Hepatology Communications最新文献

{"title":"Single-cell profiling reveals monocyte heterogeneity and association with liver fibrosis in patients with chronic HBV.","authors":"Yue Zhuo, Hongzheng Wu, Wenying Zhao, Sheng Yin, Fang Lei, Xueyang Pang, Wei Sun, Lifeng Feng, Shulei Jia, Wanzhen Li, Yang Li, Jiling Ren, Min Wang, Dongming Zhou","doi":"10.1097/HC9.0000000000000672","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000672","url":null,"abstract":"<p><strong>Background: </strong>Chronic hepatitis B (CHB) infection results in persistent liver inflammation, which ultimately leads to liver fibrosis and increases the risk of cirrhosis. Recruitment of circulating monocytes to the liver is an essential aspect that exacerbates liver fibrosis; however, the mechanism underlying their dysregulation, which contributes to this progression, remains unclear.</p><p><strong>Methods: </strong>Single-cell RNA sequencing was performed to characterize the landscape of circulating monocytes from patients with CHB and liver fibrosis (CHB group) and healthy controls (HC group). Conventional techniques were performed to validate the findings.</p><p><strong>Results: </strong>Monocytes significantly expanded in the CHB group. The proto-oncogene LIM domain only 2 (LMO2) was highly expressed in monocytes from the CHB group, which may be associated with their expansion. In addition, we noticed that a classical monocyte subcluster surged in the CHB group and highly expressed platelet-related genes such as ITGA2B, which was identified as monocyte-platelet aggregates (MPA). The frequency of MPA was significantly higher in the CHB group, positively associated with platelet and white blood cell, and negatively associated with liver fibroscan and age, which indicates that MPA may play an important role in liver inflammation in the early liver fibrosis stage. Moreover, we found that MPA displays the enrichment of chemokine signaling-associated genes, such as C-C chemokine motif ligand 5 (CCL5), and showed an increased adhesion capacity to endothelial cells. After incubation with MPA cell supernatants, pro-inflammatory factors such as IL-8 and IL-1β were upregulated in LX-2 cells, which were reversed by the addition of anti-CCL5 antibodies.</p><p><strong>Conclusions: </strong>Our data suggest that enhanced LMO2 expression in circulating monocytes may be associated with their expansion, and an increased MPA subset may participate in liver fibrosis progression. These results provide valuable insights into the etiology of liver fibrosis in patients with CHB.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 5","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11999413/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144000064","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alpha-1 antitrypsin deficiency-associated liver disease: From understudied disorder to the poster child of genetic medicine.","authors":"Malin Fromme, Fabienne Klebingat, Paul Ellis, Pavel Strnad","doi":"10.1097/HC9.0000000000000699","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000699","url":null,"abstract":"<p><p>Alpha-1 antitrypsin deficiency (AATD) constitutes an inborn disorder arising due to mutations in alpha-1 antitrypsin (AAT), a secreted protease inhibitor produced primarily in hepatocytes. It leads to diminished serum AAT levels, and this loss-of-function predisposes to chronic obstructive pulmonary disease and lung emphysema. The characteristic Pi*Z mutation results in hepatic Z-AAT accumulation. In its homozygous form (Pi*ZZ genotype), it is responsible for the majority of severe AATD cases and can cause both pediatric and adult liver disease, while the heterozygous form (Pi*MZ) is considered a disease modifier that becomes apparent primarily in the presence of other comorbidities or risk factors. In the current review, we collate conditions associated with AATD, introduce typical AAT variants, and discuss our understanding of disease pathogenesis. We present both cross-sectional and longitudinal data informing about the natural disease history and noninvasive tools that can be used for disease stratification as well as a basis for disease monitoring. Given that AATD-associated liver disease is highly heterogeneous, we discuss the risk factors affecting disease progression. While the loss-of-function lung disease is treated by weekly intravenous administration of purified AAT, recombinant modified AAT and oral protease inhibitors are currently in clinical trials. Among the liver candidates, small interfering RNA fazirsiran efficiently suppresses AAT production and is currently in phase 3 clinical trial, while several other genetic approaches, such as RNA editing, are at earlier stages. In summary, AATD represents a systemic disorder increasingly seen in the hepatologic routine and requiring thorough interdisciplinary care, since the currently ongoing clinical trials often address only one of the organs it affects.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 5","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11999460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144017280","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The global prevalence and impact of steatotic liver disease and viral infections: A systematic review and meta-analysis.","authors":"Jiajing Li, Jiahua Zhou, Pengfei Li, Yining Wang, Nathalie Ridderhof, Jaffar A Al-Tawfiq, Willem Pieter Brouwer, Kan Chen, Robert J de Knegt, Maikel P Peppelenbosch, Bettina E Hansen, Maarten F M Engel, Ming-Hua Zheng, Ziad A Memish, Mohammed Eslam, Harry L A Janssen, Qiuwei Pan, Ibrahim Ayada","doi":"10.1097/HC9.0000000000000689","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000689","url":null,"abstract":"<p><strong>Background: </strong>Steatotic liver disease (SLD) affects ~30% of adults worldwide. The global population is continuously threatened by epidemic and endemic viral diseases. This study aims to thoroughly examine the interaction between SLD and major viral diseases.</p><p><strong>Methods: </strong>We systematically searched databases from inception to April 2, 2024, for observational studies recording viral-infected adult patients with eligible data on the presence of hepatic steatosis.</p><p><strong>Results: </strong>Six hundred thirty-six eligible studies were included in the analysis of SLD prevalence. Among patients with monoinfections, the highest SLD prevalence was observed in those infected with HCV at 49% (95% CI: 47%-51%), followed by SARS-CoV-2 (39%, 95% CI [34%-44%]), HIV (39%, 95% CI [33%-44%]), and HBV (36%, 95% CI [32%-40%]). Additionally, co-infections, such as HCV-HIV and HBV-HCV, exhibit even higher SLD prevalence. The prevalence of steatohepatitis is particularly high in HIV-infected (24%, 95% CI: 17%-30%) and HCV-infected (18%, 95% CI: 13%-24%) populations. The co-existence of SLD with viral infections was associated not only with the progression of liver disease but also with more severe outcomes of the infections and poorer responses to antiviral treatment. The combination of cardiometabolic risk factors and viral-associated and host factors contributes to the higher risk of SLD in viral-infected populations.</p><p><strong>Conclusions: </strong>SLD is highly prevalent in viral-infected populations, and the reciprocal interactions between SLD and viral diseases exacerbate both conditions, leading to poorer patient outcomes in general.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 5","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11999411/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143997962","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A greater frequency of circulating CCR7loPD-1hi follicular helper T cells indicates a durable clinical cure after Peg IFN-α therapy in chronic hepatitis B patients.","authors":"Shan Ren, Xiao Lin, Wenjing Wang, Wang Xiaoxiao, Lina Ma, Yanhong Zheng, Sujun Zheng, Xinyue Chen","doi":"10.1097/HC9.0000000000000690","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000690","url":null,"abstract":"<p><strong>Background: </strong>Emerging evidence indicates that the treatment duration of pegylated interferon-α and HBsAb may predict relapse in chronic hepatitis B (CHB) patients who achieved clinical cure. However, the host immunological mechanisms contributing to clinical relapse remain poorly characterized.</p><p><strong>Objectives: </strong>This study aimed to identify the immunological factors associated with relapse in chronic hepatitis B (CHB) patients who achieved clinical cure based on pegylated interferon-alpha treatment.</p><p><strong>Methods: </strong>CHB patients who achieved HBsAg loss after discontinuing pegylated interferon-alpha therapy were enrolled and followed up for at least 96 weeks. HBcrAg and immunological markers, including the proportion of follicular helper T (Tfh) cells were assessed by flow cytometry. Peripheral blood cytokine levels were measured using a Luminex assay. The primary outcome was the correlation between immunological markers with relapse at the end of treatment (EOT) and end of follow-up (EOF).</p><p><strong>Results: </strong>A total of 456 CHB patients were included. During the 96-week follow-up period, 37 patients (8.11%) experienced a relapse. Propensity score matching was performed at a 1:2 ratio, resulting in the inclusion of 37 relapsed (R) and 74 non-relapsed (NR) patients. The NR group exhibited higher proportions of Tfh cells than the R group in both EOT and EOF (EOT: 12.52% vs. 8.78%, p=0.008; EOF: 11.38% vs. 8.29%, p=0.008). A significantly greater proportion of CCR7loPD-1hi Tfh cells was observed in the NR group at the EOT (9.4% vs. 4.5%, p=0.009). The frequency of CCR7loPD-1hi Tfh cells was significantly and positively correlated with anti-HB levels in EOT (p=0.015, r=0.392). Serum levels (median, pg/mL) of CTLA-4 (EOT: 14.87 vs. 7.84; EOF: 14.87 vs. 7.97), PD-1 (EOT: 321.44 vs. 203.96; EOF: 288.45 vs. 166.04), and TIM-3 (EOT:4487 vs. 21254; EOF:2973 vs. 1768) were significantly higher in the R group than in the NR group at both EOT and EOF (p<0.05). At EOT, the HBcrAg level was significantly greater in the R than in the NR group (3.45±0.94 vs. 2.63±0.80 log10 U/mL, p=0.003).</p><p><strong>Conclusions: </strong>Higher frequencies of CCR7loPD-1hi Tfh cells, lower levels of sCTLA-4 as well as sPD-1 in EOT were protective factors for relapse among CHB patients who experienced HBsAg loss after pegylated interferon-alpha therapy. CCR7loPD-1hiTfh cells produced insufficient IL-21 in patients who experienced recurrent disease, which resulted in a decrease in the ability of B cells to produce anti-HBs.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 5","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11999403/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143984360","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A nationwide study of primary biliary cholangitis prevalence, geographic distribution, and health care providers.","authors":"Cynthia Levy, Keri-Ann Buchanan-Peart, Joanna P MacEwan, Alina Levine, Radhika Nair, Darren Wheeler, Leona Bessonova, Aparna Goel, Robert G Gish, Alan Bonder","doi":"10.1097/HC9.0000000000000677","DOIUrl":"https://doi.org/10.1097/HC9.0000000000000677","url":null,"abstract":"<p><strong>Background: </strong>Prevalence estimates of primary biliary cholangitis (PBC) in the United States have evolved with the introduction of newer real-world data capture approaches. Little is known about the geographic distribution of PBC in the United States and the health care provider (HCP) landscape for patients with PBC. This real-world study aimed to estimate the prevalence of PBC in the United States, assess regional variability in its prevalence, and describe HCPs for patients with PBC.</p><p><strong>Methods: </strong>Patients with PBC were identified using Komodo's Healthcare Map, a large national administrative claims database. PBC prevalence per 100,000 adults was adjusted by age and gender at the 3-digit ZIP Code tabulation area level. Patients' PBC-related medical or pharmacy claims were used to determine HCP specialties and affiliations (academic vs. nonacademic); the latest claim and all claims were examined.</p><p><strong>Results: </strong>The adjusted 2021 PBC prevalence was 40.9 per 100,000 adults. The highest absolute number of patients with PBC in the United States was in heavily populated urban areas, but prevalence adjusted for population size was highest in some rural areas. Among all claims, most (83.2%) patients received care from a specialist (gastroenterologist/hepatologist) at one time. However, only approximately half (53.5%) of patients with PBC, irrespective of therapy use, were most recently treated for PBC by a specialist.</p><p><strong>Conclusions: </strong>This is the most comprehensive and contemporary estimation of PBC prevalence in the United States to date. The pockets of high prevalence of PBC located in some rural areas highlight the need to better evaluate PBC risk factors and potential barriers in access to specialist care once patients are diagnosed. Greater awareness of PBC and its management are needed.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 5","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11999412/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143963105","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The current applications and future directions of terlipressin.","authors":"Dorothy Liu, Adam Testro, Avik Majumdar, Marie Sinclair","doi":"10.1097/HC9.0000000000000685","DOIUrl":"10.1097/HC9.0000000000000685","url":null,"abstract":"<p><p>Terlipressin is a vasopressin analog with potent splanchnic vasoconstrictor properties. It has an established role in managing portal hypertensive bleeding and hepatorenal syndrome-acute kidney injury, with a growing body of evidence demonstrating improved safety and efficacy with continuous infusion-based administration compared to bolus dosing. We discuss previously reported adverse effects of terlipressin and evidence-based strategies to maximize the safety of administration. We also review the literature surrounding emerging indications for terlipressin in decompensated cirrhosis, particularly in the management of refractory ascites. Furthermore, we present data on novel ambulatory programs utilizing long-term continuous terlipressin infusion as bridging therapy for liver transplant candidates with recurrent hepatorenal syndrome-acute kidney injury, diuretic-refractory ascites, or hydrothorax.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11970894/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772078","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Screening and management of portal hypertension and varices in cirrhosis: Expert perspectives.","authors":"Robert S Brown, Kimberly A Brown, Steve Flamm, Rachel E Bejarano, Robert S Rahimi, Ashwani K Singal, Don C Rockey","doi":"10.1097/HC9.0000000000000682","DOIUrl":"10.1097/HC9.0000000000000682","url":null,"abstract":"<p><p>The prevalence of liver injury, fibrosis, and, in particular, cirrhosis in the United States is increasing in parallel to the current epidemic of metabolic dysfunction-associated steatotic liver disease and alcohol-associated liver disease. As fibrosis advances, portal hypertension occurs, and when the pressure gradient meets or exceeds 10 mm Hg, the patient is at an increased risk for decompensating events such as esophageal varices. The risk of death also increases. Therefore, decreasing the risk of progression to decompensated cirrhosis is an important management goal. The American Association for the Study of Liver Diseases recently published a guidance document to \"coalesce best practice recommendations for the identification of portal hypertension, for prevention of initial hepatic decompensation, for the management of acute variceal hemorrhage, and for reduction of the risk of recurrent variceal hemorrhage in chronic liver disease.\" In this updated guidance, the new terms \"advanced chronic liver disease\" and \"clinically significant portal hypertension\" have been proposed for routine use in clinical practice. Following recommendations for advanced chronic liver disease identification, which are largely defined by transient elastography measurements of liver stiffness, guidance is provided on the identification of clinically significant portal hypertension and early administration of nonselective beta-blocker therapy in clinically significant portal hypertension for prophylaxis. Optimal control of active bleeding, the role of preemptive TIPS, and gastric varices management are also addressed. Despite the wealth of information provided, the guidance can be difficult to put into practice, leaving non-liver-focused clinicians with an unmet need for a simplified approach to guidelines in general. To address this issue, a panel of hepatologists met to review and discuss the real-world implications of this new guidance and the result is this expert perspective review. This review aims to facilitate improvements in risk stratification and management of variceal bleeding, streamline controversial and complex issues in the recent guidance in a practical way for clinical use, and make recommendations on how to incorporate this important new guidance document into clinical practice.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11970884/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772061","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Early experience with resmetirom to treat metabolic dysfunction-associated steatohepatitis with fibrosis in a real-world setting.","authors":"Neel Ravela, Phoebe Shackelford, Nadia Blessing, Lindsay Yoder, Naga Chalasani, Niharika Samala","doi":"10.1097/HC9.0000000000000670","DOIUrl":"10.1097/HC9.0000000000000670","url":null,"abstract":"<p><strong>Background: </strong>Resmetirom was conditionally approved in the United States recently for treating metabolic dysfunction-associated steatohepatitis with stage 2 and 3 fibrosis. However, its availability to patients requires preauthorization by the payors and is dispensed only through selected specialty pharmacies.</p><p><strong>Methods: </strong>We established a multistakeholder and multistep resmetirom prescription process pivoting to a dedicated pharmacist. It incorporates liver biochemistry testing at 12 weeks and liver clinic follow-up at 6 months after starting resmetirom.</p><p><strong>Results: </strong>Fifteen hepatology providers prescribed resmetirom to 113 patients from April 1, 2024, to November 8, 2024, with histologic eligibility in 70% and noninvasive criteria in 30%. Resmetirom treatment was approved for 110 patients (97%), including 8 patients receiving the pharmaceutical company's patient assistance and 6 patients receiving bridge support to cover the co-pay. Eighty-three patients initiated resmetirom at an average of 30 days after its prescription. Adverse events were reported by 41% of patients taking resmetirom, and they were predominantly related to gastrointestinal symptoms and pruritus and/or rash with no evidence of hypersensitivity. Thirteen patients (16%) discontinued resmetirom after an average of 25.5 days (range: 2-68 d), with 11 patients discontinuing due to adverse events. The adverse events leading to discontinuation were nausea, diarrhea, and vomiting (n=4), right upper quadrant discomfort (n=2), left lower quadrant pain (n=1), rash with pruritus (n=1), pruritus and rash with indirect hyperbilirubinemia (n=1), dizziness (n=1), and mental fogginess (n=1). Follow-up liver biochemistries available in 24 patients showed no evidence of DILI.</p><p><strong>Conclusions: </strong>Our prescription pathway effectively dispensed resmetirom to nearly all patients who were prescribed resmetirom. One in 6 patients discontinued resmetirom, primarily due to side effects. This high discontinuation rate may be mitigated by modifying our follow-up from \"prescribe and forget\" to \"prescribe and closely follow.\"</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11970881/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ascites in patients with end-stage renal disease: Challenges and solutions from diagnosis to management.","authors":"Akash Roy, Anand V Kulkarni","doi":"10.1097/HC9.0000000000000687","DOIUrl":"10.1097/HC9.0000000000000687","url":null,"abstract":"<p><p>Metabolic diseases have exponentially increased in recent years, which has led to an increased prevalence of metabolic dysfunction-associated steatotic liver disease and concomitant kidney diseases. Ascites are a common presentation of cirrhosis, and renal impairment in cirrhosis is well described. However, patients with end-stage renal disease (ESRD) may also present with ascites even in the absence of cirrhosis. The literature on the management of patients with ESRD with ascites with or without concomitant cirrhosis is limited. Massive ascites in this population are often refractory to medical therapy and are associated with dismal prognosis. Pathophysiologically, increased hepatic vein hydrostatic pressure, fluid retention, increased peritoneal membrane permeability, and impaired peritoneal lymphatic drainage are proposed mechanisms for ascites in ESRD without cirrhosis. Identifying underlying cirrhosis and portal hypertension (PH) has therapeutic implications in such patients. However, diagnostic tools such as serum ascites albumin gradient and noninvasive tests to identify cirrhosis have limited utility in ESRD. Hemodialysis and continuous ambulatory peritoneal dialysis are effective but can be associated with hemodynamic compromise and peritonitis, especially in those with PH. TIPS for ascites has a limited role in the presence of ESRD due to the increased risk of HE. Kidney transplant is the treatment of choice in ESRD with ascites without PH. Simultaneous liver-kidney transplant remains the definitive treatment in the presence of PH, but is less commonly feasible, and kidney transplant alone in the presence of PH can be associated with the risk of decompensations. This review discusses the approach and management of ascites in chronic kidney disease and ESRD specifically.</p>","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11970822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143771762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatic encephalopathy predicts early post-transplant cognitive and functional impairment: The Livcog cohort study.","authors":"Marina Serper, Douglas E Schaubel, Katheryn A Q Cousins, Corey McMillan, Sumeet Asrani, Justin Boike, Julia Yoshino Benavente, Michael S Wolf","doi":"10.1097/HC9.0000000000000696","DOIUrl":"10.1097/HC9.0000000000000696","url":null,"abstract":"","PeriodicalId":12978,"journal":{"name":"Hepatology Communications","volume":"9 4","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11970804/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}