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Hepatorenal Syndrome Treatment & Management

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

Approach Considerations

Every attempt should be made to establish a precipitating cause of hepatorenal syndrome (HRS). This is particularly true for type 1 HRS, which rarely occurs spontaneously and may be associated with spontaneous bacterial peritonitis (SBP) in 25% of cases. If renal function does not improve after institution of third-generation cephalosporins for SBP, a follow-up diagnostic paracentesis is recommended 48 hours later.

Patients with HRS should be evaluated for liver transplantation, at a liver transplant center if possible. This may be more applicable for patients with type 2 HRS, who have a longer survival time, as opposed to patients with type 1 HRS, whose survival is extremely short and who may require alternative therapeutic methods (eg, TIPS, vasoconstrictors) as a bridge to transplantation.

Reasons for transferring patients to a liver transplant center include the following:

  • Assessment of candidacy for liver transplantation
  • Lack of facilities for performing dialysis at local/referring hospital
  • Entrance into study/treatment protocol for HRS at referral center

If patients are not candidates for liver transplantation, they have a poor prognosis and outpatient care will only be palliative in nature.

Guidelines from the British Society of Gastroenterology, the European Association for the Study of the Liver (EASL) and the American Association for the Study of Liver Diseases (AASLD) recommend cefotaxime as the antibiotic of choice for SBP and large-volume paracentesis for the management of ascites greater than 5 L in volume.[18] For HRS, cautious diuresis, volume expansion with albumin and the use of vasoactive drugs are recommended.



Medical Care

The ideal treatment of HRS is liver transplantation; however, because of the long waiting lists in the majority of transplant centers, most patients die before transplantation. An urgent need exists for effective alternative therapies to increase survival chances for patients with HRS until transplantation can be performed. This is reinforced by a study that reported that patients successfully treated medically for HRS before liver transplantation had posttransplantation outcome and survival comparable to that of patients who underwent transplantation without being treated for HRS. Interventions that have shown some promise are drugs with vasoconstrictor effects in the splanchnic circulation and the use of the transjugular intrahepatic portosystemic shunt (TIPS).


Numerous medications have been used to treat HRS with little, if any, effect. The pharmacologic approach has shifted, however, with greater attention now focused on the role of vasoconstrictors as opposed to the initial predominant use of vasodilators. The rationale for this change is that the initial event in HRS is vasodilatation of the splanchnic circulation and use of a vasoconstrictor may thus prevent homeostatic activation of endogenous vasoconstrictors. Promising results have been reported in small studies and case reports with agonists of vasopressin V1 receptors, such as ornipressin and terlipressin, which predominantly act on the splanchnic circulation.[21, 22, 23, 24, 25]

Although only a few controlled trials have been conducted in this arena, the results so far are encouraging and suggest an increasing role for medical therapy, given the current shortage of the donor pool in the face of an ever-increasing demand for organs.


Low-dose dopamine (2-5 mcg/kg/min) is frequently prescribed to patients with renal failure in the hope that its vasodilatory properties may improve renal blood flow. Little evidence exists to support this practice; a placebo-controlled randomized trial by Bellomo and colleagues did not demonstrate any role for low-dose dopamine in early renal dysfunction.[26] Five studies have evaluated the role of dopamine in HRS, and none have reported significant changes in RPF, GFR, or urine output.

These studies are limited by small sample size and lack of a control arm. Nonetheless, they demonstrate that dopamine administration in patients with cirrhosis, with or without HRS, does not improve renal function.


Misoprostol is a synthetic analogue of PG E1, whose use in HRS was based on the observation that these patients had low urinary levels of vasodilatory PGs.

Five studies have assessed the role of either parenteral or oral misoprostol in HRS. None of these studies demonstrated an improvement in the GFR, sodium excretion, or renal function in patients with HRS. Although Fevery et al demonstrated reversal of HRS in 4 patients, these patients also received large doses of colloids.[27] The likely scenario is that the massive administration of fluids played a predominant role here because Gines et al were unable to reproduce these findings with misoprostol alone.[28]

Renal vasoconstrictor antagonists

Saralasin, an antagonist of angiotensin II receptors, was used first in 1979 in an attempt to reverse renal vasoconstriction. Because this drug inhibited the homeostatic response to hypotension commonly observed in patients with cirrhosis, it led to worsening hypotension and deterioration in renal function. Poor results were also observed with phentolamine, an alpha-adrenergic antagonist, highlighting the importance of the SNS in maintaining renal hemodynamics in patients with HRS.

A case series by Soper et al reported an improvement in the GFR in 3 patients with cirrhosis, ascites, and HRS who received an antagonist of endothelin A receptor (BQ123).[29] All 3 patients showed a dose-response improvement in inulin and para-aminohippurate excretion, RPF, and the GFR in the absence of changes in systemic hemodynamics. These 3 patients were not candidates for liver transplantation and subsequently died. More work is needed to explore this therapeutic approach as a possible bridge to transplantation for patients with HRS.

Systemic vasoconstrictors

These medications have shown promise for the treatment of HRS; they include vasopressin analogues (ornipressin, terlipressin), somatostatin analogues (octreotide), and alpha-adrenergic agonists (midodrine).[30]

In 1956, Hecker and Sherlock used norepinephrine to treat patients with cirrhosis who had HRS; they were the first to describe an improvement in arterial pressure and urine output. However, no improvement was observed in the biochemical parameters of renal function, and all patients subsequently died.

Octapressin, a synthetic vasopressin analogue, was first used in 1970 to treat type 1 HRS. RPF and the GFR improved in all patients, all of whom subsequently died from sepsis, gastrointestinal bleeding, and liver failure. Because of these discouraging results, the use of alternate vasopressin analogues, particularly ornipressin, attracted attention. Three important studies by Lenz and colleagues demonstrated that short-term use of ornipressin resulted in an improvement in circulatory function and a significant increase in RPF and the GFR.[31, 32, 33]

The combination of ornipressin and albumin was subsequently tried by Guevera in patients with HRS.[34, 35] This was based on data suggesting that the combination of plasma volume expansion and vasoconstrictors normalized renal sodium and water handling in patients who have cirrhosis with ascites. In this important paper, 8 patients were originally to be treated for 15 days with ornipressin and albumin. Treatment had to be discontinued in 4 patients after fewer than 9 days because of complications from ornipressin use that included ischemic colitis, tongue ischemia, and glossitis. Although a marked improvement in the serum creatinine level was observed during treatment, renal function deteriorated upon treatment withdrawal. In the remaining 4 patients, the improvement in RPF and the GFR was significant and was associated with a reduction in serum creatinine levels. These patients subsequently died, but no recurrence of HRS was observed.

Due to the high incidence of severe adverse effects with ornipressin, the same investigators used another vasopressin analogue with fewer adverse effects, namely terlipressin. In this study, 9 patients were treated with terlipressin and albumin for 5-15 days. This was associated with a marked reduction in serum creatinine levels and improvement in mean arterial pressure. Reversal of HRS was noted in 7 of 9 patients, and HRS did not recur when treatment was discontinued. No adverse ischemic effects were reported, and, according to this study, terlipressin with albumin is a safe and effective treatment of HRS.

Since this early study, terlipressin has become the most studied vasopressin analogue in HRS. When used in conjunction with albumin, improvement in GFR and reduction in serum creatinine levels to below 1.5 mg/dL occur in 60-75% of patients with type 1 HRS. This may take several days, and although recurrent HRS after treatment discontinuation is uncommon (< 15%), a repeat course of terlipressin with albumin is usually effective. Ischemic complications are also rare (< 5%), but one limitation of terlipressin is its unavailability in many countries, including the United States. Under these circumstances, such agents as octreotide, albumin, and alpha-adrenergic agonists may be considered.[36]

Gluud et al reviewed 10 randomized studies to determine whether vasoconstrictor drugs reduce mortality in patients with type 1 or type 2 HRS.[37] The trials, on a total of 376 patients, investigated outcomes of HRS treatments using terlipressin alone or with albumin, using octreotide plus albumin, or using noradrenalin plus albumin. In their analysis, Gluud and colleagues found that administration of terlipressin plus albumin may lead to short-term mortality reduction in patients with type 1 HRS, but the authors saw no such reduction in patients with the type 2 form of the disease. Trials using octreotide and noradrenaline therapies were small and indicated neither harmful nor beneficial effects from these treatments. The authors advised that the response duration from terlipressin therapy be taken into account when treatment and the timing of liver transplantation are considered for patients with type 1 HRS.

In a randomized controlled trial that compared the effectiveness of terlipressin plus albumin versus midodrine and octreotide plus albumin in the treatment of HRS in 27 patients, Cavallin and colleagues found a significantly higher rate of improvement in renal function with telipressin plus albumin compared to midodrine/octreotide plus albumin.[38]

Angeli et al showed that long-term administration of midodrine (an alpha-adrenergic agonist) and octreotide improved renal function in 8 patients with type 1 HRS.[39] All patients also received albumin, and this approach was compared to dopamine at nonpressor doses. Not surprisingly, none of the patients treated with dopamine showed any improvement in renal function, but all 8 patients treated with midodrine, octreotide, and volume expansion had improvement in renal function. No adverse effects were reported in these patients. A study of 14 patients by Wong et al reported improvement in renal function in 10 patients. Three of these patients subsequently underwent liver transplantation.[40]

These studies demonstrate several important points. First, vasoconstrictors play an important role in the treatment of HRS, but further work is needed to identify the ideal agent and to determine if the addition of albumin is necessary. Another important conclusion of these studies is that patients may maintain relatively preserved renal function once therapy is discontinued. This suggests that if the precipitating factor, such as spontaneous bacterial peritonitis (SBP), is not readily identified, an irreversible decline in renal function ensues.

N-acetylcysteine (NAC): In 1999, the Royal Free group reported their experience with NAC for the treatment of HRS. This was based on experimental models of acute cholestasis, in which administration of NAC resulted in an improvement in renal function. Twelve patients with HRS were treated with intravenous NAC, without any adverse effects, and the survival rates were 67% and 58% at 1 month and 3 months, respectively (this included 2 patients who received liver transplantation after improvement in renal function). The mechanism of action remains unknown, but this interesting study encourages further optimism for medical treatment of a condition that once carried a hopeless prognosis in the absence of liver transplantation. Controlled studies with longer follow-up may help answer these pressing questions.

Dietary considerations

Institute a low-salt (2 g) diet. Do not restrict protein intake unless patient has severe encephalopathy.


Surgical Care

Peritoneovenous shunting

Peritoneovenous shunting (PVS) seems attractive in theory because it leads to plasma volume expansion and improvement of circulatory function. However, very few studies evaluating the role of PVS in this area have been performed because PVS has been used predominantly for treating refractory ascites.

This may be important for patients with type 2 hepatorenal syndrome (HRS), who often develop refractory ascites, are not candidates for orthotopic liver transplantation, and do not tolerate frequent LVPs.

PVS has no role in type 1 HRS.

Surgical shunts

No description on the treatment of HRS is complete without a brief review of the role of portacaval shunts, particularly with the introduction of TIPS.

Despite the theoretical benefit of improving portal hypertension and thus HRS with a portosystemic shunt, only a few scattered case reports have shown some benefit.

Currently, no indication exists for portacaval shunts in this setting.

Liver transplantation

Liver transplantation is the ideal treatment of HRS,[13] but it is limited by the availability of donors.

In a matched-pair study by Goldaracena et al, living (LDLT) and deceased donor liver transplantation (DDLT) led to comparable long-term outcomes in patients with HRS.[41] The investigators evaluated outcomes between 30 patients with HRS who received LDLT and 90 patients with HRS who received a full-graft DDLT. They did not identify any differences in graft survival and patient survival at 1, 3, and 5 years, and the incidence of postsurgical chronic kidney disease was similar between the two groups.[41]

Patients with HRS have a higher risk of postoperative morbidity, early mortality, and longer hospitalization. Gonwa et al reported that at least one third of patients require hemodialysis postoperatively, with a smaller percentage (5%) requiring long-term hemodialysis.[42]

Because renal dysfunction is common in the first few days following transplantation, avoiding nephrotoxic immunosuppressants generally is recommended until recovery of renal function. However, the GFR gradually improves and reaches an average of 40-50 mL/min by the sixth postoperative week. The systemic and neurohumoral abnormalities associated with HRS also resolve in the first postoperative month.

Long-term survival rates are excellent, with the survival rate at 3 years approaching approximately 60%. This is only slightly lower than the 70-80% survival rate of transplant recipients without HRS and is markedly better than the survival rate of patients with HRS not receiving transplants, which is virtually 0% at 3 years.




The importance of a nephrologist in the multidisciplinary management of patients with hepatorenal syndrome (HRS) cannot be overemphasized. Nephrologists play a critical role in assisting hepatologists and liver transplant surgeons in the management of these critically ill patients.

No controlled studies evaluating the role of dialysis in this setting have been performed, but most centers dialyze patients with HRS who are on a waiting list.

Continuous arteriovenous or venovenous hemofiltration has also been used, but the efficacy of these 2 measures has yet to be determined.

Variations of hemodialysis include the molecular adsorbent recirculating system.[9] This is a modified dialysis method that uses an albumin-containing dialysate that is recirculated and perfused online through charcoal- and anion-exchanger columns. A prospective, randomized, controlled trial showed improvement of type 1 HRS with this method, although long-term survival remained very poor, with survival of more than 1 month in only 1 of 8 patients in the treatment arm.

If transplantation is not available, hemodialysis probably will continue to be performed for patients on the waiting list.

Interventional radiologist

The use of TIPS in the treatment of HRS has yet to be established. Due to its ability to reduce portal hypertension in patients with variceal bleeding and refractory ascites, its role in HRS initially seemed logical, particularly in view of isolated reports of renal function improvement following surgical shunts in the 1970s. However, TIPS quickly fell out of favor because of high morbidity and mortality rates.

Small, uncontrolled studies indicate that TIPS may improve RPF and the GFR and reduce the activity of the RAAS and SNS in patients who have cirrhosis with types 1 and 2 HRS. Improvement in renal function is usually slow and occurs in approximately 60% of patients. However, the effects on renal function can be variable, and some patients fare worse. As a result, the role of TIPS in the treatment of HRS remains investigational because of the lack of prospective studies and the known risks of the procedure.



The main precipitating factor of type 1 HRS is spontaneous bacterial peritonitis (SBP). When this develops in patients with type 2 HRS, the probability of developing type 1 HRS is very high. This may be prevented by antibiotic prophylaxis with Bactrim or fluoroquinolones in patients with a prior history of SBP. Alternatively, patients with type 2 HRS who are on the waiting list may benefit from prophylactic antibiotics, irrespective of whether they have a prior history of SBP.

A randomized controlled trial has shown that the incidence of SBP-related renal failure is reduced if these patients are treated with antibiotics and undergo plasma volume expansion with albumin (1.5 g/kg upon diagnosis and 1 g/kg 48 h later). The incidence of HRS in patients with SBP who received albumin together with antibiotic therapy was 10% compared with an incidence of 33% in patients who did not receive albumin; in addition, hospital mortality rates were also lower in patients who received albumin expansion.

LVP is considered another risk factor for the development of HRS, which may be prevented by the administration of albumin.

Patients who have cirrhosis with ascites have a 10% chance of developing HRS at 1 year and a 40% chance at 5 years. One alternative to treatment aimed at preventing HRS is performing liver transplantation in these patients before HRS develops, particularly because risk factors for the development of HRS have been identified. With the current donor shortage, this does not seem to be a realistic possibility.

In patients with acute alcoholic hepatitis, one study reported that the administration of pentoxifylline (400 mg tid for 28 d) reduced the incidence of HRS and mortality rates (8% and 24%, respectively) compared with a placebo group (35% and 46%, respectively). However, no long-term data exist on renal function or mortality rates in these patients.

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.

  1. Betrosian AP, Agarwal B, Douzinas EE. Acute renal dysfunction in liver diseases. World J Gastroenterol. 2007 Nov 14. 13(42):5552-9. [Medline].

  2. Arroyo V. The liver and the kidney: mutual clearance or mixed intoxication. Contrib Nephrol. 2007. 156:17-23. [Medline].

  3. Lau C, Martin P, Bunnapradist S. Management of renal dysfunction in patients receiving a liver transplant. Clin Liver Dis. 2011 Nov. 15(4):807-20. [Medline].

  4. Zusman RM, Axelrod L, Tolkoff-Rubin N. The treatment of the hepatorenal syndrome with intra-renal administration of prostaglandin E1. Prostaglandins. 1977 May. 13(5):819-30. [Medline].

  5. Fernández J, Navasa M, Planas R, Montoliu S, Monfort D, Soriano G, et al. Primary prophylaxis of spontaneous bacterial peritonitis delays hepatorenal syndrome and improves survival in cirrhosis. Gastroenterology. 2007 Sep. 133(3):818-24. [Medline].

  6. Moreau R, Lebrec D. Diagnosis and treatment of acute renal failure in patients with cirrhosis. Best Pract Res Clin Gastroenterol. 2007. 21(1):111-23. [Medline].

  7. Portal AJ, Austin M, Heneghan MA. Novel approaches to assessing renal function in cirrhotic liver disease. Hepatol Res. 2007 Sep. 37(9):667-72. [Medline].

  8. Salerno F, Gerbes A, Gines P, Wong F, Arroyo V. Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. Gut. 2007 Sep. 56(9):1310-8. [Medline].

  9. Wing F, Raina N, Richardson R. Molecular adsorbent recirculating system is ineffective in the management of type 1 hepatorenal syndrome in cirrhotic patients with ascites who have failed vasoconstrictor therapy. Gut. 2009 Aug 25. [Medline].

  10. Wong F. The evolving concept of acute kidney injury in patients with cirrhosis. Nat Rev Gastroenterol Hepatol. 2015 Dec. 12 (12):711-9. [Medline].

  11. Arroyo V, Terra C, Ginès P. Advances in the pathogenesis and treatment of type-1 and type-2 hepatorenal syndrome. J Hepatol. 2007 May. 46(5):935-46. [Medline].

  12. Turban S, Thuluvath PJ, Atta MG. Hepatorenal syndrome. World J Gastroenterol. 2007 Aug 14. 13(30):4046-55. [Medline].

  13. Al-Khafaji A, Nadim MK, Kellum JA. Hepatorenal Disorders. Chest. 2015 Aug. 148 (2):550-8. [Medline].

  14. Wong F, Moore K, Dingemanse J, Jalan R. Lack of renal improvement with nonselective endothelin antagonism with tezosentan in type 2 hepatorenal syndrome. Hepatology. 2008 Jan. 47(1):160-8. [Medline].

  15. Bittencourt PL, de Carvalho GC, de Andrade Regis C, Kalil JR, Cerqueira LA, Barbosa DS, et al. Causes of renal failure in patients with decompensated cirrhosis and its impact in hospital mortality. Ann Hepatol. 2012 Jan. 11(1):90-5. [Medline].

  16. Appenrodt B, Zielinski J, Brensing KA, Heller J, Sauerbruch T, Schepke M. Degree of hepatic dysfunction and improvement of renal function predict survival in patients with HRS type I: a retrospective analysis. Eur J Gastroenterol Hepatol. 2009 Sep 29. [Medline].

  17. Angeli P, Morando F, Cavallin M, Piano S. Hepatorenal syndrome. Contrib Nephrol. 2011. 174:46-55. [Medline].

  18. Pericleous M, Sarnowski A, Moore A, Fijten R, Zaman M. The clinical management of abdominal ascites, spontaneous bacterial peritonitis and hepatorenal syndrome: a review of current guidelines and recommendations. Eur J Gastroenterol Hepatol. 2015 Dec 14. [Medline].

  19. Schepke M. Hepatorenal syndrome: current diagnostic and therapeutic concepts. Nephrol Dial Transplant. 2007 Sep. 22 Suppl 8:viii2-viii4. [Medline].

  20. Kumar A, Anel R, Bunnell E, Habet K, Zanotti S, Marshall S, et al. Pulmonary artery occlusion pressure and central venous pressure fail to predict ventricular filling volume, cardiac performance, or the response to volume infusion in normal subjects. Crit Care Med. 2004 Mar. 32(3):691-9. [Medline].

  21. Alessandria C, Ottobrelli A, Debernardi-Venon W, Todros L, Cerenzia MT, Martini S, et al. Noradrenalin vs terlipressin in patients with hepatorenal syndrome: a prospective, randomized, unblinded, pilot study. J Hepatol. 2007 Oct. 47(4):499-505. [Medline].

  22. Testro AG, Wongseelashote S, Angus PW, Gow PJ. Long-term outcome of patients treated with terlipressin for types 1 and 2 hepatorenal syndrome. J Gastroenterol Hepatol. 2007 Sep 3. [Medline].

  23. Kiser TH, Maclaren R, Fish DN. Treatment of hepatorenal syndrome. Pharmacotherapy. 2009 Oct. 29(10):1196-211. [Medline].

  24. Narahara Y, Kanazawa H, Taki Y, Kimura Y, Atsukawa M, Katakura T, et al. Effects of terlipressin on systemic, hepatic and renal hemodynamics in patients with cirrhosis. J Gastroenterol Hepatol. 2009 Aug 3. [Medline].

  25. Fabrizi F, Dixit V, Messa P, Martin P. Terlipressin for hepatorenal syndrome: A meta-analysis of randomized trials. Int J Artif Organs. 2009 Mar. 32(3):133-40. [Medline].

  26. Bellomo R, Chapman M, Finfer S, Hickling K, Myburgh J. Low-dose dopamine in patients with early renal dysfunction: a placebo-controlled randomised trial. Australian and New Zealand Intensive Care Society (ANZICS) Clinical Trials Group. Lancet. 2000 Dec 23-30. 356(9248):2139-43. [Medline].

  27. Fevery J, Van Cutsem E, Nevens F, Van Steenbergen W, Verberckmoes R, De Groote J. Reversal of hepatorenal syndrome in four patients by peroral misoprostol (prostaglandin E1 analogue) and albumin administration. J Hepatol. 1990 Sep. 11(2):153-8. [Medline].

  28. Gines A, Salmeron JM, Gines P, Arroyo V, Jimenez W, Rivera F, et al. Oral misoprostol or intravenous prostaglandin E2 do not improve renal function in patients with cirrhosis and ascites with hyponatremia or renal failure. J Hepatol. 1993 Feb. 17(2):220-6. [Medline].

  29. Soper CP, Latif AB, Bending MR. Amelioration of hepatorenal syndrome with selective endothelin-A antagonist. Lancet. 1996 Jun 29. 347(9018):1842-3. [Medline].

  30. Esrailian E, Pantangco ER, Kyulo NL, Hu KQ, Runyon BA. Octreotide/Midodrine therapy significantly improves renal function and 30-day survival in patients with type 1 hepatorenal syndrome. Dig Dis Sci. 2007 Mar. 52(3):742-8. [Medline].

  31. Lenz K, Druml W, Kleinberger G, Hortnagl H, Laggner A, Schneeweiss B, et al. Enhancement of renal function with ornipressin in a patient with decompensated cirrhosis. Gut. 1985 Dec. 26(12):1385-6. [Medline].

  32. Lenz K, Hortnagl H, Druml W, Grimm G, Laggner A, Schneeweisz B, et al. Beneficial effect of 8-ornithin vasopressin on renal dysfunction in decompensated cirrhosis. Gut. 1989 Jan. 30(1):90-6. [Medline].

  33. Lenz K, Hortnagl H, Druml W, Reither H, Schmid R, Schneeweiss B, et al. Ornipressin in the treatment of functional renal failure in decompensated liver cirrhosis. Effects on renal hemodynamics and atrial natriuretic factor. Gastroenterology. 1991 Oct. 101(4):1060-7. [Medline].

  34. Guevara M, Ginès P. Hepatorenal syndrome. Dig Dis. 2005. 23(1):47-55. [Medline].

  35. Guevara M, Rodés J. Hepatorenal syndrome. Int J Biochem Cell Biol. 2005 Jan. 37(1):22-6. [Medline].

  36. Narahara Y, Kanazawa H, Sakamoto C, Maruyama H, Yokosuka O, Mochida S, et al. The efficacy and safety of terlipressin and albumin in patients with type 1 hepatorenal syndrome: a multicenter, open-label, explorative study. J Gastroenterol. 2011 Oct 25. [Medline].

  37. Gluud LL, Christensen K, Christensen E, et al. Systematic review of randomized trials on vasoconstrictor drugs for hepatorenal syndrome. Hepatology. 2009 Sep 9. [Medline].

  38. Cavallin M, Kamath PS, Merli M, et al.; for the Italian Association for the Study of the Liver Study Group on Hepatorenal Syndrome. Terlipressin plus albumin versus midodrine and octreotide plus albumin in the treatment of hepatorenal syndrome: A randomized trial. Hepatology. 2015 Aug. 62 (2):567-74. [Medline].

  39. Angeli P, Volpin R, Gerunda G, Craighero R, Roner P, Merenda R, et al. Reversal of type 1 hepatorenal syndrome with the administration of midodrine and octreotide. Hepatology. 1999 Jun. 29(6):1690-7. [Medline].

  40. Wong F, Pantea L, Sniderman K. Midodrine, octreotide, albumin, and TIPS in selected patients with cirrhosis and type 1 hepatorenal syndrome. Hepatology. 2004 Jul. 40(1):55-64. [Medline].

  41. Goldaracena N, Marquez M, Selzner N, et al. Living vs. deceased donor liver transplantation provides comparable recovery of renal function in patients with hepatorenal syndrome: a matched case-control study. Am J Transplant. 2014 Dec. 14(12):2788-95. [Medline].

  42. Gonwa TA, Morris CA, Goldstein RM, Husberg BS, Klintmalm GB. Long-term survival and renal function following liver transplantation in patients with and without hepatorenal syndrome--experience in 300 patients. Transplantation. 1991 Feb. 51(2):428-30. [Medline].

  43. Salerno F, Cazzaniga M, Gobbo G. Pharmacological treatment of hepatorenal syndrome: a note of optimism. J Hepatol. 2007 Nov. 47(5):729-31. [Medline].

  44. Tandon P, Bain VG, Tsuyuki RT, Klarenbach S. Systematic review: renal and other clinically relevant outcomes in hepatorenal syndrome trials. Aliment Pharmacol Ther. 2007 May 1. 25(9):1017-28. [Medline].

  45. Akriviadis E, Botla R, Briggs W, Han S, Reynolds T, Shakil O. Pentoxifylline improves short-term survival in severe acute alcoholic hepatitis: a double-blind, placebo-controlled trial. Gastroenterology. 2000 Dec. 119(6):1637-48. [Medline].

  46. Arieff AI, Chidsey CA. Renal function in cirrhosis and the effects of prostaglandin A. Am J Med. 1974 May. 56(5):695-703. [Medline].

  47. Arroyo V, Bosch J, Rivera F, et al. The renin angiotensin system in cirrhosis. Its relation to functional renal failure. Bartoli E, Chiandussi L, eds. Hepatorenal Syndrome. Padua, Italy: Piccin Medical Books; 1979. 201-29.

  48. Arroyo V, Gines P, Gerbes AL, Dudley FJ, Gentilini P, Laffi G, et al. Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club. Hepatology. 1996 Jan. 23(1):164-76. [Medline].

  49. Arroyo V, Terra C, Ginès P. New treatments of hepatorenal syndrome. Semin Liver Dis. 2006 Aug. 26(3):254-64. [Medline].

  50. Arroyo V, Torre A, Guevara M. Recent advances in hepatorenal syndrome. Trop Gastroenterol. 2005 Jan-Mar. 26(1):13-20. [Medline].

  51. Bacq Y, Gaudin C, Hadengue A, Roulot D, Braillon A, Moreau R, et al. Systemic, splanchnic and renal hemodynamic effects of a dopaminergic dose of dopamine in patients with cirrhosis. Hepatology. 1991 Sep. 14(3):483-7. [Medline].

  52. Barnardo DE, Baldus WP, Maher FT. Effects of dopamine on renal function in patients with cirrhosis. Gastroenterology. 1970 Apr. 58(4):524-31. [Medline].

  53. Bennett WM, Keeffe E, Melnyk C, Mahler D, Rosch J, Porter GA. Response to dopamine hydrochloride in the hepatorenal syndrome. Arch Intern Med. 1975 Jul. 135(7):964-71. [Medline].

  54. Cárdenas A. Hepatorenal syndrome: a dreaded complication of end-stage liver disease. Am J Gastroenterol. 2005 Feb. 100(2):460-7. [Medline].

  55. Cárdenas A, Gines P. Hepatorenal syndrome. Clin Liver Dis. 2006 May. 10(2):371-85, ix-x. [Medline].

  56. Cárdenas A, Ginès P. Therapy insight: Management of hepatorenal syndrome. Nat Clin Pract Gastroenterol Hepatol. 2006 Jun. 3(6):338-48. [Medline].

  57. D'Amico G, Garcia-Tsao G, Pagliaro L. Natural history and prognostic indicators of survival in cirrhosis: a systematic review of 118 studies. J Hepatol. 2006 Jan. 44(1):217-31. [Medline].

  58. Dagher L, Patch D, Marley R, Moore K, Burroughs A. Review article: pharmacological treatment of the hepatorenal syndrome in cirrhotic patients. Aliment Pharmacol Ther. 2000 May. 14(5):515-21. [Medline].

  59. Epstein M, Berk DP, Hollenberg NK, Adams DF, Chalmers TC, Abrams HL, et al. Renal failure in the patient with cirrhosis. The role of active vasoconstriction. Am J Med. 1970 Aug. 49(2):175-85. [Medline].

  60. Esrailian E, Runyon BA. Alcoholic cirrhosis-associated hepatorenal syndrome treated with vasoactive agents. Nat Clin Pract Nephrol. 2006 Mar. 2(3):169-72. [Medline].

  61. Esrailian E, Runyon BA. Alcoholic cirrhosis-associated hepatorenal syndrome treated with vasoactive agents. Nat Clin Pract Nephrol. 2006 Mar. 2(3):169-72. [Medline].

  62. Esteva-Font C, Baccaro ME, Fernández-Llama P, Sans L, Guevara M, Ars E, et al. Aquaporin-1 and aquaporin-2 urinary excretion in cirrhosis: Relationship with ascites and hepatorenal syndrome. Hepatology. 2006 Dec. 44(6):1555-63. [Medline].

  63. Fabrizi F, Dixit V, Martin P. Meta-analysis: terlipressin therapy for the hepatorenal syndrome. Aliment Pharmacol Ther. 2006 Sep 15. 24(6):935-44. [Medline].

  64. Flint A. Clinical report on hydro-peritoneum based on an analysis of forty-six cases. Am J Med Sci. 1863. 45:306-39.

  65. Follo A, Llovet JM, Navasa M, Planas R, Forns X, Francitorra A, et al. Renal impairment after spontaneous bacterial peritonitis in cirrhosis: incidence, clinical course, predictive factors and prognosis. Hepatology. 1994 Dec. 20(6):1495-501. [Medline].

  66. Ganne-Carrie N, Hadengue A, Mathurin P, Durand F, Erlinger S, Benhamou JP. Hepatorenal syndrome. Long-term treatment with terlipressin as a bridge to liver transplantation. Dig Dis Sci. 1996 Jun. 41(6):1054-6. [Medline].

  67. Gines A, Escorsell A, Gines P, Salo J, Jiménez W, Inglada L, et al. Incidence, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites. Gastroenterology. 1993 Jul. 105(1):229-36. [Medline].

  68. Gines P, Rimola A, Planas R, Vargas V, Marco F, Almela M, et al. Norfloxacin prevents spontaneous bacterial peritonitis recurrence in cirrhosis: results of a double-blind, placebo-controlled trial. Hepatology. 1990 Oct. 12(4 Pt 1):716-24. [Medline].

  69. Gines P, Tito L, Arroyo V, Planas R, Panes J, Viver J, et al. Randomized comparative study of therapeutic paracentesis with and without intravenous albumin in cirrhosis. Gastroenterology. 1988 Jun. 94(6):1493-502. [Medline].

  70. Gines P, Uriz J, Calahorra B, Garcia-Tsao G, Kamath PS, Del Arbol LR, et al. Transjugular intrahepatic portosystemic shunting versus paracentesis plus albumin for refractory ascites in cirrhosis. Gastroenterology. 2002 Dec. 123(6):1839-47. [Medline].

  71. Ginès P, Cárdenas A, Arroyo V, Rodés J. Management of cirrhosis and ascites. N Engl J Med. 2004 Apr 15. 350(16):1646-54. [Medline].

  72. Ginès P, Guevara M, Arroyo V, Rodés J. Hepatorenal syndrome. Lancet. 2003 Nov 29. 362(9398):1819-27. [Medline].

  73. Gluud LL, Kjaer MS, Christensen E. Terlipressin for hepatorenal syndrome. Cochrane Database Syst Rev. 2006 Oct 18. CD005162. [Medline].

  74. Guevara M, Gines P, Bandi JC, Gilabert R, Sort P, Jimenez W, et al. Transjugular intrahepatic portosystemic shunt in hepatorenal syndrome: effects on renal function and vasoactive systems. Hepatology. 1998 Aug. 28(2):416-22. [Medline].

  75. Hadengue A, Gadano A, Moreau R, Giostra E, Durand F, Valla D, et al. Beneficial effects of the 2-day administration of terlipressin in patients with cirrhosis and hepatorenal syndrome. J Hepatol. 1998 Oct. 29(4):565-70. [Medline].

  76. Hadengue A, Moreau R, Bacq Y, Gaudin C, Braillon A, Lebrec D. Selective dopamine DA1 stimulation with fenoldopam in cirrhotic patients with ascites: a systemic, splanchnic and renal hemodynamic study. Hepatology. 1991 Jan. 13(1):111-6. [Medline].

  77. Halimi C, Bonnard P, Bernard B, Mathurin P, Mofredj A, di Martino V, et al. Effect of terlipressin (Glypressin) on hepatorenal syndrome in cirrhotic patients: results of a multicentre pilot study. Eur J Gastroenterol Hepatol. 2002 Feb. 14(2):153-8. [Medline].

  78. Han MK, Hyzy R. Advances in critical care management of hepatic failure and insufficiency. Crit Care Med. 2006 Sep. 34(9 Suppl):S225-31. [Medline].

  79. Heidelbaugh JJ, Sherbondy M. Cirrhosis and chronic liver failure: part II. Complications and treatment. Am Fam Physician. 2006 Sep 1. 74(5):767-76. [Medline].

  80. Kaffy F, Borderie C, Chagneau C, Ripault MP, Larzilliere I, Silvain C, et al. Octreotide in the treatment of the hepatorenal syndrome in cirrhotic patients. J Hepatol. 1999 Jan. 30(1):174. [Medline].

  81. Linas SL, Schaefer JW, Moore EE, Good JT Jr, Giansiracusa R. Peritoneovenous shunt in the management of the hepatorenal syndrome. Kidney Int. 1986 Nov. 30(5):736-40. [Medline].

  82. Martin PY, Ginès P, Schrier RW. Nitric oxide as a mediator of hemodynamic abnormalities and sodium and water retention in cirrhosis. N Engl J Med. 1998 Aug 20. 339(8):533-41. [Medline].

  83. Mitzner SR, Stange J, Klammt S, Risler T, Erley CM, Bader BD, et al. Improvement of hepatorenal syndrome with extracorporeal albumin dialysis MARS: results of a prospective, randomized, controlled clinical trial. Liver Transpl. 2000 May. 6(3):277-86. [Medline].

  84. Neri S, Pulvirenti D, Malaguarnera M, Cosimo BM, Bertino G, Ignaccolo L, et al. Terlipressin and albumin in patients with cirrhosis and type I hepatorenal syndrome. Dig Dis Sci. 2008 Mar. 53(3):830-5. [Medline].

  85. Neri S, Pulvirenti D, Malaguarnera M, Cosimo BM, Bertino G, Ignaccolo L, et al. Terlipressin and albumin in patients with cirrhosis and type I hepatorenal syndrome. Dig Dis Sci. 2008 Mar. 53(3):830-5. [Medline].

  86. O'beirne JP, Heneghan MA. Current management of the hepatorenal syndrome. Hepatol Res. 2005 Aug. 32(4):243-9. [Medline].

  87. Ortega R, Gines P, Uriz J, Cardenas A, Calahorra B, De Las Heras D, et al. Terlipressin therapy with and without albumin for patients with hepatorenal syndrome: results of a prospective, nonrandomized study. Hepatology. 2002 Oct. 36(4 Pt 1):941-8. [Medline].

  88. PAPPER S. The role of the kidney in Laennec's cirrhosis of the liver. Medicine (Baltimore). 1958 Dec. 37(4):299-316. [Medline].

  89. Perez GO, Golper TA, Epstein M. Dialysis, hemofiltration and other extracorporeal techniques in the treatment of renal complications of liver disease. Epstein M, ed. The kidney in liver disease. 4th ed. Philadelphia, Pa: Hanley & Belfus; 1996. 517-28.

  90. Restuccia T, Ortega R, Guevara M, Gines P, Alessandria C, Ozdogan O, et al. Effects of treatment of hepatorenal syndrome before transplantation on posttransplantation outcome. A case-control study. J Hepatol. 2004 Jan. 40(1):140-6. [Medline].

  91. Ruiz-del-Arbol L, Monescillo A, Arocena C, Valer P, Gines P, Moreira V, et al. Circulatory function and hepatorenal syndrome in cirrhosis. Hepatology. 2005 Aug. 42(2):439-47. [Medline].

  92. Salo J, Gines A, Quer JC, Fernandez-Esparrach G, Guevara M, et al. Renal and neurohormonal changes following simultaneous administration of systemic vasoconstrictors and dopamine or prostacyclin in cirrhotic patients with hepatorenal syndrome. J Hepatol. 1996 Dec. 25(6):916-23. [Medline].

  93. Sanyal AJ, Genning C, Reddy KR, Wong F, Kowdley KV, Benner K, et al. The North American Study for the Treatment of Refractory Ascites. Gastroenterology. 2003 Mar. 124(3):634-41. [Medline].

  94. Schepke M, Appenrodt B, Heller J, Zielinski J, Sauerbruch T. Prognostic factors for patients with cirrhosis and kidney dysfunction in the era of MELD: results of a prospective study. Liver Int. 2006 Sep. 26(7):834-9. [Medline].

  95. Schrier RW, Arroyo V, Bernardi M, Epstein M, Henriksen JH, Rodes J. Peripheral arterial vasodilation hypothesis: a proposal for the initiation of renal sodium and water retention in cirrhosis. Hepatology. 1988 Sep-Oct. 8(5):1151-7. [Medline].

  96. Sen S, Williams R, Jalan R. Emerging indications for albumin dialysis. Am J Gastroenterol. 2005 Feb. 100(2):468-75. [Medline].

  97. Senzolo M, Cholongitas E, Tibballs J, Burroughs A, Patch D. Transjugular intrahepatic portosystemic shunt in the management of ascites and hepatorenal syndrome. Eur J Gastroenterol Hepatol. 2006 Nov. 18(11):1143-50. [Medline].

  98. Singh N, Gayowski T, Yu VL, Wagener MM. Trimethoprim-sulfamethoxazole for the prevention of spontaneous bacterial peritonitis in cirrhosis: a randomized trial. Ann Intern Med. 1995 Apr 15. 122(8):595-8. [Medline].

  99. Solanki P, Chawla A, Garg R, Gupta R, Jain M, Sarin SK. Beneficial effects of terlipressin in hepatorenal syndrome: a prospective, randomized placebo-controlled clinical trial. J Gastroenterol Hepatol. 2003 Feb. 18(2):152-6. [Medline].

  100. Sort P, Navasa M, Arroyo V, Aldeguer X, Planas R, Ruiz-del-Arbol L, et al. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. N Engl J Med. 1999 Aug 5. 341(6):403-9. [Medline].

  101. de Mattos AZ, de Mattos AA, Ribeiro RA. Terlipressin versus noradrenaline in the treatment of hepatorenal syndrome: systematic review with meta-analysis and full economic evaluation. Eur J Gastroenterol Hepatol. 2015 Dec 8. [Medline].

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