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Hepatorenal Syndrome CJASN ePress. Published on April 17, 2019 as doi: 10.2215/CJN.12451018 Hepatorenal Syndrome Claire Francoz,1,2 Franc¸ois Durand,1,2 Jeffrey A. Kahn,3 Yuri S. Genyk,4 and Mitra K. Nadim5 Abstract Hepatorenal syndrome is a severe complication of end-stage cirrhosis characterized by increased splanchnic blood flow, hyperdynamic state, a state of decreased central volume, activation of vasoconstrictor systems, and extreme kidney vasoconstriction leading to decreased GFR. The contribution of systemic inflammation, a key feature of cirrhosis, in the development of hepatorenal syndrome has been highlighted in recent years. 1Hepatology and Liver The mechanisms by which systemic inflammation precipitates kidney circulatory changes during hepatorenal Intensive Care Unit, syndrome need to be clarified. Early diagnosis is central in the management and recent changes in the definition of Hospital Beaujon, hepatorenal syndrome help identify patients at an earlier stage. Vasoconstrictive agents (terlipressin in particular) Clichy, France; 2INSERM U1149, and albumin are the first-line treatment option. Several controlled studies proved that terlipressin is effective University Paris at reversing hepatorenal syndrome and may improve short-term survival. Not all patients are responders, and even Diderot, Paris, France; in responders, early mortality rates are very high in the absence of liver transplantation. Liver transplantation is and 3Division of the only curative treatment of hepatorenal syndrome. In the long term, patients transplanted with hepatorenal Gastrointestinal and Liver Disease, syndrome tend to have lower GFR compared with patients without hepatorenal syndrome. Differentiating Department of hepatorenal syndrome from acute tubular necrosis (ATN) is often a challenging yet important step because Medicine, 4Division of vasoconstrictors are not justified for the treatment of ATN. Hepatorenal syndrome and ATN may be considered Hepatobiliary, as a continuum rather than distinct entities. Emerging biomarkers may help differentiate these two conditions Pancreas, and and provide prognostic information on kidney recovery after liver transplantation, and potentially affect the Abdominal Organ Transplant, decision for simultaneous liver–kidney transplantation. Department of Clin J Am Soc Nephrol 14: ccc–ccc, 2019. doi: https://doi.org/10.2215/CJN.12451018 Surgery, and 5Division of Nephrology and Hypertension, Department of Introduction will focus on the definitions, mechanisms, and man- Medicine, Keck Advanced cirrhosis is a condition characterized by agement of hepatorenal syndrome. School of Medicine, impaired liver function, portal hypertension, in- University of Southern creased splanchnic blood volume, hyperdynamic Definition of Hepatorenal Syndrome and California, Los Angeles, California state with increased cardiac output, systemic vasodi- AKI in Cirrhosis latation, a state of decreased central blood volume, The definition of AKI in cirrhosis has undergone fl fi Correspondence: and systemic in ammatory response. AKI is one of signi cant changes over the past several years. The Dr. Mitra K. Nadim, the most severe complications of cirrhosis, occurring common theme among the definitions is use of relative Division of in up to 50% of hospitalized patients, and has been changes in serum creatinine instead of absolute cut- Nephrology and associated with higher mortality, which increases offs (e.g., .1.5 mg/dl) and identifying patients at Hypertension, Department of with severity of AKI (1). Hepatorenal syndrome is highest risk for short- and long-term mortality on the Medicine, University of one of the phenotypes of AKI that occurs in patients basis of the escalating stages within each criterion (3,4). Southern California, with advanced cirrhosis and is characterized by In 2012, the Acute Dialysis Quality Initiative (ADQI) 1520 San Pablo Street, decreased kidney blood flow that is unresponsive to recommended adaptation of the AKI Network serum Suite 4300, Los volume expansion. Hepatorenal syndrome is asso- creatinine criteria to define AKI in this patient pop- Angeles, CA 90033. fi Email: mitra.nadim@ ciated with signi cant health care resource utiliza- ulation (3). These criteria were irrespective of the cause med.usc.edu tion, with an estimated annual total direct medical of AKI and as such, hepatorenal syndrome type 1 was cost in the United States of approximately $4 billion categorized as a specific type of AKI and hepatorenal dollars (2). Refinements in the definitions have helped syndrome type 2 was categorized as a form of CKD. in the diagnosis of hepatorenal syndrome at an earlier The International Club of Ascites (ICA) further mod- stage during the course of cirrhosis. Recent advances in ified the definition of AKI on the basis of the Kidney our understanding of the pathophysiology of hepa- Disease Improving Global Outcomes serum creati- torenal syndrome suggest the involvement of systemic nine criteria, using a baseline serum creatinine within inflammation and circulatory changes in the kidney the previous 3 months (1,4). Although oliguria is not in parallel with systemic and splanchnic circulatory included in the current definition of AKI in patients changes. Although treatment of hepatorenal syn- with cirrhosis, urine output has been found to be a dromewiththeuseofvasoconstrictiveagentsin sensitive and early marker for AKI in critically ill combination with albumin has improved outcomes, patients with cirrhosis and is associated with adverse prognosis remains poor without liver transplanta- outcomes (5). Therefore, regardless of any rise in serum tion. This review, using the most recent literature, creatinine, decrease in urine output or development www.cjasn.org Vol 14 May, 2019 Copyright © 2019 by the American Society of Nephrology 1 2 Clinical Journal of the American Society of Nephrology of anuria should be considered as AKI in patients with In early stages of the disease, splanchnic vasodilation is cirrhosis until proven otherwise. moderate and reduced systemic vascular resistance is balanced Changes in the definition of AKI in patients with cirrhosis by increased cardiac output. In advanced stages, vasodilation has led to changes in the definition of hepatorenal syndrome is more pronounced because of increased synthesis of such that the cut-off value of serum creatinine was removed vasodilator factors, and cannot be balanced by the increase and replaced with ICA AKI criteria, allowing for earlier in cardiac output (Figure 1) (7). As a result, there is an effective diagnosis and treatment of patients with hepatorenal syn- arterial hypovolemia as a consequence of the disparity drome (4). A major limitation of the hepatorenal syndrome between the intravascular blood volume and the mark- criteria is that it does not allow for the coexistence of other edly dilated arterial circulation. Cirrhotic cardiomyopathy forms of acute or CKD, such as underlying diabetic ne- is a condition combining diastolic dysfunction, blunted phropathy or glomerular diseases often associated in patients increase in cardiac output after stimulations, and electro- with liver disease. Patients with underlying kidney disease mechanical abnormalities (7). Inflammatory response dur- can still develop “hepatorenal physiology”; thus the term ing cirrhosis with increased circulating levels of TNF-a may “hepatorenal disorders” has been proposed by ADQI to contribute to blunted cardiac response (8). In advanced stages describe all patients with advanced cirrhosis and concurrent of cirrhosis with ascites, decreased cardiac output seems to kidney dysfunction, which would allow these patients to be precede the occurrence of hepatorenal syndrome (9). De- properly classified and treated while maintaining the term creased cardiac output may precipitate the decline in kidney hepatorenal syndrome (3). blood flow. Eventually, changes in hemodynamics in the kidney and altered autoregulation of kidney blood flow contribute to decreased GFR. Pathogenesis of Hepatorenal Syndrome To maintain arterial pressure, systemic vasoconstrictor Cirrhosis is characterized by reduced systemic vascu- systems (the renin-angiotensin-aldosterone system, sym- lar resistance due to splanchnic arterial vasodilation (6). pathetic nervous system, and arginine vasopressin) are A B Cirrhosis and Portal Hypertension Advanced Cirrhosis and Portal Hypertension Vasodilation theory Inflammatory theory Vasodilation theory Inflammatory theory Bleeding or any other cause reducing effective volemia (diuretics, lactulose- induceddiarrhea) Splanchnic vasodilation Splanchnic vasodilation +++ Bacterial translocation Bacterial translocation +++ Effective hypovolemia Effective hypovolemia Infection Activation of Activation of Proinflammatory Proinflammatory vasoconstriction systems vasoconstriction systems cytokines cytokines +++ RAAS, SNS, AVP RAAS, SNS, AVP Cirrhotic cardiomyopathy Non-selective beta-blockers? Arterial vasoconstriction +++, Arterial vasoconstriction, Compensatory increase Insufficient increase inflammation, microvascular changes +++ inflammation, and microvascular in cardiac output in cardiac output and impaired autoregulation changes in the kidney High cardiac output Normal or low cardiac output Ascites Ascites Increased kidney susceptibility to ischemia but normal GFR Decreased GFR, AKI Figure 1. | Mechanisms involved in AKI in decompensated cirrhosis. (A) In decompensated cirrhosis, both vasodilation secondary to portal hypertension and systemic inflammation induced by gut bacterial translocation tend to induce
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