免肝硬化腹水患者AKI的發(fā)生，并積極的治療。

　　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.