New Developments in Hepatorenal Syndrome.
New Developments in Hepatorenal Syndrome.
复制标题
DOI：
10.1016/j.cgh.2017.05.041
复制
发表时间：
2018-03
期刊：
影响因子：
--
通讯作者：
Pappas SC
中科院分区：
文献类型：
--
作者：
Mindikoglu AL;Pappas SC
肝肾综合征（HRS）仍然是失代偿性肝硬化的主要并发症之一，在没有肝移植的情况下会导致死亡。由于单独使用血清肌酐（Cr）来估计肾小球滤过率（GFR）存在局限性，因此精确评估肝硬化患者的肾功能仍然存在挑战；目前的 GFR 估计模型似乎低估了肾功能障碍。纳入肾脏生物标志物的新模型（例如肝硬化 Cr-胱抑素 C GFR 方程）似乎可以更准确地估计测量的 GFR。基于血清 Cr 动态连续变化的 HRS 诊断标准发生重大变化，将 1 型 HRS 视为急性肾损伤 (AKI) 的一种特殊形式，这使得早期识别肝硬化患者肾功能障碍成为可能。 HRS的诊断标准仍然包括排除其他肾损伤原因。肾脏生物标志物在帮助区分 HRS 与肾前性氮质血症和其他肾脏疾病方面的效果令人失望。血清代谢组学分析可能是评估肾功能障碍的更强大的工具，尽管其实际临床意义仍不清楚。由于评估肝硬化肾功能的困难以及不同的 HRS 诊断标准及其应用的严格性，HRS 的确切发病率和患病率尚不清楚，但 HRS 的发生可能比预期更常见。 HRS 的病理生理学根源在于门静脉高压和内脏血管舒张导致肾血流量 (RBF) 进行性减少。肝硬化患者中进行性、明显的肾皮质缺血与利尿剂敏感性腹水向利尿剂难治性腹水和 HRS 的演变是平行的，HRS 是肝硬化肾功能不全的公认连续体。一氧化二氮（NO）产生的变化，无论是增加还是减少，都可能在这一演变的病理生理学中发挥重要作用。由细菌易位和内毒素血症引发的炎症级联反应，越来越多地被认为在急性或慢性肝衰竭的表现中很重要，也可能在 HRS 的病理生理学中发挥重要作用。主要治疗方法仍然是使用白蛋白进行血管加压治疗，试图逆转内脏血管舒张并改善 RBF。多项荟萃分析证实了升压药（主要是特利加压素和去甲肾上腺素）在改善肾功能和逆转 HRS 1 型方面的价值。其他干预措施，如肾脏替代疗法、经颈静脉肝内门体分流术 (TIPS) 和人工肝支持系统，对改善 HRS 结局的作用非常有限。肝移植仍然是 HRS 的最终治疗方法。在终末期肝病模型时代，随着器官分配政策的变化，同步肝肾移植（SLKT）的频率急剧增加。这导致更迫切需要准确预测单纯肝移植后 HRS 的天然肾脏恢复情况，以避免不必要的 SLKT。
Hepatorenal Syndrome (HRS) continues to be one of the major complications of decompensated cirrhosis leading to death in the absence of liver transplantation. Challenges in precisely evaluating renal function in the patient with cirrhosis remain due to the limitations of serum creatinine (Cr) alone in estimating glomerular filtration rate (GFR); current GFR estimating models appear to underestimate renal dysfunction. Newer models incorporating renal biomarkers, such as the Cr-Cystatin C GFR Equation for Cirrhosis appear to estimate measured GFR more accurately. A major change in the diagnostic criteria for HRS based on dynamic serial changes in serum Cr which regard HRS type 1 as a special form of acute kidney injury (AKI) promises the possibility of earlier identification of renal dysfunction in patients with cirrhosis. The diagnostic criteria of HRS still include the exclusion of other causes of kidney injury. Renal biomarkers have been disappointing in assisting with the differentiation of HRS from pre-renal azotemia and other kidney disorders. Serum metabolomic profiling may be a more powerful tool to assess renal dysfunction although the practical clinical significance of this remains unclear. As a result of the difficulties of assessing renal function in cirrhosis and the varying HRS diagnostic criteria and the rigor with which they are applied, the precise incidence and prevalence of HRS is unknown but it is likely that HRS occurs more commonly than expected. The pathophysiology of HRS is firmly rooted in the setting of progressive reduction in renal blood flow (RBF) as a result of portal hypertension and splanchnic vasodilation. Progressive, marked renal cortical ischemia in patients with cirrhosis parallels the evolution of diuretic-sensitive ascites to diuretic-refractory ascites and HRS, a recognized continuum of renal dysfunction in cirrhosis. Alterations in nitrous oxide (NO) production, both increased and decreased may play a major role in the pathophysiology of this evolution. The inflammatory cascade triggered by bacterial translocation and endotoxemia, increasingly recognized as important in the manifestations of acute on chronic liver failure, may also play a significant role in the pathophysiology of HRS. The mainstay of treatment remains vasopressor therapy with albumin in an attempt to reverse splanchnic vasodilation and improve RBF. Several meta-analyses confirm the value of vasopressors, chiefly terlipressin and noradrenaline, in improving renal function and reversing HRS type 1. Other interventions such as renal replacement therapy, transjugular intrahepatic porto-systemic shunt (TIPS), and artificial liver support systems have a very limited role to improve outcomes in HRS. Liver transplantation remains the definitive treatment for HRS. The frequency of simultaneous liver-kidney transplantation (SLKT) has increased dramatically in the Model for End-stage Liver Disease era, with changes in organ allocation policies. This has resulted in a more urgent need to accurately predict native kidney recovery from HRS after liver transplantation alone, to avoid unnecessary SLKT.
登录
查看更多内容
影响因子：
13.5
作者：
Belcher, Justin M.;Garcia-Tsao, Guadalupe;Sanyal, Arun J.;Bhogal, Harjit;Lim, Joseph K.;Ansari, Naheed;Coca, Steven G.;Parikh, Chirag R.
通讯作者：
Parikh, Chirag R.
影响因子：
29.4
作者：
Boyer, Thomas D.;Sanyal, Arun J.;Pappas, Stephen Chris
通讯作者：
Pappas, Stephen Chris
影响因子：
5.9
作者：
EPSTEIN, M;BERK, DP;MERRILL, JP
通讯作者：
MERRILL, JP
影响因子：
29.4
作者：
Akriviadis, E;Botla, R;Shakil, O
通讯作者：
Shakil, O
影响因子：
4.1
作者：
Cholongitas, Evangelos;Ioannidou, Maria;Akriviadis, Evangelos
通讯作者：
Akriviadis, Evangelos