Search Results (1,098)

Background/Objectives: Obesity is closely associated with gut microbiota dysbiosis, intestinal barrier dysfunction, and impaired glucose and lipid metabolism. However, single probiotic or prebiotic interventions often yield only limited metabolic improvements. This study aimed to evaluate the effects of a synbiotic formulation comprising Lacto-N-tetraose (LNT) and Bifidobacterium animalis subsp. lactis MN-Gup (MN-Gup) in a high-fat diet (HFD)-induced obese mouse model. Methods: In this study, an HFD-induced obese mouse model was used to investigate whether the synbiotic formulation of LNT and MN-Gup could ameliorate obesity-related metabolic dysregulation, intestinal barrier dysfunction, and gut microbiota imbalance. Mice were treated with LNT alone, MN-Gup alone, or the synbiotic at different doses. Serum biochemical parameters, glucose tolerance, lipid profiles, liver histopathology, intestinal barrier markers, gut microbiota composition, short-chain fatty acid (SCFA) levels were analyzed. Results: High-dose synbiotic intervention significantly outperformed single-component treatments in reducing weight gain, improving glucose tolerance and lipid profiles, and attenuating hepatic lipid accumulation and injury in mice. These metabolic changes were accompanied by improved markers of intestinal barrier integrity and modulation of gut microbiota composition, characterized by the enrichment of beneficial genera (e.g., Akkermansia, Leuconostoc, and Alistipes) alongside a reduction in obesity-associated taxa (including Desulfovibrionaceae_unclassified, Colidextribacter, Helicobacter, Erysipelatoclostridium, Peptococcaceae_unclassified, and Firmicutes_unclassified). Spearman correlation analysis revealed associative links between microbial alterations and host metabolic markers. Conclusions: Collectively, these findings suggest that the synbiotic formulation comprising high-dose LNT and MN-Gup offers potential benefits for managing high-fat diet-induced metabolic dysregulation in mice. Full article

Ofloxacin (OFL) and sulfamethoxazole (SMX) are common co-occurring antibiotic contaminants in aquatic environments, yet their long-term combined toxicity to freshwater fish remains poorly elucidated. In this study, adult mosquitofish (Gambusia affinis) were used as a model to investigate histopathological alterations, oxidative stress responses, gene expression, and gut microbiota changes after 30 days of exposure to environmentally relevant concentrations of OFL and SMX (0 ng/L, 50 ng/L, 1 μg/L, and 20 μg/L), either individually or in combination. The results showed that both single and combined exposures induced liver and intestinal damage. Oxidative stress responses exhibited clear tissue specificity, with activation of antioxidant defenses in the liver, whereas the intestine was mainly characterized by decreased SOD and GST activities, as well as reduced MDA content. Changes in gene expression were relatively limited, with significant alterations observed only in hepatic sod2 and hsp90 and intestinal hsp70 in certain treatment groups. Gut microbiota analysis showed that OFL exerted a stronger disruptive effect than SMX, as reflected by increased alpha diversity, reduced abundance of core genera, and functional remodeling, whereas combined exposure triggered weaker microbial community restructuring relative to single exposures. Overall, OFL and SMX induced tissue-specific toxicity in mosquitofish by causing tissue injury, oxidative stress imbalance, and gut microbiota dysbiosis, with OFL showing the stronger overall effect. Full article

Background/Objectives: Acute kidney injury (AKI) is a common complication after liver transplantation. Although intraoperative hypotension has been associated with its development, the impact of shock persistence and its hemodynamic profile remains poorly defined. Methods: This was a single-center retrospective observational study including 226 adult patients undergoing liver transplantation. Intraoperative shock was defined as a mean arterial pressure < 60 mmHg or a ≥30% decrease from baseline and was classified as hypovolemic, distributive, cardiogenic, or mixed based on pulmonary artery catheter data. AKI was defined according to Kidney Disease: Improving Global Outcomes (KDIGO) criteria within the first 7 postoperative days. Associations were assessed using adjusted logistic regression models. Results: Intraoperative shock occurred in 35.8% of patients, and the incidence of AKI was 52.2%. The presence of shock was not independently associated with AKI (adjusted OR 1.66; 95% CI 0.94–2.95). However, shock occurring in multiple phases of the procedure was associated with a higher incidence of AKI (81.8% vs. 50%; p = 0.010), greater severity, and higher mortality (27.3% vs. 3.4%; p = 0.002). In exploratory analyses, mixed shock was associated with an increased need for renal replacement therapy within 30 days (p = 0.006), persistent renal dysfunction at day 30 (p = 0.048), and higher mortality (p = 0.01), while hypovolemic shock was associated with moderate AKI (OR 6.60; p = 0.011). Conclusions: The presence of intraoperative shock alone is not independently associated with AKI. In contrast, its persistence is strongly associated with AKI development and worse clinical outcomes. Full article

Background/Objectives: Frailty is a validated predictor of waitlist mortality and perioperative risk in liver transplant candidates, but its association with early post-transplant outcomes in large real-world cohorts remains incompletely characterized. This study evaluated the association between administratively defined pre-transplant frailty and early clinical outcomes following liver transplantation. Methods: We conducted a retrospective cohort study using the TriNetX US Collaborative Research Network. Adults undergoing first-time isolated liver transplantation through February 2026 were included. Frailty was identified using ICD-10-CM codes for frailty, sarcopenia, cachexia, weakness, abnormal gait/mobility, or reduced mobility documented within 12 months before transplantation; patients coded only for nonspecific weakness were excluded from the frailty cohort. Patients underwent 1:1 propensity score matching using 18 baseline covariates, including demographics, comorbidities, laboratory values, albumin, and MELD-Na. The primary outcome was all-cause mortality at 7, 30, and 90 days. Secondary outcomes included acute kidney injury, prolonged mechanical ventilation, vasopressor requirement/hemodynamic instability, renal replacement therapy, ICU and hospital length of stay, and 90-day readmission. Sensitivity analyses used a restrictive ≥ 2-code frailty definition and substituted MELD 3.0 for MELD-Na in the propensity model. Results: Among 4860 eligible recipients, 742 had administratively defined frailty and 4118 did not. After matching, 730 patients remained in each group with well-balanced covariates. Administratively defined frailty was associated with higher mortality at 7, 30, and 90 days, with numerically smaller relative risks at later time points. It was also associated with higher risks of acute kidney injury, prolonged mechanical ventilation, vasopressor requirement/hemodynamic instability, renal replacement therapy, longer ICU and hospital stays, and 90-day readmission. Findings were directionally consistent in both sensitivity analyses. Etiology-stratified analyses were exploratory and showed no statistically significant heterogeneity across liver disease etiologies. Conclusions: In this large propensity-matched multicenter cohort, administratively defined pre-transplant frailty was associated with worse early outcomes after liver transplantation. Because frailty and several outcomes were identified using structured EHR and administrative data, findings should be interpreted as associative and hypothesis-generating. Prospective studies using validated frailty instruments and granular donor, intraoperative, and center-level variables are needed to confirm these findings. Full article

Vitis coignetiae Pulliat ex Planch, commonly referred to as “meoru” in Korea (crimson glory vine), is a grape species belonging to the Vitaceae family, native to East Asia. This study investigated the protective effects of a hot water extract prepared from the vine stems of V. coignetiae (CG) in a model of CCl₄-induced acute liver injury. Mice received oral administration of CG (100, 200, and 400 mg/kg) or silymarin (200 mg/kg) once daily for 7 consecutive days, followed by intraperitoneal injection of CCl₄ (0.5 mL/kg). CG attenuated CCl₄-induced oxidative stress, as indicated by reduced hepatic malondialdehyde production and decreased 4-hydroxynonenal-positive cells. These effects were accompanied by restoration of antioxidant defense systems, including increased glutathione levels and superoxide dismutase and catalase activities, along with increased nuclear factor erythroid 2-related factor 2 (Nrf2) mRNA expression. Hepatic inflammatory responses were also attenuated by CG treatment, with reductions in TNF-α, interleukin (IL)-1β, and IL-6 levels, inflammatory cell infiltration, and nuclear factor-κB (NF-κB) mRNA expression. Furthermore, CG attenuated apoptotic cell death, as evidenced by decreased cleaved caspase-3-positive and cleaved poly(ADP-ribose) polymerase (PARP)-positive cells. CG also lowered serum aspartate aminotransferase, alanine aminotransferase, and γ-glutamyl transferase levels, and alleviated hepatocellular degeneration in histopathological analysis. Collectively, these findings suggest that CG may exert protective effects against CCl₄-induced liver injury by regulating oxidative stress, inflammation, and apoptosis. Full article

Chronic intermittent hypoxia (CIH), the cardinal pathophysiological feature of obstructive sleep apnea, is increasingly recognized as an important modifier of metabolic dysfunction-associated steatotic liver disease (MASLD), but the underlying mechanisms remain incompletely understood. In this study, male C57BL/6 mice were fed a standard diet or a high-fat diet (HFD) and exposed to normoxia or CIH for 8 weeks. Histological, ultrastructural, biochemical, transcriptomic, proteomic, and metabolomic analyses were integrated to characterize hepatic alterations induced by CIH under metabolic stress. CIH markedly aggravated HFD-induced liver injury, as evidenced by increased body fat, hepatomegaly, serum transaminases, steatosis, mitochondrial ultrastructural alterations, and inflammatory infiltration. Mechanistically, CIH promoted hepatic lipid metabolic reprogramming by suppressing the PPARα/CPT1A fatty acid β-oxidation axis while enhancing the SREBP-1c/FASN/PLIN2 lipogenic pathway, impaired the Nrf2/HO-1/SLC7A11/GPX4 antioxidant defense system, increased lipid peroxidation and iron accumulation, and activated NF-κB/NLRP3 signaling. These findings support a multifactorial model in which CIH functions as an additional hypoxic stressor that exacerbates HFD-induced MASLD-like liver injury through coordinated metabolic, oxidative, and inflammatory dysregulation. Full article

Background/Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is now the leading cause of chronic liver disease globally, mirroring the increasing prevalence of obesity, insulin resistance, and type 2 diabetes. Early detection of hepatic steatosis is vital for cardiometabolic risk assessment; however, conventional imaging is costly and impractical for population screening. This study aimed to develop interpretable machine-learning models to predict ultrasound-detected hepatic steatosis within the MASLD spectrum using routinely available clinical and biochemical data. Methods: We analyzed data from 644 adults, 50% of whom had ultrasound-detected hepatic steatosis. Preprocessing, imputation, and feature selection were implemented within a single scikit-learn pipeline to avoid information leakage. An Elastic Net-regularized logistic regression identified the top 20 predictors, which were subsequently used across nine supervised machine learning (ML) classifiers. Model performance was evaluated via repeated stratified 5-fold cross-validation (25 resamples) using accuracy, F1 score, sensitivity, specificity, Youden’s J, balanced accuracy, and Area Under the Receiver Operating Characteristic Curve (AUROC). Interpretability was assessed using SHapley Additive exPlanations (SHAP). Results: Participants with ultrasound-detected hepatic steatosis exhibited greater adiposity, insulin resistance, and dyslipidemia compared with controls [p < 0.05 for body mass index (BMI), waist circumference, glucose, glycated hemoglobin (HbA1c), triglycerides]. Elastic Net selection highlighted Weight, Ponderal Index, Fibrosis-4 Index (FIB-4), blood urea nitrogen (BUN)/Creatinine ratio, Aspartate Aminotransferase to Platelet Ratio Index (APRI), and Visceral Adiposity Index as the strongest predictors. Logistic Regression and Gradient Boosting achieved the best performance (accuracy = 0.65 ± 0.03; AUROC = 0.71 ± 0.04; balanced accuracy = 0.66 ± 0.06), outperforming rule-based indices such as Fatty Liver Index (FLI) and Hepatic Steatosis Index (HSI) reported in the literature. SHAP analysis confirmed clinically coherent feature effects, with higher anthropometric and hepatic injury indices increasing the predicted probability of ultrasound-detected hepatic steatosis. Conclusions: Routinely available clinical and biochemical parameters can predict hepatic steatosis with moderate accuracy using transparent, interpretable ML models. Logistic Regression and Gradient Boosting provided best discrimination and robust internal performance, offering a pragmatic, low-cost approach for early identification of ultrasound-detected hepatic steatosis within the MASLD spectrum in primary and metabolic care settings. Full article

This study systematically evaluated the modulatory effects of Brassica rapa L. polysaccharides (BRP) on intestinal mucosal injury in a CTX-induced mouse model. The results showed that high-dose BRP (HBRP) significantly alleviated oxidative damage, with CAT activity increased by approximately 2-fold, SOD increased by 1.3-fold, GSH-Px increased by 70%, and MDA levels decreased by 65%. Meanwhile, liver injury was improved, as ALT and AST decreased by 35% and 55%, respectively. CTX markedly suppressed immune function, while BRP intervention significantly restored cytokine levels, with IL-1β increased by up to 2.5-fold, TNF-α by 1.3-fold, and IL-4 by 2.1-fold. In addition, BRP significantly modulated gut microbiota composition. The number of unique ASVs decreased from 316 in the normal control (NC) group to 63 in the model control (MC) group and recovered to 140 in the HBRP group. At the phylum level, Bacillota increased from 55% to 97% (MC) and decreased to 65% after BRP intervention, while Bacteroidota recovered to 25%. At the genus level, Candidatus_Arthromitus decreased from 40% to nearly 0%, whereas beneficial bacteria such as Ligilactobacillus and norank_f__Muribaculaceae were restored. Overall, BRP effectively alleviates CTX-induced intestinal injury in a dose-dependent manner through antioxidant, immunomodulatory, and gut microbiota–regulating mechanisms. Full article

Background: This study aimed to evaluate the association between comorbidity and hospital admission, hospital length of stay (LOS), and in-hospital mortality among adult trauma patients across the injury severity spectrum in South Korea, and to assess whether these associations vary according to injury severity. Methods: We conducted a retrospective cohort study using the national Community-Based Severe Trauma Survey (2019–2023). Adult patients (≥18 years) with trauma were included after excluding records with missing key exposure or outcome variables. Comorbidity was defined using the ICD-10–based Elixhauser comorbidity framework. In addition to a binary classification (any vs. none), comorbidity burden was categorized into 0, 1, 2, and ≥3 conditions to evaluate dose–response relationships. The primary outcomes were hospital admission, LOS, and in-hospital mortality. Multivariable logistic regression models were used for admission and mortality, and regression models were applied for LOS, adjusting for demographic characteristics, injury mechanism, physiologic status, and system-level factors. Effect modification by injury severity was assessed using interaction terms and ISS-stratified analyses. Results: Among 49,259 patients, 32,999 (67.0%) had at least one comorbidity. Patients with comorbidities were older, had higher injury severity, and showed higher admission rates, longer LOS, and higher in-hospital mortality compared with those without comorbidities. After adjustment, comorbidity remained independently associated with increased odds of admission, prolonged LOS, and in-hospital mortality. A dose–response relationship was observed, with increasing comorbidity burden associated with progressively worse outcomes (p for trend < 0.001). In addition, substantial heterogeneity was identified across individual comorbidities, with conditions such as metastatic cancer, liver disease, coagulopathy, renal disease, and fluid and electrolyte disorders showing stronger associations with adverse outcomes. The magnitude of these associations varied across ISS strata, indicating injury severity-dependent effects. Conclusions: In this nationwide cohort, comorbidity burden and type were important determinants of acute-care utilization and in-hospital mortality among trauma patients. Incorporating comorbidity information into early risk stratification may improve prognostic accuracy and support more efficient resource allocation and clinical decision-making across the trauma care continuum. Full article

Background/Objectives: Dietary cholesterol intake significantly influences liver health, yet the specific molecular mechanisms by which it accelerates fibrogenesis remain incompletely defined. This study aimed to characterize the dose-dependent effects of dietary cholesterol on hepatic injury and fibrogenesis, identify cholesterol-responsive gene networks through transcriptomic analysis, and investigate Annexin A2 (ANXA2) as a candidate molecular mediator linking dietary cholesterol to hepatic fibrosis progression. Methods: A CCl₄-induced liver fibrosis mouse model was established and supplemented with dietary cholesterol (1–2%). Liver injury and fibrosis were assessed by liver-to-body weight ratios, serum biochemical markers, histological analysis, and fibrogenic gene expression. RNA sequencing combined with multiple hepatic fibrosis database analyses was performed to identify potential molecular mediators. Results: Dietary cholesterol supplementation aggravated CCl₄-induced hepatic fibrosis in mice, with dose-dependent increases in liver-to-body weight ratios and serum AST and ALT levels. Histological analysis showed enhanced collagen deposition and upregulation of fibrogenic genes. By integrating RNA-sequencing with multiple hepatic fibrosis database analysis and correlation analysis, we identified Annexin A2 (ANXA2) as a cholesterol-responsive gene associated with fibrosis. Conclusions: Dietary cholesterol promotes liver fibrosis progression, and ANXA2 may act as a potential mediator linking cholesterol metabolism to hepatic fibrogenesis. Full article

Background/Objectives: Inflammation and oxidative stress are key factors contributing to the initiation and progression of liver fibrosis in chronic obstructive cholestasis. Pantothenic acid (PA) and some of its derivatives have been reported to exhibit moderate anti-inflammatory, antioxidant, and regenerative effects. This study aimed to evaluate the redox-modulating effects of PA derivatives—panthenol (PL), pantethine (PT), and hopantenic acid (HPA) in a rat model of chronic obstructive cholestasis induced by common bile duct ligation (BDL). Methods: Macroscopic, histological, and ultrastructural alterations in the liver were assessed, along with molecular markers of oxidative stress, inflammation, and parameters of the glutathione (GSH) system. Results: BDL-induced liver injury was associated with enhanced lipid peroxidation, mitochondrial structural alterations, depletion of GSH, increased levels of protein S-glutathionylation (PSSG), and elevated thiobarbituric acid-reactive substances in mitochondria. Treatment with PL and, to a lesser extent, PT was associated with attenuation of hepatocellular ultrastructural damage, reduced bile duct hyperplasia, decreased inflammatory and necrotic changes, and moderate improvement in fibrosis-related parameters. In contrast, HPA (a PA antagonist) did not demonstrate hepatoprotective effects and it was associated with more pronounced liver injury. Conclusions: Chronic BDL is accompanied by suppression of glutathione redox capacity and enhanced oxidative stress. PL and PT, but not HPA, were associated with reduced levels of protein S-glutathionylation and partial restoration of redox balance. The protective effects of PL and PT may contribute to their antifibrotic activity, potentially through direct antioxidant capacity or redox-modulating mechanisms associated with the GSH system. Full article

Quantifying the mixture effects on humans exposed remains challenging because mixture components are correlated and may act bidirectionally by exhibiting nonlinear dose-response relationships, which may contribute to subclinical organ dysfunction. The liver is a vital organ in the body with broad functions, making it vulnerable to injury as it is the first organ exposed to circulating toxicants, which can precipitate hepatic damage. Our study’s objective was to evaluate the combined and component-specific associations of a multi-chemical exposure mixture of heavy metals, polychlorinated biphenyls (PCBs), polychlorinated dibenzo-p-dioxins (dioxins), and polychlorinated dibenzofurans (furans), with liver biomarkers, and to compare concentration-based results with the toxic equivalent (TEQ) potency of the weighted results for dioxin-like compounds. In an unweighted analytic sample of U.S. adults from NHANES 2003–2004 with 947 complete cases, we examined heavy metals (cadmium, lead, and mercury), PCBs (12 congeners), dioxins (7 congeners), and furans (10 congeners) in relation to eight liver biomarkers (albumin, ALP, ALT, AST, GGT, LDH, total bilirubin, and total protein). We applied multi-exposure linear regression, weighted quantile sum (WQS) regression, quantile g-computation (qgcomp), and Bayesian kernel machine regression (BKMR), with parallel TEQ-based models using WHO 2005 TEFs for dioxin-like PCBs, dioxins, and furans. Across mixture methods, the mixture structure was chemically sparse, with a limited set of recurring contributors. Total bilirubin showed the most consistent positive mixture association across qgcomp and BKMR and persisted under TEQ weighting, with prominent PCB- and dioxin-like contributions (notably PCB81/PCB TEQs and dioxin-related components). Albumin demonstrated inverse mixture patterns in BKMR and TEQ-BKMR, with dioxin-like components (notably Dioxin3 and Dioxin3_TEQ) repeatedly emerging as key drivers. For ALT, ALP, AST, GGT, LDH, and total protein, overall mixture effects were frequently attenuated or null in qgcomp despite structured component weights, indicating bidirectional sub-mixtures and internal counterbalancing. BKMR PIPs similarly concentrated on a small number of dominant predictors (e.g., lead for ALP, mercury for ALT, PCB28 for AST, and cadmium and PCB189 for LDH), while interaction summaries provided limited evidence of stable non-additivity. Using multiple complementary mixture methods, we identified outcome-specific mixture patterns suggesting hepatobiliary vulnerability. TEQ concordance supports toxicological relevance of the dioxin-like axis, while metals and non–dioxin-like mechanisms likely contribute additional pathways. Full article

The liver is a critical organ in drug metabolism and detoxification. Ganoderma lingzhi triterpenoids, a major class of bioactive compounds in G. lingzhi extracts, exhibit liver protective effects with pharmaceutical potential. In this study, we established an acute liver injury model in mice via intraperitoneal injection of 0.25% Carbon tetrachloride(CCl₄) olive oil. Prophylactic and therapeutic administration of G. lingzhi triterpenoid extracts were evaluated using alanine aminotransferase (ALT), aspartate aminotransferase (AST), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione peroxidase (GSH-Px), tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and hepatic histopathology. Western blot analysis assessed protein expression of anti-inflammatory and antioxidant stress-related pathways (Nrf2/Keap1 and MyD88/NF-κB-p65). Intervention effects on acute liver injury were determined by measuring protein molecular weight following triterpenoid treatment. In summary, G. lingzhi triterpenoids significantly alleviate oxidative stress and inflammatory responses in mice with acute liver injury by activating the KEAP1-Nrf2 antioxidant pathway and inhibiting the NF-κB-p65 and MyD88-mediated inflammatory pathways. These triterpenoids reduced serum transaminase levels, improved hepatic histopathological damage, and exerted effective protective effect on liver tissue. This study provides experimental support for the comprehensive evaluation of G. lingzhi’s anti-inflammatory and antioxidant effects. Full article

Background: Emerging evidence indicates that the liver plays a key role in spinal cord injury (SCI) pathophysiology. Method: This study reanalysed published proteomic datasets from rat models and patients with SCI using bioinformatics and literature/database searches. The aim was to identify liver-specific molecular signatures in SCI blood samples and to link these to severity and neurological recovery at various time points (acute/sub-acute and chronic). Results: Across species, a high proportion of injury severity and neurological recovery-associated proteins were linked to liver function. Notably, non-improvers exhibited prolonged sub-acute proinflammatory responses. These changes were not restricted to classical acute-phase reactants but reflected coordinated alterations in hepatic metabolic and synthetic pathways. Pathway analysis consistently highlighted Liver X Receptor /Retinoic X Receptor (LXR/RXR), complement system/cascade and DHCR24 signalling pathways, with predicted directional changes linked to recovery status. Several proteins were identified and categorised as markers of liver dysfunction, metabolic function, complement/coagulation factors and/or acute-phase proteins. Alpha-2-HS-glycoprotein (AHSG) and afamin (AFM) were commonly dysregulated across species datasets, suggesting conserved roles in inflammation and lipid metabolism. Further associations with liver pathologies such as fibrosis and cirrhosis, particularly in non-improvers, were identified. Conclusion This work builds on emerging evidence of hepatic involvement in SCI by providing cross-species, time-resolved proteomic support for altered liver-associated protein output following injury. Together, these findings underscore the central role of hepatic responses in SCI, highlighting liver-associated proteins and pathways as candidate biomarkers that may aid in stratifying recovery trajectories and informing clinical prognostication. Full article

Background: Acute kidney injury (AKI) is a common and serious complication in patients with liver cirrhosis and is associated with poor outcomes. However, whether the association between nephrotic-range proteinuria (NRP) and severe AKI varies by liver disease severity remains unclear. Methods: This retrospective cohort study included 408 adult patients with cirrhosis stratified by Child–Pugh class (A, B, and C). Severe AKI was defined as Kidney Disease: Improving Global Outcomes stage 2–3. Multivariable logistic regression analyses were performed in the overall cohort and within each class, with the additional evaluation of interaction effects. Results: The incidence of severe AKI increased from 18.4% in class A to 38.8% in class C. In the extended multivariable model incorporating hemodynamic and inflammatory variables, nephrotic-range proteinuria was not significantly associated with severe AKI. In stratified analyses, a significant association was observed only in Child–Pugh class A. Additional analyses suggested that this relationship was attenuated after accounting for sepsis and systemic severity. Conclusions: Although NRP prevalence was similar across Child–Pugh classes, the association between NRP and severe AKI appeared to vary by disease stage, particularly before adjustment for systemic severity. Full article