Hepatorenal综合症

Arshpal Gill, Ra’ed Nassar, Ruby Sangha, Mohammed Abureesh, D. Gurala, Zeeshan Zia, Rachelle Hamadi, S. El‐Sayegh
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摘要

肝肾综合征(HRS)是临床医生在肝硬化存在时需要注意的一个重要条件。简单来说,HRS被定义为在肝硬化患者急性肾损伤(AKI)没有其他竞争病因的情况下,肌酐相对升高,血清肾小球滤过率(GFR)相对下降,同时伴有肾血浆流量(RPF)。它代表在存在严重门静脉高压症、没有肾氮血症、急性肾小管坏死或其他情况下失代偿性肝硬化的终末期并发症。这是一种排斥的诊断。认识到HRS对临床医生至关重要,因为它具有高死亡率,是移植的指征。最近对疾病病理生理学的了解改善了治疗方法,但总体预后仍然很差,I型HRS的平均生存期不到2周。一般来说,肝硬化患者的AKI和肾功能衰竭死亡率非常高,肾功能衰竭和肝硬化患者的死亡率高达60%,占重症监护病房住院患者总死亡率的86.6%。在肝硬化肾功能衰竭的各种病因中,HRS在肝硬化合并急性肾损伤患者中预后较差。HRS继续对诊断构成挑战。AKI可以发生在肾前、肾内或肾后。肾前性病因包括血容量不足、感染、使用血管扩张剂和因肾血流量减少而引起的肾功能衰竭、肾内如肾小球病变、急性肾小管坏死和肾后如梗阻。肝硬化患者易发生肾功能损害。HRS可分为快速进展型1型和缓慢进展型2型。还有其他类型的HRS,但本章将重点关注类型1 HRS和类型2 HRS。HRS被认为是急性肾损伤的功能性病因,因为它明显缺乏肾实质损害。这是急性和慢性肝病患者发生急性肾损伤的几种可能性之一。急性肾损伤(AKI)是肝硬化最严重的并发症之一。高达50%的肝硬化住院患者可发生急性肾损伤,如前所述,住院患者合并肝硬化发生AKI与死亡率增加近3.5倍相关。HRS的定义将在本章中讨论,但它的特点是急性肾损伤的一种形式,发生在晚期肝硬化患者中,导致肾血流量减少,对液体无反应,这发生在门静脉高压和脾脏血管舒张的情况下。本章将讨论HRS的发病率,识别HRS,主要关注HRS I型和II型,识别肝硬化患者肾损害的竞争病因,以及HRS的管理。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hepatorenal Syndrome
Hepatorenal Syndrome (HRS) is an important condition for clinicians to be aware of in the presence of cirrhosis. In simple terms, HRS is defined as a relative rise in creatinine and relative drop in serum glomerular filtration rate (GFR) alongside renal plasma flow (RPF) in the absence of other competing etiologies of acute kidney injury (AKI) in patients with hepatic cirrhosis. It represents the end stage complication of decompensated cirrhosis in the presence of severe portal hypertension, in the absence of prerenal azotemia, acute tubular necrosis or others. It is a diagnosis of exclusion. The recognition of HRS is of paramount importance for clinicians as it carries a high mortality rate and is an indication for transplantation. Recent advances in understanding the pathophysiology of the disease improved treatment approaches, but the overall prognosis remains poor, with Type I HRS having an average survival under 2 weeks. Generally speaking, AKI and renal failure in cirrhotic patients carry a very high mortality rate, with up to 60% mortality rate for patients with renal failure and cirrhosis and 86.6% of overall mortality rates of patients admitted to the intensive care unit. Of the various etiologies of renal failure in cirrhosis, HRS carries a poor prognosis among cirrhotic patients with acute kidney injury. HRS continues to pose a diagnostic challenge. AKI can be either pre-renal, intrarenal or postrenal. Prerenal causes include hypovolemia, infection, use of vasodilators and functional due to decreased blood flow to the kidney, intra-renal such as glomerulopathy, acute tubular necrosis and post-renal such as obstruction. Patients with cirrhosis are susceptible to developing renal impairment. HRS may be classified as Type 1 or rapidly progressive disease, and Type 2 or slowly progressive disease. There are other types of HRS, but this chapter will focus on Type 1 HRS and Type 2 HRS. HRS is considered a functional etiology of acute kidney injury as there is an apparent lack of nephrological parenchymal damage. It is one several possibilities for acute kidney injury in patients with both acute and chronic liver disease. Acute kidney injury (AKI) is one of the most severe complications that could occur with cirrhosis. Up to 50% of hospitalized patients with cirrhosis can suffer from acute kidney injury, and as mentioned earlier an AKI in the presence of cirrhosis in a hospitalized patient has been associated with nearly a 3.5-fold increase in mortality. The definition of HRS will be discussed in this chapter, but it is characterized specifically as a form of acute kidney injury that occurs in patients with advanced liver cirrhosis which results in a reduction in renal blood flow, unresponsive to fluids this occurs in the setting of portal hypertension and splanchnic vasodilation. This chapter will discuss the incidence of HRS, recognizing HRS, focusing mainly on HRS Type I and Type II, recognizing competing etiologies of renal impairment in cirrhotic patients, and the management HRS.
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