Liver Disease

KDIGO 2025 clinical practice guideline for the evaluation, management, and treatment of autosomal dominant polycystic kidney disease (ADPKD): executive summary.

Torres VE, Ahn C, Barten TRM, Brosnahan G, Cadnapaphornchai MA, Chapman AB · Kidney international · 2025

The Kidney Disease: Improving Global Outcomes (KDIGO) 2025 Clinical Practice Guideline for the Evaluation, Management, and Treatment of Autosomal Dominant Polycystic Kidney Disease (ADPKD) represents the first KDIGO guideline on this subject. Its scope includes nomenclature, diagnosis, prognosis, and prevalence; kidney manifestations; chronic kidney disease (CKD) management and progression, kidney failure, and kidney replacement therapy; therapies to delay progression of kidney disease; polycystic liver disease; intracranial aneurysms and other extrarenal manifestations; lifestyle and psychosocial aspects; pregnancy and reproductive issues; pediatric issues; and approaches to the management of people with ADPKD. The guideline has been developed with patient partners, clinicians, and researchers around the world, with the goal to generate a useful resource for healthcare providers and patients by providing actionable recommendations. The development of this guideline followed an explici

The Asian Pacific association for the study of the liver clinical practice guidelines for the diagnosis and management of metabolic dysfunction-associated fatty liver disease.

Eslam M, Fan JG, Yu ML, Wong VW, Cua IH, Liu CJ · Hepatology international · 2025

Metabolic dysfunction-associated fatty liver disease (MAFLD) affects over one-fourth of the global adult population and is the leading cause of liver disease worldwide. To address this, the Asian Pacific Association for the Study of the Liver (APASL) has created clinical practice guidelines focused on MAFLD. The guidelines cover various aspects of the disease, such as its epidemiology, diagnosis, screening, assessment, and treatment. The guidelines aim to advance clinical practice, knowledge, and research on MAFLD, particularly in special groups. The guidelines are designed to advance clinical practice, to provide evidence-based recommendations to assist healthcare stakeholders in decision-making and to improve patient care and disease awareness. The guidelines take into account the burden of clinical management for the healthcare sector.

ACG Clinical Guideline: Focal Liver Lesions.

Frenette C, Mendiratta-Lala M, Salgia R, Wong RJ, Sauer BG, Pillai A · The American journal of gastroenterology · 2024

Focal liver lesions (FLLs) have become an increasingly common finding on abdominal imaging, especially asymptomatic and incidental liver lesions. Gastroenterologists and hepatologists often see these patients in consultation and make recommendations for management of multiple types of liver lesions, including hepatocellular adenoma, focal nodular hyperplasia, hemangioma, and hepatic cystic lesions including polycystic liver disease. Malignancy is important to consider in the differential diagnosis of FLLs, and healthcare providers must be familiar with the diagnosis and management of FLLs. This American College of Gastroenterology practice guideline uses the best evidence available to make diagnosis and management recommendations for the most common FLLs.

Pharmacological landscape of endoplasmic reticulum stress: Uncovering therapeutic avenues for metabolic diseases.

Alotaibi G, Alkhammash A · European journal of pharmacology · 2025

The endoplasmic reticulum (ER) plays a fundamental role in maintaining cellular homeostasis by ensuring proper protein folding, lipid metabolism, and calcium regulation. However, disruptions to ER function, known as ER stress, activate the unfolded protein response (UPR) to restore balance. Chronic or unresolved ER stress contributes to metabolic dysfunctions, including insulin resistance, non-alcoholic fatty liver disease (NAFLD), and neurodegenerative disorders such as Parkinson's disease and Alzheimer's disease. Recent studies have also highlighted the importance of mitochondria-ER contact sites (MERCs) and ER-associated inflammation in disease progression. This review explores the current pharmacological landscape targeting ER stress, focusing on therapeutic strategies for rare metabolic and neurodegenerative diseases. It examines small molecules such as tauroursodeoxycholic acid (TUDCA) and 4-phenylbutyric acid (4-PBA), repurposed drugs like 17-AAG (17-N-allylamino-17demethoxygeld

Pathogenesis and Management of Intestinal Failure-Associated Liver Disease.

Abi-Aad SJ, Lovell M, Khalaf RT, Sokol RJ · Seminars in liver disease · 2025

Long-term parenteral nutrition (PN) has considerably improved the management of intestinal failure (IF) in children and adults, particularly those with short bowel syndrome; however, it carries a significant risk of hepatotoxicity, specifically, intestinal failure-associated liver disease (IFALD), also known as PN-associated liver disease. This review provides an update on the latest understanding of IFALD pathogenesis, emerging therapies, and ongoing challenges in the management of this complication. A number of factors are associated with the development of IFALD. PN lipid emulsions, phytosterol exposure, bacterial dysbiosis, an altered gut-liver axis, and episodes of sepsis disrupt bile acid homeostasis and promote liver inflammation in the active phase of IFALD, favoring the development of PN-associated cholestasis (PNAC) and the more chronic form of steatohepatitis with fibrosis. Based on the identification of pathophysiological pathways, potential therapies are being studied in p

Roles and Mechanisms of Choline Metabolism in Nonalcoholic Fatty Liver Disease and Cancers.

Chen X, Qiu W, Ma X, Ren L, Feng M, Hu S · Frontiers in bioscience (Landmark edition) · 2024

Choline participates in three major metabolic pathways: oxidation, phosphorylation, and acetylation. Through oxidation, choline is converted to betaine and contributes to methyl metabolism and epigenetic regulation. Through phosphorylation, choline participates in phospholipid metabolism, and serves as the precursor of phosphocholine, phosphatidylcholine, glycerophosphocholine, and other essential compounds, thereby modulating lipid metabolism and transport. Through acetylation, choline is transformed into acetylcholine in cholinergic neurons, playing a vital role in neurotransmission. Moreover, gut microbiota can metabolize choline into trimethylamine-N-oxide, and be involved in the pathogenesis of various diseases such as nonalcoholic fatty liver disease (NAFLD), cancer, cardiovascular disease, etc. Since choline metabolism is implicated in the development of NAFLD and diverse cancers, including liver cancer, it may serve as a therapeutic target for these diseases in the future. Curr

Somatic loss-of-function mutations in CIDEB reduce hepatic steatosis by increasing lipolysis and fatty acid oxidation.

Zeng Q, Patel S, Wang X, Hsieh MH, Li Z, Ren X · Journal of hepatology · 2026

Somatic and germline CIDEB mutations are associated with protection from chronic liver diseases. The mechanistic basis and whether CIDEB suppression would be an effective therapy against fatty liver disease remain unclear. Twenty-one CIDEB somatic mutations were introduced into cells to assess functionality. In vivo screening was used to trace Cideb mutant clones in mice fed normal chow, western diet (WD), and choline-deficient, L-amino acid-defined, high-fat diet (CDA-HFD). Constitutive and conditional Cideb knockout mice were generated to study Cideb in liver disease. Isotope tracing was used to evaluate fatty acid oxidation and de novo lipogenesis. Transcriptomics, lipidomics, and metabolic analyses were utilized to explore molecular mechanisms. Double knockout models (Cideb/Atgl and Cideb/Pparα) tested mechanisms underlying Cideb loss. Most CIDEB mutations impaired function, and loss-of-function clones were positively selected under CDA-HFD but not all steatogenic diets. Ci

An unbiased ranking of murine dietary models based on their proximity to human metabolic dysfunction-associated steatotic liver disease (MASLD).

Vacca M, Kamzolas I, Harder LM, Oakley F, Trautwein C, Hatting M · Nature metabolism · 2024

Metabolic dysfunction-associated steatotic liver disease (MASLD), previously known as non-alcoholic fatty liver disease, encompasses steatosis and metabolic dysfunction-associated steatohepatitis (MASH), leading to cirrhosis and hepatocellular carcinoma. Preclinical MASLD research is mainly performed in rodents; however, the model that best recapitulates human disease is yet to be defined. We conducted a wide-ranging retrospective review (metabolic phenotype, liver histopathology, transcriptome benchmarked against humans) of murine models (mostly male) and ranked them using an unbiased MASLD 'human proximity score' to define their metabolic relevance and ability to induce MASH-fibrosis. Here, we show that Western diets align closely with human MASH; high cholesterol content, extended study duration and/or genetic manipulation of disease-promoting pathways are required to intensify liver damage and accelerate significant (F2+) fibrosis development. Choline-deficient models rapidly induc

NUP85 alleviates lipid metabolism and inflammation by regulating PI3K/AKT signaling pathway in nonalcoholic fatty liver disease.

Wu YC, Yan Q, Yue SQ, Pan LX, Yang DS, Tao LS · International journal of biological sciences · 2024

Nonalcoholic fatty liver disease (NAFLD) is one of the common causes of chronic liver disease in the world. The problem of NAFLD had become increasingly prominent. However, its pathogenesis is still indistinct. As we all know, NAFLD begins with the accumulation of triglyceride (TG), leading to fatty degeneration, inflammation and other liver tissues damage. Notably, structure of nucleoporin 85 (NUP85) is related to lipid metabolism and inflammation of liver diseases. In this study, the results of researches indicated that NUP85 played a critical role in NAFLD. Firstly, the expression level of NUP85 in methionine-choline-deficient (MCD)-induced mice increased distinctly, as well as the levels of fat disorder and inflammation. On the contrary, knockdown of NUP85 had the opposite effects. In vitro, AML-12 cells were stimulated with 2 mm free fatty acids (FFA) for 24 h. Results also proved that NUP85 significantly increased in model group, and increased lipid accumulation and inflammation

Hepatitis

WHO

The WHO provides fact sheets and global strategies on hepatitis, highlighting the disease burden, prevention, diagnosis, and treatment efforts worldwide.

Liver Diseases

NIH/MedlinePlus

MedlinePlus offers comprehensive information on various liver diseases, including symptoms, diagnosis, treatment options, and prevention, targeted at a general audience.

Liver disease

NHS

The NHS provides accessible information on liver disease, covering common types, causes, symptoms, diagnosis, and treatment, aimed at public understanding and awareness.

A Phase 1, Open-Label, Parallel-Group, Single-Dose Study to Evaluate the Pharmacokinetics of GS-5816 in Subjects With Normal Renal Function and Severe Renal Impairment

n=19 · NCT02002767 · COMPLETED · COMPLETED

The primary objective of the study is to evaluate the single-dose pharmacokinetics (PK) of velpatasvir (formerly GS-5816) in participants with severe renal impairment using matched healthy participants as a control group.

Safety and Efficacy Evaluation of IM83 CAR-T Cells for Patients Wirh Advanced Liver Tumors

n=12 · NCT05123209 · UNKNOWN · UNKNOWN

This is a open-label, single center, cohort study to determine the efficacy and safety of IM83 CAR-T cells in patients with advanced Liver Tumors.

Comparison of Diuretic Effect With Furosemide Alone Versus the Combination of Furosemide and Albumin in Cirrhotic Patients

n=21 · NCT04216784 · TERMINATED · TERMINATED

A common complication of the progression of cirrhosis is fluid retention (ascites, edema, or pleural effusion). Loop diuretics are the treatment of choice for fluid retention in cirrhotic patients; however, many of these patients demonstrate diuretic resistance, requiring higher doses of the diuretics to achieve adequate diuresis. The cause of this diuretic resistance is hypothesized to be secondary to hypoalbuminemia which has led some providers to give human albumin in combination with loop diuretics to increase intravascular volume and facilitate diuresis. However, this practice remains controversial because minimal data exists to support its efficacy. The purpose of this study is to compare the efficacy of diuretics alone versus diuretics in combination with albumin in cirrhotic patients presenting with fluid retention.