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Introduction: Hepatitis C virus (HCV) may recur after liver transplantation (LT) in the severe form of fibrosing cholestatic hepatitis (FCH). The prognosis dramatically improved by the use of direct acting antivirals (DAAs). The aim of the present study was to describe the change in histological features of FCH after virological eradication.
Methods: From the ANRS CUPILT cohort we included 17 patients who presented FCH and at least two graft biopsies, one before DAA-treatment and one after. A single expert pathologist, blinded for clinical outcome, retrospectively confirmed the diagnosis of FCH and progression of fibrosis.
Results: Diagnosis of FCH was made after a median [IQR] 6.0 [3.1-11.8] months after LT, and the median interval between diagnosis and onset of treatment was 1.2 [0.7-6.1] months. The rate of viral eradication was 94.1%. The median delay between the pre-treatment and the treatment biopsies was 12.5 [11.1-20.0] months. Between the end of treatment and the second biopsy, the delay was 5.3 [0.6-7.4] months. Fibrosis stage worsened in 10 patients (58.8%); 6 patients had cirrhosis (35.3%). Chronic rejection appeared in 4 (23.5%) patients.
Conclusion: Our results suggest that, despite viral eradication in patients presenting FCH after LT, fibrosis progression was observed in half of patients. This should encourage monitoring fibrosis progression despite HCV cure.
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http://dx.doi.org/10.1016/j.clinre.2022.102024 | DOI Listing |
Clin Kidney J
September 2025
Department of Nephrology. University Clinical Hospital, INCLIVA, Valencia. RICORS Renal Instituto de salud Carlos III, Valencia. Spain.
Metabolic dysfunction-associated steatotic liver disease (MASLD) has emerged as a major contributor to systemic metabolic dysfunction and is increasingly recognized as a risk enhancer for both cardiovascular disease (CVD) and chronic kidney disease (CKD). This review explores the complex interconnections between MASLD, CVD, and CKD, with emphasis on shared pathophysiological mechanisms and the clinical implications for risk assessment and management. We describe the crosstalk among the liver, heart, and kidneys, focusing on insulin resistance, chronic inflammation, and progressive fibrosis as key mediators.
View Article and Find Full Text PDFFront Public Health
September 2025
Department of Nephrology and Institute of Nephrology, Sichuan Provincial People's Hospital, School of Medicine, University of Electronic Science and Technology of China, Chengdu, China.
Background: Chronic kidney disease (CKD), a global health challenge, is closely linked to renal fibrosis progression. Copper, an essential trace element, influences cellular functions, yet its role in CKD-related fibrosis remains unclear. This study explores the causal relationship between serum copper levels and renal fibrosis in CKD.
View Article and Find Full Text PDFEnviron Int
September 2025
State Key Laboratory of Environmental Chemistry and Toxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, Beijing 100085, China; College of Sciences, Northeastern University, Shenyang 110004, China; School of Environment, Hangzhou Institute for Advanced Study, Univ
Exposure to nanoplastics (NPs), a pervasive environmental pollutant, presents potential health risks. Pulmonary exposure to NPs has been shown to disrupt both pulmonary metabolic status and immune homeostasis, leading to concerns about their impact on respiratory health and systemic well-being. However, the underlying linkage and mechanisms remain elusive.
View Article and Find Full Text PDFNat Cell Biol
September 2025
Department of Medicine, Division of Pulmonary and Critical Care Medicine, Massachusetts General Hospital, Harvard Medical School, Boston, MA, USA.
Durotaxis, cell migration along stiffness gradients, is linked to embryonic development, tissue repair and disease. Despite solid in vitro evidence, its role in vivo remains largely speculative. Here we demonstrate that durotaxis actively drives disease progression in vivo in mouse models of lung fibrosis and metastatic pancreatic cancer.
View Article and Find Full Text PDFEcotoxicol Environ Saf
September 2025
Department of Cardiology, the Second Affiliated Hospital of Anhui Medical University, Hefei 230601, China; School of Basic Medicine, Anhui Medical University, Hefei 230032, China. Electronic address:
Renal fibrosis represents a critical pathological mechanism driving the progression of chronic kidney disease toward end-stage renal failure, primarily characterized by the proliferation and deposition of connective tissue within the renal tissue. Triclosan is a widely used synthetic antibacterial agent, and previous studies have demonstrated that TCS exposure interferes with renal fibrosis. However, the pathogenetic mechanism between TCS and renal fibrosis is still unclear.
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