Diagnostic Criteria Of Hepatorenal Syndrome Research Articles

Hepatorenal syndrome: Updates.

Hepatorenal syndrome: Updates.

Do old urinary biomarkers have a place in the new definition of hepatorenal syndrome in the Egyptian cirrhotic patients? A single-center experience

BackgroundHepatorenal syndrome is still a diagnosis of exclusion despite new classification.AimsTo validate the accuracy of urinary neutrophil gelatinase-associated lipocalin, interleukin-18, and kidney injury molecule-1 in the new diagnostic criteria of hepatorenal syndrome in Egyptian patients with hepatitis C virus-related liver cirrhosis using serum creatinine as a gold standard test for acute kidney injury.MethodsOne-hundred twenty cirrhotic patients with ascites were recruited and divided into two groups depending on the presence or absence of renal impairment, and 40 age- and sex-matched cirrhotic patients without ascites used as controls participated in the study. Urinary biomarkers were measured and compared with conventional biomarkers used to assess kidney function (serum creatinine, estimated glomerular filtration rate).ResultsThe mean urinary neutrophil gelatinase-associated lipocalin, interleukin-18, and kidney injury molecule-1 were statistically significantly higher in patients with hepatorenal syndrome and were found to be helpful in the early detection with cutoff values of 125 ng/ml, 34.8 pg/ml, and 3.1 pg/ml, respectively.ConclusionsUrinary neutrophil gelatinase-associated lipocalin, interleukin-18, and kidney injury molecule-1 levels are higher in patients with cirrhotic ascites complicated by HRS-AKI using the new definition of HRS, but IL-18 has lower sensitivity and specificity for the prediction of HRS-AKI as compared to NGAL and KIM-1.

Guideline updates for definition, diagnosis and management of hepatorenal syndrome

Hepatorenal syndrome (HRS) is a unique form of acute kidney injury (AKI) developing in patients with end‐stage liver disease. AKI is a frequent complication in advanced cirrhosis patients which is associated with increased hospital admissions and decreased survival. The definition of AKI in cirrhosis has been recently modified and the new diagnostic criteria are based on small changes in serum creatinine with respect to previous values, occurring within a short period of time.
 Systemic circulatory dysfunction and marked kidney vasoconstriction play a key role in the development of HRS. The modification of the AKI definition has also led to a change in the diagnostic criteria of HRS. The new diagnostic criteria are based on AKI stages and there is no need to reach a specific serum creatinine threshold. The use of the new HRS definition may lead to an earlier identification of renal impairment and better prognostic stratification. According to these new criteria, treatment with vasoconstrictors and albumin for the management of HRS will be started at lower serum creatinine values, with expected higher response rates. There are consistent data showing that some urine biomarkers, particularly NGAL (neutrophil gelatinase‐associated lipocalin), may be useful in daily clinical practice for the differential diagnosis of the cause of AKI in cirrhosis. Various HRS treatment regimens are available worldwide and all are designed to increase the mean arterial pressure by increasing the central blood volume and decreasing splanchnic vasodilation, and to serve as bridge to liver transplantation.

Cirrhosis and Complications of Portal Hypertension

Cirrhosis is the most advanced stage of all the different types of chronic liver diseases. It is defined as a diffuse disorganization of normal hepatic structure by extensive fibrosis associated with regenerative nodules. Hepatic fibrosis is potentially reversible if the causative agent is removed. However, advanced cirrhosis leads to major alterations in the hepatic vascular bed and is usually irreversible. Cirrhosis is a progressive and severe clinical condition associated with considerable morbidity and high mortality. It leads to a wide spectrum of characteristic clinical manifestations, mainly attributable to hepatic insufficiency and portal hypertension. Major complications of portal hypertension include ascites, gastrointestinal (GI) variceal bleeding, hepatic encephalopathy (HE), renal failure, and bacterial infections. In recent years, major advances in the understanding of the natural history and pathophysiology of cirrhosis and the treatment of its complications have led to improved management, quality of life, and life expectancy of patients with this disease. Cirrhosis is also a risk factor for developing hepatocellular carcinoma (HCC). Decompensated cirrhosis carries a poor short-term prognosis; thus, orthotopic liver transplantation (OLT) should always be considered in suitable candidates. This chapter describes the epidemiology, etiology and genetic factors, pathogenesis, diagnosis, general management, and treatment of cirrhosis. Complications of cirrhosis are discussed, including ascites, spontaneous bacterial peritonitis, dilutional hyponatremia, hepatorenal syndrome, variceal bleeding, hepatopulmonary syndrome and postpulmonary hypertension, HE, and HCC. Indications and contraindications for liver transplantation are described. Figures show liver biopsy results and ultrasound images in cirrhosis from hepatitis C, a patient with tense ascites, transjugular intrahepatic portosystemic shunting (TIPS), large esophageal varices with red spots, and HCC. Tables outline the main causes of cirrhosis and the diagnostic methods for identifying them, the Child-Pugh score, diagnostic criteria for hepatorenal syndrome, grades of HE, and indications for liver transplantation.This chapter contains 6 highly rendered figures, 8 tables, 73 references.

Hepatorenal syndrome in the era of acute kidney injury.

Acute kidney injury (AKI) is a frequent complication of patients with advanced cirrhosis that it is associated with increased hospital admissions and decreased survival. The definition of AKI in cirrhosis has been recently modified and the new diagnostic criteria are based on small changes in serum creatinine with respect to previous values, occurring within a short period of time. The use of this new definition may lead to an earlier identification of renal impairment and better prognostic stratification. Hepatorenal syndrome (HRS) is a unique form of AKI developing in patients with end-stage liver disease. Systemic circulatory dysfunction and marked kidney vasoconstriction play a key role in the development of HRS. The modification of the definition of AKI has also led to a change in the diagnostic criteria of HRS. The new diagnostic criteria are based on AKI stages and there is no need to reach a specific serum creatinine threshold. According to these new criteria, treatment with vasoconstrictors and albumin for the management of HRS will be started at lower serum creatinine values, with expected higher response rates. Finally, there are consistent data showing that some urine biomarkers, particularly NGAL (neutrophil gelatinase-associated lipocalin), may be useful in daily clinical practice for the differential diagnosis of the cause of AKI in cirrhosis.

Diagnostic criteria of hepatorenal syndrome and modern methods of therapy (literature review)

Hepatorenal syndrome (HRS) is a variant of functional renal failure in acute or chronic liver pathology. Type 1 HRS entails a rapidly progressive decline in kidney function within few days and without liver transplantation, 95,0 % of patients die within the next few weeks. With type 2 HRS, kidney function remains stable or gradually declining over several months. HRS diagnosis is based on the exclusion of other causes of renal failure. Pathophysiological changes in renal failure in the case of HRS are quite complex – they include an increase in the synthesis of vasoactive substances, which lead to a decrease in renal perfusion, a decrease in resistance in peripheral arteriovenous anastomosis, the development of portal hypertension, ascites, a decrease in colloidal osmotic pressure and a consistently increasing delay of sodium and water in the kidneys. HRS therapy is based on acid-base balance and anemia correction, intravenous administration of albumin, paracentesis, the removal of nephrotoxic agents and the renal replacement therapy is only symptomatic. areast-font-family:Times New Roman;mso-bidi-font-family:Times New Roman; mso-ansi-language:EN-US;mso-fareast-language:EN-US;mso-bidi-language:AR-SA'>, 420012

Pathophysiological basis of portal hypertension and the new concept of acute kidney injury in patients with liver cirrhosis

Recently, the International Club of Ascites (ICA) has developed a new expert consensus on the diagnosis and treatment of acute kidney injury (AKI) in patients with liver cirrhosis, which reflects the new concept of AKI management in patients with liver cirrhosis. This consensus emphasizes the increase in the absolute value of serum creatinine (SCr) and establishes a new staging system for AKI, which may help to evaluate disease progression and recovery. In addition, the new management concept also emphasizes that when AKI progresses to stage 2/3 or still progresses after comprehensive treatment, a diagnosis can be made and vasoconstrictors and albumin can be used as long as the patient meets the other diagnostic criteria for hepatorenal syndrome, regardless of SCr level.

New Developments in Hepatorenal Syndrome

Hepatorenal syndrome (HRS) continues to be one of the major complications of decompensated cirrhosis, leading to death in the absence of liver transplantation. Challenges in precisely evaluating renal function in the patient with cirrhosis remain because of the limitations of serum creatinine (Cr) alone in estimating glomerular filtration rate (GFR); current GFR estimating models appear to underestimate renal dysfunction. Newer models incorporating renal biomarkers, such as the Cr-Cystatin C GFR Equation for Cirrhosis appear to estimate measured GFRmore accurately. A major change in the diagnostic criteria for HRS based on dynamic serial changes in serum Cr that regard HRS type 1 as a special form of acute kidney injury promises the possibility of earlier identification of renal dysfunction in patients with cirrhosis. The diagnostic criteria of HRS still include the exclusion of other causes of kidney injury. Renal biomarkers have been disappointing in assisting with the differentiation of HRS from prerenal azotemia and other kidney disorders. Serum metabolomic profiling may be a more powerful tool to assess renal dysfunction, although the practical clinical significance ofthis remains unclear. As a result of the difficulties of assessing renal function in cirrhosis and the varying HRS diagnostic criteria and the rigor with which they are applied, the precise incidence and prevalence of HRS is unknown, but it is likely that HRS occurs more commonly than expected. The pathophysiology of HRS is rooted firmly in the setting of progressive reduction in renal blood flow as a result of portal hypertension and splanchnic vasodilation. Progressive marked renal cortical ischemia in patients with cirrhosis parallels the evolution of diuretic-sensitive ascites to diuretic-refractory ascites and HRS, a recognized continuum of renal dysfunction in cirrhosis. Alterations in nitrous oxide production, both increased and decreased, may play a major role in the pathophysiology of this evolution. The inflammatory cascade, triggered by bacterial translocation and endotoxemia, increasingly recognized as important in the manifestation of acute-on-chronic liver failure, also may play a significant role in the pathophysiology of HRS. The mainstay of treatment remains vasopressor therapy with albumin in an attempt to reverse splanchnic vasodilation and improve renal blood flow. Several meta-analyses have confirmed thevalue of vasopressors, chiefly terlipressin and noradrenaline, in improving renal function and reversing HRS type 1. Other interventions such as renal replacement therapy, transjugular intrahepatic portosystemic shunt, and artificial liver support systems have a very limited role in improving outcomes in HRS. Liver transplantation remainsthe definitive treatment for HRS. The frequency of simultaneous liver-kidney transplantation has increased dramatically in the Model for End-stage Liver Disease era, with changes in organ allocation policies. This has resulted in a more urgent need to predict native kidney recovery from HRS after liver transplantation alone, to avoid unnecessary simultaneous liver-kidney transplantation.

Cirrhosis and Complications of Portal Hypertension

Cirrhosis is the most advanced stage of all the different types of chronic liver diseases. It is defined as a diffuse disorganization of normal hepatic structure by extensive fibrosis associated with regenerative nodules. Hepatic fibrosis is potentially reversible if the causative agent is removed. However, advanced cirrhosis leads to major alterations in the hepatic vascular bed and is usually irreversible. Cirrhosis is a progressive and severe clinical condition associated with considerable morbidity and high mortality. It leads to a wide spectrum of characteristic clinical manifestations, mainly attributable to hepatic insufficiency and portal hypertension. Major complications of portal hypertension include ascites, gastrointestinal (GI) variceal bleeding, hepatic encephalopathy (HE), renal failure, and bacterial infections. In recent years, major advances in the understanding of the natural history and pathophysiology of cirrhosis and the treatment of its complications have led to improved management, quality of life, and life expectancy of patients with this disease. Cirrhosis is also a risk factor for developing hepatocellular carcinoma (HCC). Decompensated cirrhosis carries a poor short-term prognosis; thus, orthotopic liver transplantation (OLT) should always be considered in suitable candidates. This chapter describes the epidemiology, etiology and genetic factors, pathogenesis, diagnosis, general management, and treatment of cirrhosis. Complications of cirrhosis are discussed, including ascites, spontaneous bacterial peritonitis, dilutional hyponatremia, hepatorenal syndrome, variceal bleeding, hepatopulmonary syndrome and postpulmonary hypertension, HE, and HCC. Indications and contraindications for liver transplantation are described. Figures show liver biopsy results and ultrasound images in cirrhosis from hepatitis C, a patient with tense ascites, transjugular intrahepatic portosystemic shunting (TIPS), large esophageal varices with red spots, and HCC. Tables outline the main causes of cirrhosis and the diagnostic methods for identifying them, the Child-Pugh score, diagnostic criteria for hepatorenal syndrome, grades of HE, and indications for liver transplantation.This chapter contains 6 highly rendered figures, 8 tables, 73 references.

Cirrhosis and Complications of Portal Hypertension

Cirrhosis is the most advanced stage of all the different types of chronic liver diseases. It is defined as a diffuse disorganization of normal hepatic structure by extensive fibrosis associated with regenerative nodules. Hepatic fibrosis is potentially reversible if the causative agent is removed. However, advanced cirrhosis leads to major alterations in the hepatic vascular bed and is usually irreversible. Cirrhosis is a progressive and severe clinical condition associated with considerable morbidity and high mortality. It leads to a wide spectrum of characteristic clinical manifestations, mainly attributable to hepatic insufficiency and portal hypertension. Major complications of portal hypertension include ascites, gastrointestinal (GI) variceal bleeding, hepatic encephalopathy (HE), renal failure, and bacterial infections. In recent years, major advances in the understanding of the natural history and pathophysiology of cirrhosis and the treatment of its complications have led to improved management, quality of life, and life expectancy of patients with this disease. Cirrhosis is also a risk factor for developing hepatocellular carcinoma (HCC). Decompensated cirrhosis carries a poor short-term prognosis; thus, orthotopic liver transplantation (OLT) should always be considered in suitable candidates. This chapter describes the epidemiology, etiology and genetic factors, pathogenesis, diagnosis, general management, and treatment of cirrhosis. Complications of cirrhosis are discussed, including ascites, spontaneous bacterial peritonitis, dilutional hyponatremia, hepatorenal syndrome, variceal bleeding, hepatopulmonary syndrome and postpulmonary hypertension, HE, and HCC. Indications and contraindications for liver transplantation are described. Figures show liver biopsy results and ultrasound images in cirrhosis from hepatitis C, a patient with tense ascites, transjugular intrahepatic portosystemic shunting (TIPS), large esophageal varices with red spots, and HCC. Tables outline the main causes of cirrhosis and the diagnostic methods for identifying them, the Child-Pugh score, diagnostic criteria for hepatorenal syndrome, grades of HE, and indications for liver transplantation.This chapter contains 6 highly rendered figures, 8 tables, 73 references.

Acute kidney injury in liver cirrhosis: new definition and application.

The traditional diagnostic criteria of renal dysfunction in cirrhosis are a 50% increase in serum creatinine (SCr) with a final value above 1.5 mg/dL. This means that patients with milder degrees of renal dysfunction are not being diagnosed, and therefore not offered timely treatment. The International Ascites Club in 2015 adapted the term acute kidney injury (AKI) to represent acute renal dysfunction in cirrhosis, and defined it by an increase in SCr of 0.3 mg/dL (26.4 µmoL/L) in <48 hours, or a 50% increase in SCr from a baseline within ≤3 months. The severity of AKI is described by stages, with stage 1 represented by these minimal changes, while stages 2 and 3 AKI by 2-fold and 3-fold increases in SCr respectively. Hepatorenal syndrome (HRS), renamed AKI-HRS, is defined by stage 2 or 3 AKI that fulfils all other diagnostic criteria of HRS. Various studies in the past few years have indicated that these new diagnostic criteria are valid in the prediction of prognosis for patients with cirrhosis and AKI. The future in AKI diagnosis may include further refinements such as inclusion of biomarkers that can identify susceptibility for AKI, differentiating the various prototypes of AKI, or track its progression.

Population Based Trends in the Incidence of Hospital Admission for the Diagnosis of Hepatorenal Syndrome: 1998-2011.

Background and Objectives. Hepatorenal syndrome carries a high risk of mortality. Understanding the incidence and mortality trends in hepatorenal syndrome will help inform future studies regarding the safety and efficacy of potential therapeutic interventions. Design and Methods. We conducted a retrospective cohort study using the Nationwide Inpatient Sample. We identified hospitalizations from January 1998–June 2011 with a primary diagnosis of hepatorenal syndrome. To characterize the incidence trends in monthly hepatorenal syndrome hospitalizations, we fit a piecewise linear model with a change point at January 2008. We examined hospital and patient characteristics before and after the change point. Results. Hospital admissions with a diagnosis of hepatorenal syndrome increased markedly between September of 2007 and March of 2008. Comparing patients who were admitted with a diagnosis of hepatorenal syndrome prior to 2008 with those after 2008, we found that length of stay increased while the mortality of patients admitted for hepatorenal syndrome decreased. Conclusion. The revision of the diagnostic criteria for hepatorenal syndrome may have contributed to the increase in the incidence of admissions for hepatorenal syndrome. However, the changes in the principles of hepatorenal syndrome management may have also contributed to the increase in incidence and lower mortality.

Systemic vascular resistance and fluid status in patients with decompensated liver cirrhosis with or without functional renal failure in Egypt.

Background:Functional renal failure and cardiovascular dysfunction are common complications of liver cirrhosis. This study aimed to evaluate cardiac performance, systemic vascular resistance (SVR) and fluid status in patients with decompensated liver cirrhosis either with or without functional renal failure.Methods:Sixty patients diagnosed as having decompensated liver cirrhosis were divided into two groups. Group 1 included 30 patients with decompensated liver cirrhosis with ascites and with creatinine values ≤ 1.5 mg/dl. Group 2 included 30 azotemic decompensated cirrhotic patients with diagnostic criteria of hepatorenal syndrome (HRS). Also, 20 healthy subjects, of matched age and sex to the Group 1 and Group 2 patients, were included in the study as the control group. All patients and normal controls were subjected to clinical examination, laboratory evaluation, ECG, abdominal ultrasonography and echocardiographic studies.Results:The echocardiographic and ECG data showed significant increase in LAD (P<0.01, P<0.01), AoD (P<0.05, P<0.01), interventricular septum thickness (IVST) (P<0.01, P<0.01), posterior wall thickness (PWT) (P<0.01, P<0.01), EDD (P<0.01, P<0.01), ESD (P<0.05, P<0.01), left ventricular (LV) mass (P<0.01, P<0.01), and Corrected QT (QTc) (P<0.01, P<0.01) interval with significant decrease in SVR (P<0.01, P<0.01). Additionally, there was significant decrease in IVC diameter in both patients groups compared to the control group (P<0.01, P<0.01).Conclusion:Patients with decompensated liver cirrhosis have low SVR, and Doppler echocardiography provides an easy noninvasive tool to assess this finding. Also, these patients demonstrate small inferior vena cava (IVC) diameter with normal collapsibility, which indicates low effective plasma volume. Measuring IVC diameter and collapsibility are of value in the prediction of intravascular fluid status in liver cirrhosis. This is especially true with renal dysfunction. Early addition of oral vasoconstrictors in decompensated patients may correct the SVR and circulatory dysfunction and hinder HRS occurrence.

Sepsis-induced acute kidney injury in patients with cirrhosis.

Acute kidney injury (AKI) is a common and life-threatening complication in patients with cirrhosis. Recently, new criteria for the diagnosis of AKI have been proposed in patients with cirrhosis by the International Club of Ascites. Almost all types of bacterial infections can induce AKI in patients with cirrhosis representing its most common precipitating event. The bacterial infection-induced AKI usually meets the diagnostic criteria of hepatorenal syndrome (HRS). Well in keeping with the "splanchnic arterial vasodilation hypothesis", it has been stated that HRS develops as a consequence of a severe reduction of effective circulating volume related to splanchnic arterial vasodilation and to an inadequate cardiac output. Nevertheless, the role of bacterial infections in precipitating organ failures, including renal failure, is enhanced when their course is characterized by the development of a systemic inflammatory response syndrome (SIRS), thus, when sepsis occurs. Sepsis has been shown to be capable to induce "per se" AKI in animals as well as in patients conditioning also the features of renal damage. This observation suggests that when precipitated by sepsis, the pathogenesis and the clinical course of AKI also in patients with cirrhosis may differentiate to a certain extent from AKI with another or no precipitating factor. The purpose of this review is to describe the features of AKI precipitated by bacterial infections and to highlight whether infection and/or the development of SIRS may influence its clinical course, and, in particular, the response to treatment.

Hepatorenal Syndrome

Hepatorenal syndrome (HRS) is a form of functional renal failure that develops as a consequence of portal hypertension in cirrhosis of the liver or other processes that acutely raise portal pressure, such as fulminant liver failure or severe alcoholic hepatitis. Its development is an independent risk factor for a poor post–liver transplantation outcome. This review addresses the epidemiology, pathophysiology, classification of subtypes of HRS, incidence, evaluation of the cirrhotic patient with renal insufficiency, prevention of HRS, and management. A figure shows the sequence of circulatory abnormalities in HRS, and a table lists the summary of the diagnostic criteria for HRS as established by the International Ascites Club. This review contains 1 highly rendered figure, 1 table, and 28 references.

Hepatorenal syndrome

Renal dysfunction is commonly seen in patients with end stage liver disease. Prognosis of patients who develop hepatorenal syndrome (HRS) is dismal with a median survival of around six months without liver transplantation. Advances in understanding of the pathophysiology of HRS has lead to evolving ideas regarding the definition and diagnostic criteria of HRS. In addition, recent pharmacological and other therapeutic innovations provide hope to patients of HRS. This is a review of diagnostic criteria, etio-pathogenesis and therapeutic options for patients of HRS based on the available evidence in literature.

Hepatorenal Syndrome: A Critical Update

Acute kidney injury (AKI) is common in cirrhotic patients with ascites. Although not the primary etiology of AKI in cirrhotic patients, hepatorenal syndrome (HRS) is a unique form of AKI that develops only in cirrhotic patients. Intense renal vasoconstriction is the hallmark of HRS. Different mechanisms contribute to renal vasoconstriction, with splanchnic vasodilatation and reduced effective blood volume playing a central role. Diagnostic criteria for HRS have been developed and were recently modified, but diagnosing HRS and differentiating it from other causes of AKI in cirrhotic patients continues to be a difficult task in some patients. Given its overall dismal prognosis, strategies to prevent HRS have been developed and proved to be effective in reducing HRS prevalence among cirrhotic patients. Liver transplantation is the ultimate treatment, but more than one treatment modality can be utilized as a bridge to transplantation. This review provides an update on our current understanding of HRS with emphasis on the underlying pathophysiological mechanisms involved, difficulties in diagnosis, and different treatment modalities.

Impact of hepatorenal syndrome and liver transplantation

Hepatorenal syndrome (HRS) is an extremely detrimental complication of cirrhosis, with dismal survival in untreated patients. Continued advances in understanding the pathophysiology of HRS have improved HRS recognition and facilitated development of effective treatment strategies. In this article, we review current concepts in HRS pathophysiology, guidelines for HRS diagnosis, effective treatment options presently available, and controversies surrounding liver versus liver-kidney transplant in transplant candidates. Published diagnostic criteria for HRS have improved early recognition and intervention in HRS. Increasing data support vasoconstrictor therapy for HRS reversal. Several randomized controlled trials clearly demonstrate efficacy of terlipressin therapy in HRS reversal; although comparable studies are lacking with norepinephrine, preliminary findings suggest that this regime may be the preferred alternative when terlipressin is unavailable for use. In transplant candidates without response to vasoconstrictor therapies, mounting evidence supports simultaneous liver-kidney transplantation if prolonged pretransplant dialysis is required. Prompt identification and therapy initiation in transplant candidates with HRS may improve transplantation rates and posttransplantation outcomes. Future studies identifying optimal vasoconstrictor regimens, alternative therapies, and factors predictive of response to therapy are needed. The appropriate use of simultaneous liver-kidney transplants in patients with HRS remains controversial and requires further analysis by the transplant community.

Diagnosis, treatment and survival of patients with hepatorenal syndrome: A survey on daily medical practice

Hepatorenal syndrome (HRS) is a severe complication of cirrhosis with ascites. The International Ascites Club recommended strict diagnostic criteria and treatment with vasoconstrictors and albumin. Aim of this prospective cohort study was to investigate the prevalence of HRS, diagnostic criteria, treatment and 3-month outcome in the daily-clinical-practice. Two-hundred-fifty-three patients with cirrhosis and renal failure consecutively admitted to 21 Italian hospitals were recruited. The prevalence of HRS was 45.8% (30% type-1 and 15.8% type-2). In 36% of cases HRS was presumed because not all diagnostic criteria could be fulfilled. In 8% of cases HRS was superimposed on an organic nephropathy. Patients with HRS type-1 were younger and showed higher leukocyte count, higher respiratory rates, and worse liver function scores. Sixty-four patients with HRS type-1 received vasoconstrictors (40 terlipressin and 24 midodrine/octreotide). A complete response was obtained in 19 cases (30%) and a partial response in 13 (20%). Age was the only independent predictor of response (p=0.033). Three-month survival of patients with HRS type-1 was 19.7%. Survival was better in patients who responded to therapy. Age (p=0.017), bilirubin (p=0.012), and creatinine increase after diagnostic volume expansion (p=0.02) independently predicted death. The mortality rate was 97% among patients with at least two negative predictors. The diagnostic criteria of HRS in our daily-clinical-practice could not be completely fulfilled in one third of cases. The treatment with vasoconstrictors and albumin was widely implemented. Mortality was strongly predicted by simple baseline variables.

Diagnosis, prevention and treatment of hepatorenal syndrome in cirrhosis

Hepatorenal syndrome (HRS) is a serious complication of end-stage liver disease, occurring mainly in patients with advanced cirrhosis and ascites, who have marked circulatory dysfunction,1 as well as in patients...