The Use of Rifaximin in Patients With Cirrhosis.

Rifaximin is an oral nonsystemic antibiotic with minimal gastrointestinal absorption and broad-spectrum antibacterial activity covering both gram-positive and gram-negative organisms. Rifaximin is currently used worldwide in patients with cirrhosis for preventing recurrent HE because its efficacy and safety have been proven by large randomized clinical trials. In the last decade, experimental and clinical evidence suggest that rifaximin could have other beneficial effects on the course of cirrhosis by modulating the gut microbiome and affecting the gut-liver axis, which in turn can interfere with major events of the pathophysiological cascade underlying decompensated cirrhosis, such as systemic inflammatory syndrome, portal hypertension, and bacterial infections. However, the use of rifaximin for prevention or treatment of other complications, including spontaneous bacterial peritonitis or other bacterial infections, is not accepted because evidence by clinical trials is still very weak. The present review deals in the first part with the potential impact of rifaximin on pathogenic mechanisms in liver diseases, whereas in the second part, its clinical effects are critically discussed. It clearly emerges that, because of its potential activity on multiple pathogenic events, the efficacy of rifaximin in the prevention or management of complications other than HE deserves to be investigated extensively. The results of double-blinded, adequately powered randomized clinical trials assessing the effect of rifaximin, alone or in combination with other drugs, on hard clinical endpoints, such as decompensation of cirrhosis, acute-on-chronic liver failure, and mortality, are therefore eagerly awaited.

Effectiveness of terlipressin for prevention of complications after major liver resection - A randomized placebo-controlled trial.

BACKGROUND: Elevated portal pressure in response to major liver resection is associated with impaired liver regeneration and increased postoperative complications. Terlipressin, a splanchnic vasoconstrictor used for treatment of hepatorenal syndrome, was tested for reduction of complications and renal protection after liver resection. METHODS: A randomized double-blinded placebo-controlled trial including patients undergoing elective major liver resection was performed. Terlipressin was administered to patients in the intervention group for five days. The primary outcome parameter was the incidence of a clinical composite endpoint of following liver specific complications 6 weeks after surgery: liver failure, ascites, bile leakage, intra-abdominal abscess and operative mortality. Postoperative kidney function was assessed as a secondary endpoint. RESULTS: 150 patients (mean age 63.4 years, 73.3% male) were included. No difference was found in the composite endpoint between the placebo and intervention group (32.8% versus 30.8%, relative risk 1.066, 95%CI 0.643 to 1.769, p = 0.85). Patients receiving terlipressin showed a significant lower decrease in postoperative estimated glomerular filtration rate compared to placebo (two way ANOVA, p = 0.005). CONCLUSION: Perioperative administration of terlipressin during major liver surgery did not affect a composite endpoint of liver specific complications, but significantly protected from postoperative deterioration of kidney function compared to placebo. CLINICALTRIALS. GOV IDENTIFIER: NCT01921985.

Deoxyribonuclease partially ameliorates thioacetamide-induced hepatorenal injury.

Several recent studies have shown that liver injury is associated with the release of DNA from hepatocytes. This DNA stimulates innate immunity and induces sterile inflammation, exacerbating liver damage. Similar mechanisms have been described for acute renal injury. Deoxyribonuclease degrades cell-free DNA and can potentially prevent some of the induced tissue damage. This study analyzed the effects of thioacetamide-induced hepatorenal injury on plasma DNA in rats. Plasma DNA of both nuclear and mitochondrial origin was higher in thioacetamide-treated animals. Administration of deoxyribonuclease resulted in a mild, nonsignificant decrease in total plasma DNA and plasma DNA of mitochondrial origin but not of nuclear origin. This was accompanied by a decrease in bilirubin, creatinine, and blood urea nitrogen as markers of renal function. In conclusion, the study confirmed the hepatotoxic and nephrotoxic effect of thioacetamide. The associated increase in cell-free DNA seems to be involved in hepatorenal pathogenesis because treatment with deoxyribonuclease resulted in a partial prevention of hepatorenal injury. Further experiments will focus on the effects of long-term treatment with deoxyribonuclease in other clinically more relevant models. Clinical studies should test endogenous deoxyribonuclease activity as a potential risk determinant for kidney or liver failure.NEW & NOTEWORTHY Thioacetamide-induced hepatorenal injury resulted in higher plasma cell-free DNA. Deoxyribonuclease decreased average cell-free DNA of mitochondrial origin but not nuclear origin. Deoxyribonuclease partially prevented hepatorenal injury in rats.

[Is there a role for pentoxifylline in the treatment of alcoholic hepatitis?]. / ¿Tiene algún papel la pentoxifilina en el tratamiento de la hepatitis alcohólica?

Despite better knowledge of the pathogenesis of severe alcoholic hepatitis (AH), corticosteroids are still the treatment recommended by clinical guidelines, pentoxifylline being the second-line option for non-responders to corticosteriods and for patients with contraindications. Pentoxifylline is a phosphodiesterase inhibitor with an anti-TNF effect and has been reported to reduce mortality and the incidence of hepatorenal syndrome in severe AH. After the first report, several studies, of distinct quality, have tested the efficacy of pentoxifylline in different scenarios. The conclusions of these studies are that pentoxifylline seems to improve survival in comparison to placebo but has lower efficacy than corticosteroids, with no improvement in survival when added to corticosteroids or in non-responders to steroid therapy. The role of pentoxifylline in severe alcoholic hepatitis is even more doubtful after the results of a very recent controlled study that showed no beneficial effect on survival at 1, 3 and 12 months of follow up, although a very recent network meta-analysis reported a beneficial effect of pentoxifylline alone or with corticosteroids on short-term survival. In conclusion, pentoxifylline has no clear beneficial effects in severe AH but could perhaps be used in patients with a contraindication to corticosteroids. However, the recommendations of clinical guidelines should be reconsidered and it is essential to search for new therapeutic targets for this disease.

Human serum albumin, systemic inflammation, and cirrhosis.

Human serum albumin (HSA) is one of the most frequent treatments in patients with decompensated cirrhosis. Prevention of paracentesis-induced circulatory dysfunction, prevention of type-1 HRS associated with bacterial infections, and treatment of type-1 hepatorenal syndrome are the main indications. In these indications treatment with HSA is associated with improvement in survival. Albumin is a stable and very flexible molecule with a heart shape, 585 residues, and three domains of similar size, each one containing two sub-domains. Many of the physiological functions of HSA rely on its ability to bind an extremely wide range of endogenous and exogenous ligands, to increase their solubility in plasma, to transport them to specific tissues and organs, or to dispose of them when they are toxic. The chemical structure of albumin can be altered by some specific processes (oxidation, glycation) leading to rapid clearance and catabolism. An outstanding feature of HSA is its capacity to bind lipopolysaccharide and other bacterial products (lipoteichoic acid and peptidoglycan), reactive oxygen species, nitric oxide and other nitrogen reactive species, and prostaglandins. Binding to NO and prostaglandins are reversible, so they can be transferred to other molecules at different sites from their synthesis. Through these functions, HSA modulates the inflammatory reaction. Decompensated cirrhosis is a disease associated systemic inflammation, which plays an important role in the pathogenesis of organ or system dysfunction/failure. Although, the beneficial effects of HAS have been traditionally attributed to plasma volume expansion, they could also relate to its effects modulating systemic and organ inflammation.

Treatment with metadoxine and its impact on early mortality in patients with severe alcoholic hepatitis.

BACKGROUND & AIM: Despite treatment with glucocorticoids, mortality remains high in patients with severe alcoholic hepatitis. Oxidative stress and depletion of mitochondrial glutathione are implicated factors in liver injury. The aim of this study was to evaluate the impact of the addition of metadoxine, a drug which possesses a multifactorial mechanism of action, including antioxidant properties, to standard treatment with glucocorticoids in patients with severe alcoholic hepatitis. MATERIAL AND METHODS: This randomized open label clinical trial was performed in Mexico's General Hospital (Registry Key DIC/10/107/03/043). We randomized 70 patients with severe alcoholic hepatitis. The first group received prednisone (40 mg/day), and the second group received prednisone (40 mg/day) plus metadoxine tablets (500 mg three times daily). The duration of treatment in both groups was 30 days. Survival at 30 and 90 days, development of complications, adverse events and response to treatment (Lille model) were assessed. RESULTS: In the group receiving metadoxine, significant improvements were observed, as follows: survival at 30 days (74.3 vs. 45.7%, P = 0.02); survival at 90 days (68.6 vs. 20.0%, P = 0.0001). There was less development or progression of encephalopathy (28.6 vs. 60.0%, P = 0.008) and hepatorenal syndrome (31.4 vs. 54.3%, P = 0.05), and the response to treatment (Lille model) was higher in the metadoxine group (0.38 vs. 0.63, P = 0.001; 95% CI 0.11 to 0.40). There were no differences between groups regarding the development or progression of variceal hemorrhage or infection. The incidence of adverse events, mainly gastrointestinal, was similar in both groups. CONCLUSIONS: Addition of metadoxine to glucocorticoid treatment improves the short-term survival of patients with severe alcoholic hepatitis and diminishes the development or progression of encephalopathy and hepatorenal syndrome.

Allopurinol Prevents Cirrhosis-Related Complications: A Quadruple Blind Placebo-Controlled Trial.

BACKGROUND: Complications associated with liver cirrhosis are various and potentially fatal. The treatment options to counteract hepatic decompensation are limited. Therefore, the study aimed to explore the use of allopurinol in preventing the recurrence of liver cirrhosis-related complications. METHODS: One hundred patients with hepatic decompensation were randomized into 1:1 ratio to receive either allopurinol 300 mg or placebo tablets once daily for 6 months. The primary endpoint was the incidence of cirrhosis-related complications (overt ascites, spontaneous bacterial peritonitis, variceal bleeding, hepatorenal syndrome, and hepatic encephalopathy). RESULTS: Six months following treatment, allopurinol reduced the relative risk (RR) of any first complication experienced after enrollment by 56% (hazard ratio [HR] 0.44; 95% confidence interval [CI], 0.27-0.62); P ˂ .001). Allopurinol decreased the RR of overt ascites by 67% (HR 0.33; 95% CI, 0.0098-0.94); P = .039] and reduced the RR of spontaneous bacterial peritonitis by about 75% (HR 0.25; 95% CI, 0.05-0.76; P = .01). Likewise, allopurinol was linked to an 80% reduction in the RR of developing hepatorenal syndrome (HR 0.2; 95% CI, 0.04-0.87; P = .033). CONCLUSION: Allopurinol significantly decreased the recurrence of overall liver cirrhosis-related complications. Therefore, allopurinol may constitute a promising agent for patients with hepatic decompensation. These positive outcomes could be a result of its ability to reduce bacterial translocation and inflammation. GOV IDENTIFIER: NCT005545670.

Long-term administration of rifaximin improves the prognosis of patients with decompensated alcoholic cirrhosis.

BACKGROUND AND AIM: Cirrhotic patients are predisposed to intestinal bacterial overgrowth with translocation of bacterial products which may deteriorate liver hemodynamics. Having shown that short-term administration of rifaximin improves liver hemodynamics in decompensated cirrhosis, we conducted this study to investigate the effect of intestinal decontamination with rifaximin on the long-term prognosis of patients with alcohol-related decompensated cirrhosis (Child-Pugh > 7) and ascites. METHODS: Patients who had received rifaximin and showed improved liver hemodynamics were enrolled in the current study and continued to receive rifaximin (1200 mg/day). Each patient was matched by age, sex, and Child-Pugh grade to two controls and followed up for up to 5 years, death or liver transplantation. Survival and risk of developing portal hypertension-related complications were compared between rifaximin group and controls. RESULTS: Twenty three patients fulfilled the inclusion criteria and matched with 46 controls. Patients who received rifaximin had a significant lower risk of developing variceal bleeding (35% vs. 59.5%, P = 0.011), hepatic encephalopathy (31.5% vs. 47%, P = 0.034), spontaneous bacterial peritonitis (4.5% vs. 46%, P = 0.027), and hepatorenal syndrome (4.5% vs. 51%, P = 0.037) than controls. Five-year cumulative probability of survival was significantly higher in patients receiving rifaximin than in controls (61% vs. 13.5%, P = 0.012). In the multivariate analysis, rifaximin administration was independently associated with lower risk of developing variceal bleeding, hepatic encephalopathy, spontaneous bacterial peritonitis, hepatorenal syndrome, and higher survival. CONCLUSIONS: In patients with alcohol-related decompensated cirrhosis, long-term rifaximin administration is associated with reduced risk of developing complications of portal hypertension and improved survival.

[Hepatorenal syndrome]. / Hepatorenales Syndrom.

Hepatorenal syndrome (HRS) is a unique form of acute renal failure occurring in patients with advanced cirrhosis or acute liver failure. In patients with ascites the incidence of HRS is 8 % and in end-stage liver disease 75 % of patients suffer from HRS. Vasodilation of splanchnic arteries with subsequent decrease of effective blood volume, arterial pressure and renal vasoconstriction is hypothesized to be the central pathophysiological mechanism leading to acute renal failure. Moreover, cardiac output might be decreased in advanced cirrhosis. There are two types of HRS: while HRS type 1 is characterized by a rapid progression to acute renal failure often triggered by a precipitating event, e. g. bacterial peritonitis, which can rapidly develop into multiorgan failure, HRS type 2 shows a more steadily or slowly progressive course to renal failure with increasing ascites. Type 1 HRS has the worst prognosis. Treatment options include pharmacological treatment with vasoconstrictors and albumin and placement of transjugular intrahepatic portosystemic shunts (TIPS) but can only partially improve the survival rate. Liver transplantation is the ultimate and only definitive treatment of patients with HRS.

[Challenges and advances in diagnostics, prevention and treatment of hepatorenal syndrome].

Hepatorenal syndrome (HRS) is an exclusion diagnosis in patients with decompensated liver cirrhosis. True hepatic functional insufficiency is sometimes unobvious. Differential diagnostics of HRS encounters difficulty despite new diagnostic criteria. HRS can be prevented by the correct treatment of portal hypertension and hepatic insufficiency under careful monitoring. Effective conservative therapy may significantly change the short-term prognosis and facilitate remission in selected patients. Terlipressin is the agent of choice for HRS therapy aimed at the promotion of intrahospital survival for the subsequent referral of the patient to liver transplantation.

Prevention of Hepatorenal Insufficiency Associated with Lead Exposure by Hibiscus sabdariffa L. Beverages Using In Vivo Assay.

Lead pollution is a major environmental challenge worldwide. Therefore, dietary interventions that are aimed at preventing lead's deleterious effects on body organs are needed. The study's goal was to study and compare the protective effect of cold and hot beverages of Roselle (Hibiscus sabdariffa L.) red calyces (CRB and HRB, respectively) on liver and kidney insufficiency associated with lead exposure in male rats. Adult albino rats (32 males) were divided into four groups of equal number, including a normal control (group 1), while groups from 2 to 4 received lead acetate (20 mg/kg body weight/day) and were kept untreated (group 2). The 3rd and the 4th groups received CRB and HRB (0.5 ml/100 g body weight/day), respectively, for 6 weeks. The gain in the body and relative weights of the liver and kidneys were calculated. Liver and kidney functions were determined in serum, while lead, delta-aminolevulinic acid dehydratase, and oxidative stress markers were established in tissues. Specimens from the liver and kidney of sacrificed rats were histopathologically examined. The total activity of antioxidants and total content of anthocyanin of both beverages were determined. Lead exposure resulted in its accumulation in tissues, leading to overweight and liver and kidney insufficiency along with oxidative stress, which was further confirmed by histological staining. CRB was more efficient than HRB in preventing the deleterious effects of lead intoxication. Due to their antioxidant properties, the present study proved that Roselle red calyx beverages, particularly the cold ones, are protective agents against lead-associated disorders in a rat model.

Management of refractory ascites and hepatorenal syndrome.

One of the most common manifestations of the development of portal hypertension in the patient with cirrhosis is the appearance of ascites. Once ascites develops, the prognosis worsens and the patient becomes susceptible to complications such as bacterial peritonitis, hepatic hydrothorax, hyponatremia, and complications of diuretic therapy. As the liver disease progresses, the ascites becomes more difficult to treat and many patients develop renal failure. Most patients can be managed by diuretics which, when used correctly, will control the ascites. Spontaneous bacterial peritonitis can be treated effectively, but portends a worse prognosis. Once the ascites becomes refractory to diuretics, liver transplantation is the best option, although use of transjugular intrahepatic portosystemic shunts will control the ascites in many patients. Lastly, the development of hepatorenal syndrome indicates the patient's liver disease is advanced, and transplantation again is the best option. However, use of vasoconstrictors may improve renal function in some patients, helping in their management while they await a liver transplant.

Enteral nutrition with or without N-acetylcysteine in the treatment of severe acute alcoholic hepatitis: a randomized multicenter controlled trial.

BACKGROUND & AIMS: Severe acute alcoholic hepatitis is associated with a high mortality rate. Oxidative stress is involved in the pathogenesis of acute alcoholic hepatitis. Previous findings had also suggested that enteral nutritional support might increase survival in patients with severe acute alcoholic hepatitis. Therefore, the aim of the present study was to evaluate the efficacy of N-acetylcysteine in combination with adequate nutritional support in patients with severe acute alcoholic hepatitis. METHODS: Patients with biopsy-proven acute alcoholic hepatitis and mDF ≥32 were randomized to receive N-acetylcysteine intravenously or a placebo perfusion along with adequate nutritional support for 14 days. The primary endpoint was 6-month survival; secondary endpoints were biological parameter evolution and infection rate. RESULTS: Fifty-two patients were randomized in the study (28 into the N-acetylcysteine arm, 24 into the control arm), and among them, five were excluded from the analysis for protocol violation. The two groups did not differ in baseline characteristics. Survival rates at 1 and 6 months in N-acetylcysteine and control groups were 70.2 vs. 83.8% (p=0.26) and 62.4 vs. 67.1% (p=0.60), respectively. Early biological changes, documented infection rate at 1 month, and incidence of hepatorenal syndrome did not differ between the two groups. CONCLUSIONS: In this study, high doses of intravenous N-acetylcysteine therapy for 14 days conferred neither survival benefits nor early biological improvement in severe acute alcoholic hepatitis patients with adequate nutritional support. However, these results must be viewed with caution, since the study suffered from a lack of power.

Hepatorenal syndrome.

Acute kidney injury (AKI) secondary to hepatorenal syndrome (HRS) is an ominous complication of end-stage liver disease (ESLD). In HRS, splanchnic and peripheral vasodilatation with reduction in effective arterial volume causes activation of mechanisms leading to intense renal vasoconstriction and functional AKI. HRS is a diagnosis of exclusion and all other causes of AKI (especially prerenal azotemia) have to be considered and excluded. Spontaneous bacterial peritonitis (SBP) frequently precipitates HRS and should be ruled out in all ESLD patients presenting with AKI. Prompt therapy of SBP with intravenous antibiotics and albumin lessens the risk of developing HRS. Combined use of intravenous albumin, splanchnic and/or peripheral vasoconstrictors, and renal replacement therapy (RRT) are only bridges to early liver transplantation (or combined liver-kidney transplantation in selected patients). Transplantation is the only definitive way of improving the long-term prognosis. Close collaboration between hospitalists/internists managing HRS patients and hepatology and nephrology consultants is critically important.

Renal failure in patients with cirrhosis: hepatorenal syndrome and renal support strategies.

PURPOSE OF REVIEW: The development of hepatorenal syndrome in liver cirrhosis leads to an increased morbidity and mortality in patients with cirrhosis. Currently, there are no proven methods for the treatment or prevention of hepatorenal syndrome except to maintain adequate hemodynamics and intravascular volume in this patient population. These patients will frequently require renal replacement therapy when presenting for hepatic transplantation. RECENT FINDINGS: New consensus definitions have been published in order to create uniform standards for classifying and diagnosing acute kidney injury. Two such groups are the Acute Dialysis Quality Initiative (ADQI) and the Acute Kidney Injury Network (AKIN), which have proposed approaches to defining criteria for acute kidney injury. Recent literature supports not only the role of splanchnic vasodilation and systemic vasoconstriction but also heart failure in the pathogenesis of hepatorenal syndrome. The practice of using vasoconstrictor and intravenous albumin therapy for the treatment of hepatorenal syndrome is ongoing with a growing body of recent data supporting the use of vasopressin analogs as the first-line therapy in the ICU setting with knowledge of the possible cardiovascular side-effects. SUMMARY: Hepatorenal syndrome, HRS, is a diagnosis of exclusion. There are two forms of hepatorenal syndrome: type 1 hepatorenal syndrome and type 2 hepatorenal syndrome. Type 1 HRS is rapidly progressive and portends a very poor prognosis and has a high mortality rate. Type 2 is more indolent while still associated with an overall poor prognosis. Treatment of HRS is largely still supportive. It is imperative to maintain euvolemia and hemodynamics in this patient population to optimize renal perfusion and preserve renal function. Renal replacement therapy may be necessary in this chronically ill patient population, if renal function deteriorates such that the kidneys cannot maintain metabolic and volume homeostasis. Further research is still necessary as to the prevention and effective treatment for hepatorenal syndrome.

[Prevention and treatment of hepatorenal syndrome by acute intestinal obstruction].

Results of treatment were analyzed in 358 patients with acute bowel obstruction resulted from a variety of causes. Algorithm for control of liver and renal function disturbances in dynamics was estimated basing on the markers for hepatorenal failure. It is shown that differentiated approach to extracorporal detoxification combined with enterosorbtion and complex therapy allows preventing hepatorenal failure and decreasing lethality and terms of hospitalization.

Albumin: Indications in chronic liver disease.

Albumin is currently employed as a plasma expander to prevent and treat specific complications of cirrhosis with ascites, such as the prevention of paracentesis-induced circulatory dysfunction and renal dysfunction induced by spontaneous bacterial peritonitis, as well as the diagnosis and treatment of acute kidney injury and hepatorenal syndrome. Recently, evidence has shown that long-term albumin administration in patients with decompensated cirrhosis reduces mortality and incidence of complications, eases the management of ascites, is cost effective, and has a good safety profile.

Management of hepatorenal syndrome.

Hepatorenal syndrome is a form of acute or sub-acute renal failure which develops in patients with chronic liver disease. In contrast to other forms of acute renal failure it may be reversible using pharmacological agents. The pathogenesis involves splanchnic vasodilatation and intense renal vasoconstriction. Increasing intravascular volume and prolonged treatment with vasoconstrictor drugs reverses renal failure in a significant proportion of patients. Agents currently used include the vasopressin analogues terlipressin and the alpha1-adrenoceptor agonist midodrine. The somatostatin analogue octreotide has been used in combination therapy but is ineffective as monotherapy. Intravenous albumin is an important adjunctive treatment both in the prevention and treatment of hepatorenal syndrome. Increasing intravascular volume using TIPS (transjugular intrahepatic stent shunt) is effective in some patients and may be useful in maintaining patients who have initially responded to pharmacological therapy. Despite improvements in survival, long term prognosis is still poor and generally depends on the degree of reversibility of the underlying liver disease or access to liver transplantation.

Primary and secondary prophylaxis of spontaneous bacterial peritonitis: current state of the art.

Introduction: Spontaneous bacterial peritonitis represents a frequent and severe complication in cirrhotic patients with ascites. In daily practice, the diagnosis of spontaneous bacterial peritonitis might be challenging in the absence of the typical signs and symptoms of infection such as fever or leukocytosis. Areas covered: Aim of this review is to revise the current state of the art on primary and secondary spontaneous bacterial peritonitis. Literature search in Medline/Pubmed was performed. Expert opinion: Historically, gram-negative bacteria were the most frequent etiologic agents of spontaneous bacterial peritonitis, with Escherichia coli and Klebsiella spp. being the most frequently isolated bacteria. However, major changes in this regard occurred over the last few decades with an increasing prevalence of gram-positive, quinolone-resistant, and multidrug-resistant bacteria. In particular, the increasing prevalence of quinolone-resistant bacteria challenged the prominent role of norfloxacin in spontaneous bacterial peritonitis prevention. Given the high mortality rate and the risk of developing the hepatorenal syndrome, prophylaxis of spontaneous bacterial peritonitis is indicated in three high-risk populations: patients with acute gastrointestinal hemorrhage, patients with low total protein content in ascitic fluid and advanced cirrhosis, and patients with a previous history of spontaneous bacterial peritonitis (secondary prophylaxis).

Effect of low dose albumin administration in spontaneous bacterial peritonitis on renal function and survival.

BACKGROUND AND STUDY AIMS: Current guidelines favour albumin administration during spontaneous bacterial peritonitis (SBP). However, its use is limited in clinical practice and low doses are preferred. The aim of our study was to determine the effect of low dose albumin perfusion during SBP on mortality and prevention of hepatorenal syndrome (HRS) in cirrhotic patients. PATIENTS AND METHODS: A retrospective study including consecutive patients with SBP hospitalized from 2002 to 2015 was performed. All patients were treated by intravenous empiric antibiotics associated with albumin infusion (30 g/day the first and third day) irrespective of patient's weight. The diagnosis of HRS was assessed according to the International Ascites Club criteria. The survival, the frequency of HRS and any disturbance in renal function were recorded. RESULTS: Fourty nine patients (sex ratio = 0.81, mean age 60.6 years [23-89]) were included. Main cause of cirrhosis was hepatitis B and C in 42.9% of cases. 63.3% were of Child Pugh C score%. The first line intravenous antibiotic treatment was based on cefotaxime in 87.8% of cases, followed by ofloxacin in 6.1% of cases. The outcome was favourable in 85.7% of cases. HRS was observed in 9 patients (18.3%) within 18 months [1-55]. Otherwise, 10 patients (20.4%) experienced an increase in creatinine level despite of albumin perfusion. The immediate mortality was 4%, and the six months survival was of 81.8%. CONCLUSION: Despite even a low dose administration of albumin during SBP, renal dysfunction and HRS occurred less than described in literature. These results associated with cost considerations could suggest to use such an intervention during SBP or to select high risk patients who must receive albumin perfusion during SBP.