The bacterial translocation of intestinal germs, the gradual decrease in systemic vascular resistances, the hepatic vascular neoformation are potential risk factors. The fall in mean arterial pressure is compensated by increase in cardiac output and by activation of renin-angiotensin-aldosterone system RAAS and sympathetic nervous system SNS to improve systemic vascular resistence.
These compensatory mechanisms ultimately have repercussions on kidney function causing reduced glomerular filtration rate GFR and further water retention thereby worsening the water overload. The ensuing hemodynamic instability may give rise to many clinical events that further interfere with the compensatory mechanisms. These include the onset of spontaneous bacterial peritonitis, gastrointestinal bleeding and post-paracentesis circulatory dysfunction[ 12 ].
The renal impairment is worsened by a progressive cardiac dysfunction known as cirrhotic cardiomyopathy. The latter is characterized by diastolic impairment with septal ventricular hypertrophy, blunted ventricular response to stress, systolic and diastolic dysfunction, and electrophysiological abnormalities prolongation of QT interval [ 7 ]. Furthermore it is possible that several intracellular signaling pathways are involved.
On the other hand the activation of renin-angiotensin system and salt retention play a role in diastolic disfunction. Recent studies have stated myocardial dysfunction in cirrhosis as a contributing, or even a precipitant factor, of HRS[ 13 , 14 ].
HRS may also arise in patients with acute liver failure as shown in Akriviadis et al[ 16 ]: They considered patients with alcoholic hepatitis of whom 28 developed HRS after a four-week follow-up. Despite discrepancies in literature data, the prevalence of HRS has dropped in recent years, probably as a result of a better understanding of its pathophysiology and improved clinical management[ 19 ].
Nonetheless the long-term survival of HRS patients remains poor and the only effective treatment for this condition is liver transplantation. Since then, advances in our understanding of HRS pathogenesis and the introduction of new therapies led to repeated revisions of the criteria.
The latest version of excludes the use of creatinine clearance due to its poor correlation with kidney function in patients with cirrhosis , and has eliminated minor criteria sodium excretion fraction, urinary output deemed less sensitive and specific.
This type of HRS can develop spontaneously but more often tends to follow a precipitating event, mostly spontaneous bacterial peritonitis or other infections like pneumonia, urinary tract infections or cellulitis[ 24 ]. Other potential risk factors include viral, alcoholic, toxic or ischemic hepatitis e. Spontaneous bacterial peritonitis are leading trigger of HRS.
Diuretic treatment has been suggested as a potential trigger of HRS, but there are no clear supportive data for this. This type presents as a less severe and more gradual decline in renal function associated with refractory ascites. The increase in creatinine is gradual with mean values of 1. The average survival rate is six to eight months after onset. The differential diagnosis between the two types of HRS is based on the rate of progression and extent of renal impairment, whereas the pathophysiological differences have not yet been fully clarified.
A spontaneous recovery is rare in both cases unless there is a significant improvement in liver function. The differential diagnosis between HRS, other causes of kidney disease and septic shock remain extremely difficult.
Despite the widespread circulation of the IAC criteria, a serum creatinine cut-off of 1. AKI is defined as the abrupt loss of kidney function resulting in a 0. The aim is to apply the AKI criteria to decompensated cirrhotic patients for an early identification of kidney failure and thereby implementing prompt aggressive treatment[ 26 ]. Two recent prospective studies assessed the applicability of the AKI criteria in patients with cirrhosis.
The study by Fagundes et al[ 27 ] on patients and another by Piano et al[ 28 ] on cirrhotic patients both divided the populations into two groups based on kidney function. Nonetheless, a recent editorial by Arroyo et al[ 29 ] pointed to a lack of evidence demonstrating the real advantage of the IAC guidelines with respect to AKI criteria. The stratification of cirrhotic patients according to single organ damage kidney, liver or brain appears to simplify the complex changes occurring in patients with decompensated liver failure.
However, further studies are required to establish the clinical utility of this concept[ 30 ]. In all patients with acute renal failure and even more in patients with cirrhosis, serum creatinine may not reflect the reduction of kidney function with a significant difference between male and female.
Because of that it was proposed using cystain C as alternative marker of renal function. Seo et al[ 31 ] and Sharawey et al[ 32 ] showed that serum cystatin C level is a good marker for predicting HRS and survival in patients with cirrhotic ascites. As there are currently no specific tests to identify HRS, diagnosis rests on the exclusion of other causes of kidney failure. It is important to establish the etiology of kidney injury in order to institute the appropriate treatment.
The parameters traditionally used to distinguish AKI from chronic kidney disease CKD urinary sodium concentration, serum and urine osmolarity are not applicable in patients with cirrhosis and ascites. Likewise, serum urea values are usually reduced in cirrhotic patients due to the impaired hepatic synthesis. Belcher et al[ 36 ] proposed the use of urinary biomarkers of AKI to improve the diagnostic process: urinary levels of neutrophil gelatinase-associated lipocalin NGAL , interleukin 18 IL , kidney injury molecule-1 and liver fatty acid-binding protein are elevated in liver disease patients with kidney injury due to acute tubular necrosis.
Two recent trials studied patients admitted to hospital for cirrhosis-induced complications. They both demonstrated that raised urinary levels of NGAL may serve to distinguish functional kidney damage from acute tubular necrosis or necrosis arising in HRS[ 37 , 38 ]. Barreto et al[ 39 ] confirmed that urinary NGAL predicts clinical outcome, namely persistent kidney injury and mortality at three months in hospitalized patients with cirrhosis and bacterial infections.
Although further clinical trials are required, NGAL appears to predict short-term mortality in cirrhotic patients. Renal biopsy is not used for diagnostic purposes but can be entertained when a decline in renal function is associated with active urinary sediment or clinical status not corresponding to IAC criteria or unresponsive to therapy.
The current therapeutic armamentarium includes drugs with specific vasoconstrictive effects on the splanchnic circulation in addition to renal and liver replacement therapies which can be artificial or natural liver transplantation. Liver transplant remains the only truly effective treatment but is limited by the high mortality rate in HRS patients and the shortage of available organs.
A recent literature review by Fabrizi et al[ 40 ] noted that pre-transplant kidney function is the most important predictor for patient survival after liver transplant.
If multiorgan damage is present, some patients, especially those with type I HRS, may require a high level of care, and admission to an intensive care facility. In addition, a patient-tailored diet and physical rehabiligation program should be planned and each patient assessed for eligibility for liver transplantation to avoid aggressive treatment. The aim of treatment must be to stabilize patients until liver transplantation and optimize their clinical condition for a successful transplant[ 6 ].
Medical management is targeted at the pathogenetic mechanisms underlying HRS. The ideal treatment is designed to improve liver function by exerting splanchnic vasoconstriction and renal vasodilation to reduce portal hypertension and raise systemic arterial pressure[ 34 ].
The specific drug approach is based on the use of vasoconstrictor agents terlipressin, norepinephrine, midodrine to correct circulatory changes. As reported in a review by Davenport et al[ 41 ], intravenous administration of terlipressin and albumin is currently the treatment of choice for patients with type I and type II HRS, resulting in an overall reduction in short-term mortality rates.
The vasopressin synthetic analogue terlipressin is a V1 agonist of the receptors expressed on vascular smooth muscle cells in the splanchnic circulation. It is enzymatically transformed from the inactive to biologically active form lysine-vasopressin with a longer half-life than other vasopressin analogues, e.
The vasoconstrictive effect of terlipressin corrects the circulatory dysfunction typical of end-stage liver disease, indirectly rebalancing intrarenal vasoconstriction and lowering levels of renin, noradrenaline and ultimately serum creatinine. As a result, the kidney regains control of its self-regulatory system. In addition, terlipressin has a major impact on the portal circulation reducing portal venous flow and porto-systemic pressure with a concomitant increase in hepatic arterial blood flow and an improvement in hepatocellular oxygenation.
Terlipressin can be administered as an intravenous bolus starting from a dose of 0. The dosage can be doubled after three days of treatment if there is no improvement in serum creatinine i.
Continuous infusion is associated with a better clinical response and fewer side-effects[ 48 ]. Albumin serves to expand the circulating plasma volume by raising the oncotic pressure. In addition, it has metabolic, immune and vasoconstrictor effects by binding to endotoxins, nitric oxide, bilirubin and fatty acids[ 49 , 50 ]. The average recovery time is seven days up to a maximum of two weeks after which terlipressin should be suspended if there is no improvement in kidney function[ 54 ].
Terlipressin has an acceptable side-effects profile. Side effects include abdominal pain with cramps and diarrhea until intestinal ischemia; cardiac tachiarrhythmias and chest pain can be observed, in generale ECG monitoring is recommended.
Vasoconstriction induced by terlipressin may cause also cyanosis, livedo reticularis, necrosis of the skin and extremities[ 53 ]. If patient shows side effects the dosage should be reduced or administration discontinued. Continuous infusion is safer and less burdened by side effects[ 52 ]. Their data confirm the regression of HRS in a significant number of treated patients but no effect on survival rates.
The association albumin and terlipressin showed an improvement of survival rates for positive effects of albumin on cardiac function, on the reduction of nitric oxid and on improving the responsiveness of arterial wall to vasoconstrictors. Terlipressin is not available in the United States and Canada so therapeutic protocols with other vasoconstrictor agents need to be considered in those countries.
The alpha-adrenergic receptor agonist norepinephrine has proved effective in the treatment of HRS. Continuous norepinephrine infusion at a dose of 0. The maximum period of treatment must not exceed 2 wk[ 57 , 58 ]. Neither treatment proved superior to the other and the outcome was broadly the same in terms of HRS regression. Noradrenaline can be deemed as effective as terlipressin but its lower costs makes it an interesting option for the treatment of HRS.
Another alpha-adrenergic agent, midodrine, can be considered a good alternative to terlipressin and is the drug most commonly used in the United States. Midodrine is a prodrug metabolized by the liver into its active metabolite desglymidodrine and then excreted in the urine. Midodrine can be administered orally initial dose 7. Albumin must be associated at the usual dose[ 6 ]. Midodrine dosage has a major effect on its effectiveness: Patients treated at the maximum dose have shown a complete response to therapy, whereas octreotide administered alone has no effect on kidney function[ 62 ].
The creation of a portosystemic shunt to treat refractory ascites can improve renal function in cirrhotic patients as it increases venous return of splanchnic blood to the right heart thereby raising the effective arterial blood volume and reducing hepatic sinusoidal pressure. Despite its side-effects namely the high incidence of hepatic encephalopathy , TIPS can be used in the short term to gain potential benefits in patients awaiting liver transplant[ 64 , 65 ].
HRS patients, particularly those with type I, may need to undergo dialysis because of metabolic acidosis or hyperkalemia due to water or sodium retention or less frequently uremic intoxication. RRT is among the so-called bridging therapies designed to support patients awaiting liver transplant, but there is no evidence that dialysis improves the long-term survival of patients not eligible for transplantation[ 66 ].
By definition, patients with cirrhosis are at higher risk of bleeding and hemodynamic complications hypotension, arrythmias hampering the decision to initiate and manage dialysis treatment. Continuous renal replacement therapy CRRT is usually preferred to intermittent dialysis due to its greater hemodynamic stability ensuring fewer fluctuations in intracranial pressure.
However, prospective studies show that the choice of RRT has no significant effect on survival rates in patients awaiting liver transplantation[ 68 - 71 ].
Anticoagulation of the extracorporeal circuit is needed to maintain the filter patency without increasing the risk of hemorrhage. Regional citrate anticoagulation emerged as possible alternative but no specific protocols are currently recommended for patients with liver diseases[ 72 ]. Peritoneal dialysis is an option to resolve ascites and correct other complications of cirrhosis without exposing patients to the complications of hemodialysis[ 73 , 74 ].
The precise timing and dose of RRT have yet to be established but some studies demonstrate that the early initiation and maintenance of a constantly negative fluid balance have a positive effect on survival rates[ 75 ]. RRT removes water-soluble toxins whereas most of the molecules accumulated in the course of liver failure are linked to albumin and hence are not removed by conventional hemodialysis. Liver support systems are designed to enhance and optimize these results, increasing the removal of water-soluble toxins and those linked to albumin.
To date these treatments have served as bridging therapies for patients awaiting liver transplantation. Molecular adsorbent recirculating system MARS combines the conventional CRRT monitor or a standard hemodialysis machine with an albumin dialysate circuit. The albumin dialysate, in its turn, is regenerated by a low flux dialysis filter and two adsorber cartridges, one filled with activated charcoal, the other with an anion exchanger resin.
The regenerated albumin solution is then ready for new uptake of toxins from the blood, entering the circuit through a high permeability filter to undergo standard dialysis to remove water-soluble toxins. The eight patients treated with MARS had significantly better survival rates at 30 d than patients receiving standard medical therapy. After a one-year follow-up, Donati et al[ 78 ] reported that among 64 patients treated with MARS, the best survival rates were found in the 11 patients who subsequently underwent liver transplant.
The same authors observed an improvement in both systolic and diastolic blood pressure in 5 patients with type 2 HRS treated with MARS and standard medical therapy.
The Prometheus system consists of a primary circuit plasma filter and dialyzer and a secondary circuit adsorbent filters to remove bilirubin for the combined removal of toxin albumin-bound and water-soluble molecules using a fractionated plasma separation and adsorption FPSA system.
Unlike MARS, the plasma is separated from the blood through a high cut-off point polysulfone membrane kDa, albumin permeable and purified from the albumin-bound toxins by direct adsorption on resin-containing cartridges.
The purified plasma is then returned to the blood circuit through a high efficiency dialyzer to remove water-soluble toxins. The HELIOS study on patients with liver failure treated with standard medical therapy vs extracorporeal treatment showed no significant advantage in terms of overall survival except in the subgroup of patients with type I HRS treated with FPSA who had a significant survival benefit[ 79 ].
Liver transplantation remains the treatment of choice in HRS patients despite its mortality rate which is particularly high in patients with type I HRS whose survival is so poor that many die while awaiting transplant.
Renal sodium excretion, serum creatinine and neurohormonal levels may normalize within a month whereas renovascular resistance may take more than a year to return to normal after transplantation[ 81 , 82 ]. Organ allocation is mainly based on the MELD score, a system devised to stratify disease severity on the basis of laboratory parameters serum creatinine, bilirubin and INR to assign organs according to the so-called sickest first policy[ 83 ].
Considering all liver transplant recipients, those with HRS are more exposed to post-transplant complications, at greater risk of developing CKD and have a shorter overall survival[ 84 , 85 ]. RRT prior to liver transplant is an important predictive factor. Patients undergoing hemodialysis for more than eight weeks have a markedly reduced probability of renal recovery and a combined liver-kidney transplant is recommended in these cases[ 87 , 88 ]. Vasopressor treatment of HRS before liver transplant does not seem to affect subsequent patient outcome[ 89 ].
Nonetheless, Angeli et al[ 83 ] reported that liver transplantation may be delayed in patients treated with vasopressors following a response to treatment and hence an improvement in clinical and hemodynamic status. There are no specific recommendations as to post-transplant immunosuppressive therapy, but it may be advisable to delay the start of cyclosporine or tacrolimus to h after transplantation to enhance renal recovery as suggested by Guevara and Arroyo[ 90 ].
HRS is a life-threatening complication arising in patients with liver cirrhosis and triggered by a series of complex hemodynamic and neurohormonal changes linked to the liver disease. The condition carries a very poor prognosis and high morbidity and mortality rates.
Recent years have seen a reduction in HRS prevalence and an improvement in patient outcome probably reflecting a better understanding of HRS pathophysiology and advances in therapeutic strategies.
Treatment consists of medical management mainly based on vasopressor administration , surgery TIPS or instrumental therapies e. Although the therapeutic armamentarium at our disposal will control the syndrome and obtain temporary remission, there is no guarantee of disease resolution.
The only effective treatment offering patients the hope of complete recovery is liver transplantation or combined kidney-liver transplant in selected cases. The decision to embark on transplantation must be carefully assessed in HRS patients considering all the potential factors likely to influence transplant surgery and its outcome.
Conflict-of-interest statement: The authors do not have any disclosures to report. Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers.
Peer-review started: April 15, First decision: May 13, Article in press: September 18, National Center for Biotechnology Information , U. Journal List World J Nephrol v. World J Nephrol. Published online Nov 6. Author information Article notes Copyright and License information Disclaimer. Orsola University Hospital, Bologna, Italy. Published by Baishideng Publishing Group Inc. All rights reserved. This article has been cited by other articles in PMC.
Abstract Acute kidney injury AKI is a common complication in patients with end-stage liver disease and advanced cirrhosis regardless of the underlying cause. Open in a separate window. Figure 1. Table 1 Diagnostic criteria for hepatorenal syndrome. HRS: Hepatorenal syndrome. Table 2 Characteristics of type I and type II hepatorenal syndrome. Table 3 Risk factors for the onset of hepatorenal syndrome. Table 4 Differential diagnosis of renal failure in cirrhosis. Pre-renal History of fluid loss, gastrointestinal bleeding, treatment with diuretics or non-steroidal anti-inflammatory drugs Organic Medical history, laboratory tests cryoglobulinemia, complementemia, etc.
Obstructive Ultrasound imaging Chronic kidney disease Anemia, proteinuria, secondary hyperparathyroidism, ultrasound evidence of renal cortical thinning. Table 5 Prevention of hepatorenal syndrome and general patient management strategies. Medical management Medical management is targeted at the pathogenetic mechanisms underlying HRS. Transjugular intrahepatic portosystemic shunt The creation of a portosystemic shunt to treat refractory ascites can improve renal function in cirrhotic patients as it increases venous return of splanchnic blood to the right heart thereby raising the effective arterial blood volume and reducing hepatic sinusoidal pressure.
Molecular adsorbent recirculating system Molecular adsorbent recirculating system MARS combines the conventional CRRT monitor or a standard hemodialysis machine with an albumin dialysate circuit. Fractionated plasma separation and absorption Prometheus The Prometheus system consists of a primary circuit plasma filter and dialyzer and a secondary circuit adsorbent filters to remove bilirubin for the combined removal of toxin albumin-bound and water-soluble molecules using a fractionated plasma separation and adsorption FPSA system.
Liver transplantation Liver transplantation remains the treatment of choice in HRS patients despite its mortality rate which is particularly high in patients with type I HRS whose survival is so poor that many die while awaiting transplant.
Footnotes Conflict-of-interest statement: The authors do not have any disclosures to report. References 1. Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis. Unopposed splanchnic arterial vasodilation may cause a decrease in effective arterial volume which in turn triggers the activation of vasoconstrictors[ 23 , 34 ]. Vasoconstrictors that have been widely used for type 1 HRS include vasopressin analogues ornipressin and terlipressin , a somatostatin analogue octreotide , and alpha-adrenergic analogues midodrine and noradrenalin.
In most studies, albumin was administered concurrently. The vasopressin analogues are effective in causing marked splanchnic vasoconstriction. Ornipressin, although effective in treating HRS, may cause significant ischemic side effects and is not currently recommended for the management of HRS[ 35 ].
However, it is important to note that GFR was not normalized in most patients who responded[ 37 , 39 ]. Small, short-term, non-randomized studies suggest that treatment with terlipressin may also improve renal function in patients with type 2 HRS[ 34 ]. Terlipressin is not currently licensed for use in North America, but a double-blind, randomized, placebo-controlled trial is now being conducted in the USA and Germany in patients with type 1 HRS.
Alpha-1 adrenoreceptor agonists and a somatostatin analogue are readily available in North America and have been studied in type 1 HRS. In type 1 HRS, alpha-1 agonists have only been used in combination with other agents. Few nonrandomized, prospective studies have evaluated treatment with both midodrine and octreotide[ 45 - 47 ].
In the study by Wong et al[ 46 ], 10 of 14 patients with HRS treated with midodrine, octreotide, and albumin had their serum creatinine stable at less than 1. The use of noradrenalin in combination with intravenous albumin and furosemide was studied in 12 patients[ 48 ]. These small studies suggest a short-term benefit in improving renal function in HRS patients, although larger, randomized studies are required before recommending the routine use of these agents in clinical practice.
Other drugs, such as N-acetylcysteine and misoprostol, have been proposed as therapy for HRS, but have not been well-studied.
Patients with HRS who progress to severe renal failure can be initiated on renal replacement therapy RRT , generally given as continuous hemofiltration. Dialysis is usually used as a bridge in patients who are awaiting liver transplantation, and is not recommended for patients who are unlikely to recover from liver failure or are unlikely to receive liver transplantation because of other contraindications. Survival on dialysis is generally dependent on the severity of liver disease[ 52 ].
There are only a few small studies evaluating the effects of dialysis in HRS[ 53 , 54 ]. In the prospective study by Witzke et al[ 53 ], 30 patients with Child-Pugh C cirrhosis and HRS were treated with continuous veno-venous hemodialysis CVVHD if they were on mechanical ventilation, or with intermittent hemodialysis if they were not on mechanical ventilation.
No patients on mechanical ventilation survived for more than 30 d, but 8 of 15 patients who were not on mechanical ventilation survived for more than 30 d. The absence of a control group and lack of randomization make it difficult to draw any firm conclusions from this study. Liver transplantation LT is the only effective and permanent treatment for HRS[ 10 , 14 , 56 , 57 ] that cures both the liver and renal failure. Patients who undergo LT may sometimes require postoperative hemodialysis.
It is preferable to delay administration of cyclosporine or tacrolimus until renal impairment improves in these patients, as these drugs may further worsen renal function. The issue of whether to transplant a kidney in addition to a liver LKT, combined liver kidney transplantation is an important one as well. A renal biopsy may be helpful in some patients to identify the etiology of the renal failure and to determine the presence and extent of glomerular scarring[ 59 ].
LKT should be reserved for patients with irreversible renal failure, including HRS patients who are on dialysis for more than 8 wk or patients with progressive primary renal disease[ 59 ]. It is not clear if the advances in management of HRS in recent years have had an impact on post-transplant outcomes. However, the study had only 9 patients with HRS and as correctly stated by the authors, further confirmation in a larger series of patients is required.
Clearly, further prospective studies are needed to guide transplant physicians to determine whether they should transplant the liver and the kidney or the liver alone in patients with liver failure and kidney failure. Renal failure occurs commonly in patients with severe liver disease and its causes are multifactorial. Patients with type 1 HRS generally have a fatal outcome without expedited liver transplantation.
Therapy with terlipressin and albumin looks promising, but there is a paucity of data to make firm conclusions. Use of other vasoconstrictors or TIPS remains experimental.
The only proven treatment option is expedited liver transplantation. Dialysis is often used as a bridge to liver transplantation, but there are no controlled studies to support renal replacement therapy in type 1 HRS. Further research is necessary to better elucidate the mechanisms of HRS and to identify treatment strategies to reduce morbidity and mortality in patients with liver disease.
National Center for Biotechnology Information , U. Journal List World J Gastroenterol v. World J Gastroenterol. Published online Aug Author information Article notes Copyright and License information Disclaimer. Author contributions: All authors contributed equally to the work. All rights reserved. This article has been cited by other articles in PMC. Keywords: Acute renal failure, End stage liver disease, Hepatorenal syndrome, Transjugular intrahepatic portosystemic shunts, Dialysis, Liver transplantation.
Open in a separate window. Figure 1. Table 1 Clinical types of HRS. Table 2 Diagnostic criteria of hepatorenal syndrome 1. Table 3 Non-invasive therapies.
Twenty-three patients had adverse events that may have been terlipressin-related. No adverse effects related to AVP. None survived by d 15 in placebo group.
Of 8 patients who received terlipressin alone, 2 responded. One patient had ischemic side effects finger ischemia. The study included types 1 and 2 HRS patients numbers in each group not specified. No side effects reported. Patients with improved renal function had less severe cirrhosis than patients without. Patients without a precipitating factor for HRS or who responded to terlipressin were more likely to survive.
One had severe bronchospasms after terlipressin administration, and subsequently died. Treatment was stopped in 4 patients on the d protocol because of ischemic complications. No significant side effects. The other 9 died during follow-up. No ischemic complications. Transient myocardial ischemia was observed in 1 patient. One patient did not complete the study due to pancreatitis. This study looked at the acute effect of one dose of midodrine. The results include cirrhotic patients without HRS.
One of them responded to retreatment, but treatment was stopped in the other because of a ventricular tachyarrhythmia. Treatment was stopped in another patient because of intestinal ischemia. HRS rapidly recurred when octreotide was stopped, and did not respond to further octreotide infusion. Table 4 Invasive therapies. There was 1 TIPS-related death. Five responders received TIPS; their renal function continued to improve. TIPS was performed in responders who were stable.
Two of the five responders who did not receive TIPS underwent liver transplantation, and their SCr remained normal at the time of liver transplantation. Renal function improved significantly after TIPS in all patients who responded to terlipressin.
Mean survival was 4. None of these patients underwent liver transplantation or received TIPS or vasopressin analogues during the observation period. Renal function improved in all patients. Of the 5 patients with type 1 HRS, 3 remained anuric, but there was normalization of SCr in the other 2 patients.
SCr was normalized in both patients with type 2 HRS by the end of treatment. Renal replacement therapy Patients with HRS who progress to severe renal failure can be initiated on renal replacement therapy RRT , generally given as continuous hemofiltration.
Transplantation Liver transplantation LT is the only effective and permanent treatment for HRS[ 10 , 14 , 56 , 57 ] that cures both the liver and renal failure. References 1. Hecker R, Sherlock S. Electrolyte and circulatory changes in terminal liver failure.
Definition and diagnostic criteria of refractory ascites and hepatorenal syndrome in cirrhosis. International Ascites Club. The Kidney in Cirrhosis. Ann Intern Med. Disorders of Renal Function. Renal Failure in Patients with Cirrhosis of the Liver. Clinical and Pathologic Characteristics. Am J Med. Recovery from "hepatorenal syndrome" after orthotopic liver transplantation. N Engl J Med. Incidence, predictive factors, and prognosis of the hepatorenal syndrome in cirrhosis with ascites.
Frequency and type of renal and electrolyte disorders in fulminant hepatic failure. Br Med J. Renal duplex Doppler ultrasonography: a noninvasive predictor of kidney dysfunction and hepatorenal failure in liver disease. Dagher L, Moore K. The hepatorenal syndrome. Renal failure in the patient with cirrhosis. The role of active vasoconstriction.
Renal failure in patients with cirrhosis of the liver. Evaluation of intrarenal blood flow by para-aminohippurate extraction and response to angiotensin. Moore K.
Clin Sci Lond ; 92 — Hepatorenal syndrome. Nitric oxide as a mediator of hemodynamic abnormalities and sodium and water retention in cirrhosis. Renal function abnormalities, prostaglandins, and effects of nonsteroidal anti-inflammatory drugs in cirrhosis with ascites. An overview with emphasis on pathogenesis.
Sympathetic nervous activity, renin-angiotensin system and renal excretion of prostaglandin E2 in cirrhosis. Relationship to functional renal failure and sodium and water excretion. Eur J Clin Invest. Peripheral arterial vasodilation hypothesis: a proposal for the initiation of renal sodium and water retention in cirrhosis.
Antidiuretic hormone and the pathogenesis of water retention in cirrhosis with ascites. Semin Liver Dis. Pathogenesis of the hepatorenal syndrome.
Annu Rev Med. Circulatory function and hepatorenal syndrome in cirrhosis. Systemic, renal, and hepatic hemodynamic derangement in cirrhotic patients with spontaneous bacterial peritonitis. Hepatorenal syndrome: a dreaded complication of end-stage liver disease.
Am J Gastroenterol. Arroyo V. Physiopathology of refractory ascites and the hepatorenal syndrome. Renal impairment after spontaneous bacterial peritonitis in cirrhosis: incidence, clinical course, predictive factors and prognosis. Effect of intravenous albumin on renal impairment and mortality in patients with cirrhosis and spontaneous bacterial peritonitis. Randomized comparative study of therapeutic paracentesis with and without intravenous albumin in cirrhosis.
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Arch Intern Med. Diagnosis of functional kidney failure of cirrhosis with Doppler sonography: prognostic value of resistive index. Pentoxifylline improves short-term survival in severe acute alcoholic hepatitis: a double-blind, placebo-controlled trial. Amelioration of hepatorenal syndrome with selective endothelin-A antagonist.
Improvement in renal function in hepatorenal syndrome with N-acetylcysteine. Moreau R, Lebrec D. The use of vasoconstrictors in patients with cirrhosis: type 1 HRS and beyond. Reversibility of hepatorenal syndrome by prolonged administration of ornipressin and plasma volume expansion.
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