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Hepatorenal Syndrome

  • Author: Deepika Devuni, MBBS; Chief Editor: BS Anand, MD  more...
Updated: Jan 13, 2016


Hepatorenal syndrome (HRS) is the development of renal failure in patients with advanced chronic liver disease[1]  and, occasionally, fulminant hepatitis, who have portal hypertension and ascites. Estimates indicate that at least 40% of patients with cirrhosis and ascites will develop HRS during the natural history of their disease.

During the 19th century, Frerichs and Flint made the original description of renal function disturbances in liver disease. They described oliguria in patients with chronic liver disease in the absence of proteinuria and linked the abnormalities in renal function to disturbances present in the systemic circulation. In the 1950s, the clinical description of HRS by Sherlock, Popper, and Vessin emphasized the functional nature of the syndrome, the coexistence of systemic circulatory abnormalities, and its dismal prognosis. Further studies in the following 2 decades demonstrated that renal failure occurred because of vasoconstriction of the renal circulation and intense systemic arteriolar vasodilatation resulting in reduced systemic vascular resistance and arterial hypotension.

In HRS, the histological appearance of the kidneys is normal, and the kidneys often resume normal function following liver transplantation. This makes HRS a unique pathophysiological disorder that provides possibilities for studying the interplay between vasoconstrictor and vasodilator systems on the renal circulation.[2, 3]

Relevant studies include those implicating the renin-angiotensin-aldosterone system (RAAS), the sympathetic nervous system (SNS), and the role of renal prostaglandins (PGs).[4] Strong associations have been reported between spontaneous bacterial peritonitis (SBP) and HRS and the use of vasopressin analogues with volume expanders in the management and prevention of HRS. Although a similar syndrome may occur in acute liver failure, HRS is usually described in the context of chronic liver disease. Despite some encouraging studies of new pharmacological therapies, the development of HRS in people with cirrhosis portends a dismal prognosis because renal failure is usually irreversible unless liver transplantation is performed.[5, 6, 7, 8, 9]

Acute kidney injury (AKI) (increase in serum creatinine by 0.3 mg/dL in less than 48 hour or an increase in serum creatinine by 50% from a stable baseline reading within 3 months) has been proposed to characterize renal dysfunction in patients with cirrhosis, in which type 1 HRS would be reclassified as HRS-AKI.[10] Stage 1 AKI would be classified as an increase in serum creatinine level by 0.3 mg/dL or a 50% increase, whereas stages 2 and 3 AKI would be a doubling and tripling, respectively, of serum creatinine levels.[10]



The hallmark of HRS is renal vasoconstriction, although the pathogenesis is not fully understood. Multiple mechanisms are probably involved and include an interplay between disturbances in systemic hemodynamics, activation of vasoconstrictor systems, and a reduction in the activity of the vasodilator systems. The hemodynamic pattern of patients with HRS is characterized by increased cardiac output, low arterial pressure, and reduced systemic vascular resistance. Renal vasoconstriction occurs in the absence of reduced cardiac output and blood volume, which is in contrast to most clinical conditions associated with renal hypoperfusion.[11, 12, 13]

Although the pattern of increased renal vascular resistance and decreased peripheral resistance is characteristic of HRS, it also occurs in other conditions, such as anaphylaxis and sepsis. Doppler studies of the brachial, middle cerebral, and femoral arteries suggest that extrarenal resistance is increased in patients with HRS, while the splanchnic circulation is responsible for arterial vasodilatation and reduced total systemic vascular resistance.

The RAAS and SNS are the predominant systems responsible for renal vasoconstriction. The activity of both systems is increased in patients with cirrhosis and ascites, and this effect is magnified in HRS. In contrast, an inverse relationship exists between the activity of these 2 systems and renal plasma flow (RPF) and the glomerular filtration rate (GFR). Endothelin is another renal vasoconstrictor present in increased concentration in HRS, although its role in the pathogenesis of this syndrome has yet to be identified.[14] Adenosine is well known for its vasodilator properties, although it acts as a vasoconstrictor in the lungs and kidneys. Elevated levels of adenosine are more common in patients with heightened activity of the RAAS and may work synergistically with angiotensin II to produce renal vasoconstriction in HRS. This effect has also been described with the powerful renal vasoconstrictor, leukotriene E4.

The vasoconstricting effect of these various systems is antagonized by local renal vasodilatory factors, the most important of which are the PGs. Perhaps the strongest evidence supporting their role in renal perfusion is the marked decrease in RPF and the GFR when nonsteroidals, medications known to sharply reduce PG levels, are administered.

Nitric oxide (NO) is another vasodilator believed to play an important role in renal perfusion. Preliminary studies, predominantly from animal experiments, demonstrate that NO production is increased in people with cirrhosis, although NO inhibition does not result in renal vasoconstriction due to a compensatory increase in PG synthesis. However, when both NO and PG production are inhibited, marked renal vasoconstriction develops.

These findings demonstrate that renal vasodilators play a critical role in maintaining renal perfusion, particularly in the presence of an overactivity of renal vasoconstrictors. However, whether vasoconstrictor activity becomes the predominant system in HRS and whether reduction in activity of the vasodilatory system contributes to this have yet to be proven.

Various theories have been proposed to explain the development of HRS in cirrhosis. The 2 main theories are the arterial vasodilation theory and the hepatorenal reflex theory. The former theory not only describes sodium and water retention in cirrhosis, but also may be the most rational hypothesis for the development of HRS. Splanchnic arteriolar vasodilatation in patients with compensated cirrhosis and portal hypertension may be mediated by several factors, the most important of which is probably NO. In the early phases of portal hypertension and compensated cirrhosis, this underfilling of the arterial bed causes a decrease in the effective arterial blood volume and results in homeostatic/reflex activation of the endogenous vasoconstrictor systems.

Activation of the RAAS and SNS occurs early with antidiuretic hormone secretion, a later event when a more marked derangement in circulatory function is present. This results in vasoconstriction not only of the renal vessels, but also in vascular beds of the brain, muscle, spleen, and extremities. The splanchnic circulation is resistant to these effects because of the continuous production of local vasodilators such as NO.

In the early phases of portal hypertension, renal perfusion is maintained within normal or near-normal limits as the vasodilatory systems antagonize the renal effects of the vasoconstrictor systems. However, as liver disease progresses in severity, a critical level of vascular underfilling is achieved. Renal vasodilatory systems are unable to counteract the maximal activation of the endogenous vasoconstrictors and/or intrarenal vasoconstrictors, which leads to uncontrolled renal vasoconstriction. Support for this hypothesis is provided by studies in which the administration of splanchnic vasoconstrictors in combination with volume expanders results in improvement in arterial pressure, RPF, and the GFR.

The alternative theory proposes that renal vasoconstriction in HRS is unrelated to systemic hemodynamics but is due to either a deficiency in the synthesis of a vasodilatory factor or a hepatorenal reflex that leads to renal vasoconstriction. Evidence points to the vasodilation theory as a more tangible explanation for the development of HRS.



Risk factors for developing hepatorenal syndrome (HRS) have been reported based on a large series of patients with cirrhosis and ascites and, for the most part, are related to circulatory and renal function. Three important and easily recognized risk factors are low mean arterial blood pressure (<80 mm Hg), dilutional hyponatremia, and severe urinary sodium retention (urine sodium <5 mEq/L). Interestingly, patients with advanced liver disease, defined by a high Child-Pugh score or worsening parameters of liver function, such as albumin, bilirubin, and prothrombin levels, are not at a higher risk of developing HRS.

In some patients, HRS may occur spontaneously, whereas in others, it may be associated with infections (particularly spontaneous bacterial peritonitis [SBP]), acute alcoholic hepatitis, or large-volume paracentesis without albumin replacement. SBP precipitates type 1 HRS in approximately 20% of patients despite appropriate and timely diagnosis, treatment, and resolution of infection. Large-volume paracentesis without albumin replacement can precipitate type 1 HRS in up to 15% of patients. Although renal failure occurs in up to 10% of cirrhotics with gastrointestinal bleeding, this is usually in the presence of hypovolemic shock, suggesting that renal failure is related to acute tubular necrosis rather than HRS.

The following is a list of risk factors associated with the development of HRS in patients with cirrhosis who are nonazotemic. All measurements were obtained after a minimum of 5 days on a low-salt diet and without diuretics.

  • Low urinary sodium excretion (<5 mEq/L)
  • Low serum sodium (dilutional hyponatremia)
  • Reduced free-water excretion after water load
  • Low mean arterial pressure
  • High plasma renin activity
  • Increased plasma norepinephrine
  • Low plasma osmolality
  • High urine osmolality
  • High serum potassium
  • Previous episodes of ascites
  • Absence of hepatomegaly
  • Presence of esophageal varices
  • Poor nutritional status
  • Moderately increased serum urea (>30 mg/dL)
  • Moderately increased serum creatinine (>1.5 mg/dL)
  • Moderately reduced GFR (<50 mL/min)


United States statistics

Hepatorenal syndrome (HRS) is common, with a reported incidence of 10% among hospitalized patients with cirrhosis and ascites.[15] In decompensated cirrhotics, the probability of developing HRS with ascites ranges between 8-20% per year and increases to 40% at 5 years. An estimated 35-40% of patients with end-stage liver disease (ESLD) and ascites will develop HRS.[13]

International incidence

The incidence of HRS globally is similar to that in the United States.

Race-, sex-, and age-related demographics

People of all races who have chronic liver disease are at risk for HRS.

Frequency is equal in both sexes.

Most patients with chronic liver disease are in their fourth to eighth decades of life.



Type 1 hepatorenal syndrome (HRS) has a median survival of 2 weeks, with few patients surviving more than 10 weeks.[16]  Type 2 HRS has a median survival of 3-6 months.


Physicians need to be aware that 2 different forms of HRS are described.[17]  Although their pathophysiology is similar, their manifestations and outcomes are different.

Type 1 HRS is characterized by rapid and progressive renal impairment and is most commonly precipitated by spontaneous bacterial peritonitis (SBP). Type 1 HRS occurs in approximately 25% of patients with SBP, despite rapid resolution of the infection with antibiotics. Without treatment, the median survival of patients with type 1 HRS is less than 2 weeks, and virtually all patients die within 10 weeks after the onset of renal failure.

Type 2 HRS is characterized by a moderate and stable reduction in the GFR and commonly occurs in patients with relatively preserved hepatic function. These patients are often diuretic-resistant with a median survival of 3-6 months. Although this is markedly longer than type 1 HRS, it is still shorter compared to patients with cirrhosis and ascites who do not have renal failure.


Progressive liver failure, as manifested by worsening encephalopathy, jaundice, and coagulopathy, is a preterminal condition if liver transplantation is not performed. 


Patient Education

Patients who have cirrhosis with ascites must be informed that they are at a risk of developing HRS and they must be informed about the dismal prognosis this carries in the absence of liver transplantation. They should be very cautious when new medications are prescribed by physicians not familiar with their care and must avoid known nephrotoxic agents such as nonsteroidals and aminoglycosides. Any deterioration in their clinical condition should result in a prompt call to their physician to determine if they have developed HRS.

For patient education resources, see Infections Center and Digestive Disorders Center, as well as Cirrhosis and Liver Transplant.

Contributor Information and Disclosures

Deepika Devuni, MBBS Resident Physician, Department of Internal Medicine, University Of Connecticut School of Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Received salary from Medscape for employment. for: Medscape.

Chief Editor

BS Anand, MD Professor, Department of Internal Medicine, Division of Gastroenterology, Baylor College of Medicine

BS Anand, MD is a member of the following medical societies: American Association for the Study of Liver Diseases, American College of Gastroenterology, American Gastroenterological Association, American Society for Gastrointestinal Endoscopy

Disclosure: Nothing to disclose.

Additional Contributors

Ann Ouyang, MBBS Professor, Department of Internal Medicine, Pennsylvania State University College of Medicine; Attending Physician, Division of Gastroenterology and Hepatology, Milton S Hershey Medical Center

Disclosure: Nothing to disclose.


Sandeep Mukherjee, MB, BCh, MPH, FRCPC Associate Professor, Department of Internal Medicine, Section of Gastroenterology and Hepatology, University of Nebraska Medical Center; Consulting Staff, Section of Gastroenterology and Hepatology, Veteran Affairs Medical Center

Sandeep Mukherjee, MB, BCh, MPH, FRCPC is a member of the following medical societies: Royal College of Physicians and Surgeons of Canada

Disclosure: Merck Honoraria Speaking and teaching; Ikaria Pharmaceuticals Honoraria Board membership

Hemant K Roy, MD Associate Professor of Medicine, Section of Gastroenterology, Feinberg School of Medicine at Northwestern University, Evanston-Northwestern Healthcare

Disclosure: Nothing to disclose.

Rowen K Zetterman, MD Director, Faculty Mentoring Programs, University of Nebraska Medical Center; Dean Emeritus, Creighton University School of Medicine

Rowen K Zetterman, MD, is a member of the following medical societies: Alpha Omega Alpha, American Association for the Study of Liver Diseases, American College of Gastroenterology, American College of Physicians, and American Medical Association

Disclosure: Nothing to disclose.

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