Falla hepática aguda / Acute liver failure

La falla hepática aguda es la pérdida súbita de la función hepática en un corto plazo en un paciente sin enfermedad hepática previa, que se acompaña de coagulopatía y encefalopatía. Es una entidad rara con una incidencia muy baja que afecta especialmente a personas jóvenes. La principal causa en países desarrollados es la toxicidad por acetaminofén, mientras que en los países subdesarrollados son las hepatitis virales. El curso natural de la enfermedad es la progresión rápida a muerte por falla orgánica multisistémica, sepsis o edema cerebral. Después del diagnóstico, los pacientes deben remitirse tempranamente a la unidad de cuidado intensivo y a centros que ofrezcan trasplante hepático. La supervivencia sin trasplante hepático hasta hace pocos años era menor al 15%; sin embargo, en la actualidad puede ser hasta del 50%, dependiendo de la causa, y está relacionada con tratamientos específicos, la disponibilidad de trasplante hepático y una atención óptima en las unidades de cuidados intensivos. El trasplante hepático se constituye en el tratamiento de elección para los pacientes con falla hepática aguda y criterios de mal pronóstico del King's College.

Acute liver failure is the severe short-term liver function impairment in a patient without previous liver disease, which is accompanied by coagulopathy and encephalopathy. It is a rare condition with a very low incidence that affects young people. The leading cause in developed countries is acetaminophen toxicity, while in developing countries is mainly caused by viral hepatitis. The natural course is characterized by a rapid progression to death due to multisystemic organ failure, sepsis, or cerebral edema. After diagnosis, patients must be transferred to the intensive care unit and liver transplantation centers. Survival without liver transplantation until a few years ago was less than 15%; however, currently it can be up to 50% depending on the cause, and it is related to specific treatments, availability of liver transplantation and optimal care in the intensive care units. Liver transplantation is the treatment of choice for patients with acute liver failure and King's College criteria for poor prognosis.

Study of gastrointestinal manifestations in Dengue fever

Background: Dengue is an arthropod borne viral haemorrhagic fever. In India between 2015-2017, 790 deaths have been recorded according to NVBDCP data. Gastrointestinal manifestations are among the most common manifestations in dengue fever, and are most often missed due to lack of awareness. This study aims to find the spectrum of Gastrointestinal manifestations and correlation of GI manifestations with severity of Dengue.Methods: A cross-sectional observational study was conducted on 100 consecutive cases of serologically confirmed Dengue fever. Patients were examined clinically, and laboratory data was assessed till they got discharged. Gastrointestinal manifestations of dengue fever were noted and analyzed.Results: This study included 100 consecutive cases of dengue fever. Mean age of the study population was 32.48+12.40 years of them 77 were males and 23 were female patients. Gastrointestinal manifestations were noted in 96% of the patients. GI manifestations noted were Nausea in 71%, Elevation of transaminases in 59%, vomiting in 54%, pain abdomen in 31%, Ascites in 24% hepatomegaly in 14%, diarrhoea in 13%, Acalculous cholecystitis in 13%, Acute fulminant hepatitis in 6%, Upper GI bleed in 6%, splenomegaly in 5%, and Acute pancreatitis in 4% of patients. Of these, GI manifestations like nausea, vomiting, pain abdomen, GI bleed, ascites, jaundice, elevation of transaminases, acute fulminant hepatitis and acute pancreatitis correlated with severity of Dengue fever . Conclusion: Gastrointestinal manifestations in Dengue fever are much more common than once thought of. In our study it was found in 96 percent of patients making it most common manifestations in dengue fever. Transaminitis and Atypical GI manifestations like acute pancreatitis, acute fulminant hepatitis may indicate severe Dengue. The differential diagnosis of an acute febrile syndrome with abdominal pain or gastrointestinal symptoms in patients living in endemic areas should include Dengue fever.

Successful Treatment of Neonatal Herpes Simplex Infection Presenting as Fulminant Hepatitis with Acyclovir and Peritoneal Dialysis

Disseminated neonatal herpes simplex virus (HSV) infection is a severe disease with a high mortality rate. Here, we report the patient presented with fulminant hepatic failure secondary to HSV infection followed by renal failure without any mucocutaneous symptoms. The patient recovered after treatment with acyclovir and peritoneal dialysis. This is the first known case of a patient in Korea who survived disseminated HSV infection with fulminant liver failure followed by renal failure without undergoing liver transplantation.

Enterovirus como agente causal de Hepatitis fulminante neonatal

El enterovirus es un virus ARN que pertenece a la familia Picornavirididae. La mayoría de los casos en infección en recién nacidos son producidos por los Enterovirus del grupo Coxsackie B y Echovirus. El método diagnóstico de elección para la detección del Enterovirus es la aplicación de la reacción en cadena de la polimerasa (PCR) para buscar la presencia de RNA de Enterovirus en LCR, suero o mucosas. A continuación se describe un caso de un neonato varón con antecedente de prematuridad de 36 semanas quién presentó hepatitis fulminante y coagulación intravascular diseminada secundaria a enterovirus.

Enterovirus is an RNA virus belonging to the family Picornaviridae. Most infections in newborns are caused by the Enterovirus group Coxsackie B and Echovirus. The diagnostic method for detection of Enterovirus is the application of the chain reaction (PCR) for the presence of Enterovirus RNA in cerebral spinal fluid, serum or mucous membranes. Here is a case of a newborn male child 36 week with fulminant hepatitis and disseminated intravascular coagulation secondary to enterovirus infection.

Long Term Outcomes of Pediatric Liver Transplantation According to Age

Liver transplantation (LT) has been the key therapy for end stage liver diseases. However, LT in infancy is still understudied. From 1992 to 2010, 152 children had undergone LT in Seoul National University Hospital. Operations were performed on 43 patients aged less than 12 months (Group A) and 109 patients aged over 12 months (Group B). The mean age of the recipients was 7 months in Group A and 74 months in Group B. The patients' survival rates and post-LT complications were analyzed. The mean Pediatric End-stage Liver Disease score was higher in Group A (21.8) than in Group B (13.4) (P = 0.049). Fulminant hepatitis was less common in Group A (4.8%) than in Group B (13.8%) (P = 0.021). The post-transplant lymphoproliferative disorder and portal vein complication were more common in Group A (14.0%, 18.6%) than in Group B (1.8%, 3.7%) (P = 0.005). However, the 1, 5, and 10 yr patient survival rates were 93%, 93%, and 93%, in Group A and 92%, 90%, and 88% in Group B (P = 0.212). The survival outcome of pediatric LT is excellent and similar regardless of age. LTs in infancy are not riskier than those of children.

How to Manage Hepatitis B Infection.

Hepatitis B is a potentially life-threatening infection caused by the hepatitis B virus (HBV), which attacks the liver and causes both acute and chronic disease. Presence of virus in infected host relies on demonstration of hepatitis B surface antigen/ hepatitis B virus-DNA (HBsAg/HBV-DNA) in serum/liver tissue. No treatment is required for acute hepatitis B. Patients with immunosuppressed state like chronic liver failure, transplant recipient and patients on cancer chemotherapy with acute hepatitis B may be treated with antivirals under study protocol or at expert centers. Screening of family members for HBsAg and anti- HBs is recommended. If both the markers are negative they should be vaccinated and vaccine success should be confirmed with anti-HBs testing.

Falência hepática aguda / Acute liver failure

Falência hepática aguda é uma síndrome clínica devastadora, com alta taxa de mortalidade, apesar dos recentes avanços da terapia intensiva. Determinar a causa tem importantes implicações prognósticas, e o transplante de fígado é um tratamento que salva vidas em casos selecionados. O conhecimento das últimas diretrizes e protocolos pode levar a melhores resultados.

Acute liver failure is a devasting clinical syndrome, with high mortality rate, despite critical care advances. Determining the cause has important prognostic implications, and the orthotopic liver transplantation is a life-saving treatment in select cases. Knowledge of the latest guidelines and treatment protocols can lead to improved patient case.

Manejo de la hepatitis B aguda grave y fulminante / Management of acute fulminant hepatitis B

Fulminant hepatitis B virus infection occurs in less than 1percent of acutely infected patients. Acute hepatitis Baccounts for 2-42 percent of the total of fulminant hepatitis cases depending on the geographic area. This infection is associated with 65-93 percent of mortality, without liver transplantation. Its pathogenesis is related to a severe immune response to infected hepatocytes, causing massive cytolysis and liver failure. During the last 3 decades its prognosis has improved due to better medical support in intensive care units, the use of liver transplantation and an improvement in the prevention and management of its complications. More recently the use of liver support devices (MARS, Prometheus, and BAL) has been considered in this situation as a bridge to liver transplantation. Recurrent hepatitis B virus reinfection of the graft was a major issue in the past, but currently with the use of hepatitis B immunoglobulin (HBIg) and oral antiviral therapy, the prognosis has improved, leading to excellent graft and patient outcomes after liver transplantation. There is controversial data on the use of oral antiviral therapy among fulminant hepatitis patients. While some authors have shown beneficial effects, other communications have failed to demonstrate any benefits. Nevertheless, many experts currently recommend the use of oral antiviral therapy in this setting due to their relative safety and potential benefits. This paper reviews the current view on management issues in reference to the patient with fulminant hepatic failure due to acute hepatitis B.

La hepatitis fulminante por virus de hepatitis B ocurre en menos del 1 por ciento de los casos de hepatitis B aguda. Del total de hepatitis fulminantes, entre el 2-42 por ciento son causadas por hepatitis B aguda, dependiendo del lugar geográfico donde se estudia. Se asocia a elevada mortalidad, entre 65-93 por ciento, sin el uso de trasplante hepático. Su patogenia se relaciona a una significativa respuesta inmune a hepatocitos infectados, determinando citolisis masiva y falla hepática. En las últimas 3 décadas el pronóstico de esta patología ha mejorado gracias al soporte médico en unidades de tratamiento intensivo, a la implementación del trasplante hepático, y a la mejoría en la prevención y manejo de sus complicaciones. Más recientemente se ha usado dispositivos de soporte hepático (MARS, Prometheus, BAL), como un puente al trasplante hepático. La reinfección del injerto con hepatitis B era una consideración importante en el pasado, pero con el uso de gamaglobulina específica para hepatitis B y el tratamiento antiviral oral, su pronóstico ha mejorado, determinando un excelente pronóstico del injerto y del paciente a largo plazo post trasplante hepático. Existen datos controversiales referentes al uso de antivirales orales durante una hepatitis fulminante, pues algunos autores muestran beneficios en esta condición, pero otros no han demostrado un beneficio real. Sin embargo, muchos expertos actualmente recomiendan su uso en este escenario, pues son seguros y pueden tener un potencial beneficio. Este artículo revisa el manejo actual del paciente con hepatitis fulminante por hepatitis B aguda.

Preliminary study on immunologic mechanism of chemokine receptor CXCR3 and its ligands involved in mouse fulminant hepatitis / 中华微生物学和免疫学杂志

Objective To investigate the role of the chemokine receptor CXCR3 and its ligands in the migration of lymphocytes and acute hepatic failure. Methods BALB/cJ mice (6-8 weeks, female) were intraperitoneally injected with 100 PFU mouse hepatitis virus-3(MHV-3). The proportions and numbers of T cells and NK cells in liver, spleen, and blood as well as the expression of CXCR3 in T cells, and NK cells post MHV-3 infection was analyzed by flow cytometry. The hepatic mRNA level of the CXCR3-associated chemokines(CXCL9 and CXCL10) was detected by real-time PCR. A transwell migration assay was used to assess the chemotactic effect of MHV-3-infected hepatocytes and CXCL10 on the splenic lymphocytes. Results Following MHV-3 infection, the number of hepatic NK cells and T cells and the frequencies of hepatic NK cells and T cells expressing CXCR3 increased markedly; however, in the spleen and peripheral blood, they both decreased significantly. Moreover, the hepatic mRNAs levels of CXCL9 and CXCL10 were significantly elevated post infection. The transwell migration assay demonstrated that MHV-3-infected hepatocytes have the capacity to attract and recruit the splenic NK cells and T cells, and CXCL10 plays a key role in lymphocyte mobilization from the spleen. Conclusion Interactions between CXCR3 and its ligands (CXCL9 and CXCL10),especially CXCL10 may play a key role in the recruitment of intrahepatic lymphocytes and subsequent necroinflammation and acute hepatic failure in MHV-3 infection.

Clinical & molecular characterization of human TT virus in different liver diseases.

Background & objectives: TT virus (TTV) is a newly discovered non-enveloped, single stranded DNA virus of high genotypic variability, found frequently in patients with acute or chronic hepatitis of non A-G aetiology. This study was carried out to look for the presence of TTV and its genotypes in patients with different types of liver diseases from northern India. Methods: A total of 262 serum samples from patients of acute viral hepatitis (AVH; n=72), fulminant hepatic failure (FHF; n=49), chronic active hepatitis (CAH; n=93) and liver cirrhosis (LC; n=48), were analyzed for hepatitis A-G viral markers. TTV DNA was detected in all cases by nested polymerase chain reaction (PCR) using the primers from N22 and untranslated (UTR) region. TTV-DNA was also tested in 150 volunteer blood donors. Direct nucleotide sequencing of N22 amplicons were carried out to look into the prevalent TTV genotypes. Results: TTV-DNA was detected in 73.6, 59.2, 21.5 and 29.1 per cent cases with AVH, FHF, CAH and cirrhosis, respectively. In AVH and FHF groups, TTV showed co-infection with all A-G hepatitis cases whereas in CAH and cirrhosis groups, TTV co-infection observed with HBV, HCV and HGV. TTV-DNA was detected in 45.3 per cent volunteer blood donors. No statistically significant difference was observed amongst the mean liver function profile of UTR PCR positive and negative cases in different liver disease groups except AVH cases, in whom the various biochemical parameters between TTV positive and TTV negative patients were marginally significant. However, no significant evidence of biochemical or histological deterioration of the liver was observed in TTV positive cases amongst FHF, CAH and cirrhosis. Predominance of genotype 1a was observed in all the cases from north India. Interpretation & conclusions: TTV is a frequent virus isolated from patients with various types of liver diseases as well as in healthy individuals from northern India. TTV has no effect on biochemical markers of associated liver diseases. Genotype 1a was the most predominant type in different liver disease groups. The occurrence of TTV did not further influence the course of the disease.

Fulminant hepatic failure in an infant with severe dengue infection.

Fulminant hepatic failure due to dengue infection is rare, although mild liver dysfunction is common. Here we report a fatal case of fulminant hepatitis in an infant infected with dengue 3 serotype. Attention must be given to the use of hepatotoxic drugs in some cases of dengue especially in infants.

Construction of mTNFR1shRNA Plasmid and its Biological Effects on MHV-3 Induced Fulminant Hepatitis in BALB/cJ Mice / 中国病毒学·英文版

Previous study on TNFRl-mediated hepatocyte apoptosis has been implicated in the development of fulminant viral hepatitis.To interfere with the potentially effective target,plasmid named p-mTNFR1shRNA complimentary to the sequence responsible for mTNFR1 was also constructed and further confirmed by sequence analysis.To investigate the effect of mTNFR1shRNA plasmid on mTNFR1 expression in vivo and the disease progress in MHV-3 induced fulminant hepatitis mice model.By hydrodynamic injection of mTNFRlshRNA plasmid,the survival rate of mice,hepatic pathological change were examined and compared between mice with/without mTNFR1 shRNA plasmid intervention.The expression of mTNFR1 was detected by Real-time PCR,immunohistochemistry staining.The mTNFR1 shRNA plasmid significantly reduced mTNFR1 expression in vivo,markedly ameliorates inflammatory infiltration,prolonged the survival time period and elevated the survival rate from 0 up to 13.3% in Balb/cJ mice with MHV-3 induced fulminant hepatitis.This study was designed to explore the opportunity of RNA interference technique in inhibiting TNFR1 expression,which has been reported to be involved in the development of a variety of diseases including fulminant viral hepatitis and severe chronic hepatitis B.

Construction of the Eukaryotic Expression Vectors and the microRNA Expression Plasmids of Human Fas and TNFR1 Gene and Their Biological Effects in vitro / 华中科技大学学报(医学版)

Objective To construct the eukaryotic expression plasmids of human Fas and TNFR1 gene(pcDNA3.0-hFas and pcDNA3.0-hTNFR1)and microRNA(miRNA)expression plasmid of hFas and hTNFR1 named p-hFasmiRNA and p-hTNFR1miRNA,and to investigate their inhibitory effects in vitro.Methods The eukaryotic expression plasmids of human Fas and TNFR1 gene were constructed(pcDNA3.0-hFas and pcDNA3.0-hTNFR1)and have been shown successfully to express hFas and hTNFR1 protein.miRNA expression plasmids of hFas and hTNFR1 named p-hFasmiRNA and p-hTNFR1miRNA complimentary to the sequence responsible for hFas and hTNFR1 respective were constructed,meanwhile irrelevant miRNA plasmid was used as a control.By respective co-transfection of p-hFasmiRNA and pcDNA3.0-hFas,p-hTNFR1 miRNA and pcDNA3.0-hTNFR1 expression construct into 293T cells,the inhibition of hFas and hTNFR1 expression was analyzed by real-time PCR and Western blot.Results The experiments showed the significant inhibitory effect of p-hFasmiRNA on hFas and p-hTNFR1miRNA on hTNFR1 expression at 48 h post-transfection both at RNA level and protein level as well in 293T cell lines with the inhibitory efficiency being as high as 87% for hFas and 80% for hTNFR1,respectively.Conclusion The p-hFasmiRNA and p-hTNFR1miRNA were constructed successfully,and it was verified that they could specifically inhibit the hFas and hTNFR1 expression at the cellular level.

Fulminant hepatitis failure in adults and children from a Public Hospital in Rio de Janeiro, Brazil

Fulminant hepatic failure (FHF) is characterized by massive hepatocellular injury, whose physiopathology is still unclear. Hepatitis B (HBV) is probably the most common viral cause of FHF, while hepatitis A (HAV) virus seem occurs less frequently. However, the host and viral factors that determine the outcome of these infections are poorly understood. In the present study, viral load and genotyping determining regions of HAV and HBV genomes were sequenced. Eight FHF patients and one patient with severe acute hepatitis (SAH) were included. Liver and blood samples were collected during liver transplantation or necropsy procedures. HAV-RNA and HBV-DNA were extracted from serum, biopsy and paraffin liver. Nucleotide sequencing of HAV-RNA was performed from VP1/2A and HBV-DNA from PreS/S region. The amplified samples were quantified by Real-Time PCR. The cases of HAV infection were due to subgenotype IA. The cases of HBV infection were due to genotype A2 and D4. The case of HAV/HBV coinfection was infected by genotype IA and D3. Hepatitis A and B infection were associated with genotypes most prevalent in Brazil. In hepatitis A infection the mean of period evolution was 13 days. In hepatitis B, FHF patients infected by genotype D have a shorter period of evolution than FHF patients infected by genotype A (mean 15 v. 53 days). There was no association with genotype-determining region with the severity of hepatitis, however nucleotide differences and high viral load could be observed among FHF.

Four patients with hepatitis A presenting with fulminant hepatitis and acute renal failure and who underwent liver transplantation / 대한간학회지

Hepatitis A is generally known as a mild, self-limiting disease of the liver, but in rare instances it can progress to fulminant hepatitis, which may require liver transplantation for recovery. Such cases are known to be related to old age and underlying liver disease. We report four cases of hepatitis A in which patients presented with fulminant hepatitis and acute renal failure and underwent liver transplantation. The following common features were observed in our cases: (1) occurrence in relatively old age (> or =39 years old), (2) association with acute renal failure, (3) presence of hepatomegaly, and (4) microscopic features of submassive hepatic necrosis.

Hepatitis B-cuadro clínico / Hepatitis B-clinical history

Las manifestaciones clínicas de la hepatitis viral tipo B tienen un amplio abanico de presentaciones, dependiendo de muchos factores, algunos desconocidos y otros, perfectamente identificables: subtipo del virus, características genéticas del huésped, estado inmunológico en el momento de la inoculación, carga viral y vía de entrada de dicha inoculación, entre los más importantes. La clínica de la hepatitis viral por virus B tanto aguda como crónica puede ser desde síntomas inespecíficos sin ictericia, a un cuadro severo con ictericia y encefalopatía. La hepatitis B que se manifiesta por primera vez, se clasifica como hepatitis aguda y hepatitis fulminante. La hepatitis B no aguda se clasifica en hepatitis subaguda o prolongada, hepatitis crónica persistente y hepatitis crónica activa.

The clinical manifestations of hepatitis B has a wide spectrum of presentations that depend on many factors, some are unknown and others very well identifiable: virus subtypes, genetic characteristics of the host, immunological status at the time of inoculation, viral burden, and entrance pathway of such inoculation, among others. The clinical case of acute and chronic hepatitis type B, can show either unspecific symptoms without jaundice or a severe case of jaundice and encephalopathy. The hepatitis B that manifests for the first time is classified as acute hepatitis and fulminant.

Preliminary study effect of artificial liver support on HBV cccDNA in patients with fulminant hepatitis B / 重庆医科大学学报

Objective:To establish a new fluorescence-based quantitative PCR assay for detecting hepatitis B virus covalently closed circular DNA(HBV cccDNA).To explore the effect of artificial liver support system(ALSS)on total HBV DNA and HBV cccDNA in sera of patients with fulminant hepatitis B.Methods:The serum specimens from 50 patients of fulminant hepatitis B prior to and after treatment with ALSS were collected.Then HBV cccDNA was quantitatively detected by fluorescent PCR with specific primer set and Taqman probe.And the results were analyzed by SAS8.0 statistics software.Results:We successfully established a new fluorescence-based quantitative PCR method for HBV cccDNA.HBV cccDNA was detectable in sera of the patients with fulminant hepatitis B.The level of total HBV DNA and HBV cccDNA decreased significantly following plasma exchange in ALSS.The levels of total HBV DNA and HBV cccDNA had positive correlation with degree of PT,ALT,andAST.Total HBV DNA also had positive correlation with HBV cccDNA.Conclusion:The level of total HBV DNA and HBV cccDNA has positive correlation with degree of PT,ALT,and AST,which might be indication of hepatocyte damage.The finding that significant decrease in total HBV DNA and HBV cccDNA after plasma exchange in ALSS may provide a clue of further research about the fulminant hepatitis B treated with ALSS.

Construction of shRNA of Fulminant Hepatitis Related Gene mfgl2 and Investigation of Its Biological Effects in vitro / 中国病毒学

This study was designed to explore the RNA interference technique in inhibition of the expression of the mouse fibrinogen like protein 2 (mfgl2), which has been reported to be involved in the development a variety of diseases including fulminant viral hepatitis. A plasmid named p-mfgl2shRNA,complementary to the sequence of mfgl2 was constructed, while another short hairpin RNA (shRNA)which was a mutated form of the mfgl2shRNA sequences was used as a control. A plasmid named pEGFP-mfgl2 expressing the mfgl2-EGFP fusion protein was also constructed for the screening of the effect of p-mfgl2shRNA on mfgl2 expression. By cotransfection of p-mfgl2shRNA and pEGFP-mfgl2 or pcDNA3.1-mfgl2 expression construct into CHO cells or HeLa cells, the inhibition of mfgl2 expression by mfgl2shRNA was analyzed by direct observation through fluorescent microscopy, FACS, RT-PCR and immunohistochemistry staining. The experiments showed the significant inhibitory effect of p-mfgl2shRNA on mfgl2 expression at 48h post-transfection in both CHO and Hela cell lines with the inhibitory efficiency as high as 80.1%. The study demonstrated that the construct of p-mfgl2shRNA successfully interfered with the mfgl2 expression in vitro.

Acute liver failure in children / 소아과

Acute liver failure (ALF) is a very rare but devastating illness in children. Specific treatment to recovery is often not available, and the underlying cause of the liver failure is often unknown and diverse especially in children. Liver transplantation has increased the chance of survival; however it needs an optimal timing to reach the best result which is not familiar to pediatrician. This article discusses the current knowledge of the epidemiology, backgrounds and factors to be considered before establishing the treatment of ALF in children.

A Case of Acute Renal Failure Associated with Acute Fulminant Hepatitis A / 대한신장학회잡지

Hepatitis A is a common cause of acute hepatitis throughout the world and is usually a mild self-limiting disease of the liver, but rarely presents as fulminant hepatitis in 0.14-0.35% of acute hepatitis A. Acute renal failure requiring dialysis in acute hepatitis A is also exceeding rare. We here report an unusual case of acute renal failure associated with acute fulminant hepatitis A. A previously healthy 22-year-old female was admitted to our hospital with nausea and vomiting of 1 day duration. Biochemical tests on admission revealed a marked increase of serum AST 19,810 IU/L, ALT 10,340 IU/L, total bilirubin 5.7 mg/dL, BUN 32.7 mg/dL and creatinine 4.4 mg/dL. Prothrombin time was prolonged to 40.3 seconds (INR 5.85). Random urine Na+ was 121.5 mmol/L and fractional excretion of sodium 22%. IgM antibody to hepatitis A virus was positive, while serology tests for hepatitis B and C virus, HIV, cytomegalovirus and Epstein-Barr virus were negative. On the 4th day of admission, hepatic encephalopathy and diuretics-resistant pulmonary edema developed. Lactulose treatment was performed for hepatic encephalopathy, and intermittent hemodialysis and continuous venovenous hemodialysis for pulmonary edema and uremia. On day 21, her urine output increased up to 1,000 cc with progressive improvement in renal function. She was discharged on day 32, with her serum creatinine of 2.0 mg/dL and total bilirubin of 4.7 mg/dL.