Schiano, Thomas D.

ABSTRACT Background and Aims Clinically significant portal hypertension (CSPH; hepatic venous pressure gradient (HVPG) ≥ 10 mmHg) is a severe complication of chronic liver disease, with increased risk of variceal bleeding and liver decompensation (at HVPG ≥ 12 mmHg). This study evaluated the performance of multiparametric (mp)MRI for diagnosing CSPH and predicting liver decompensation, compared to ultrasound‐based shear wave elastography (SWE) and blood tests. Methods In this prospective single‐centre study (2018–2022), 59 patients (M 30, mean age 52.7 years) underwent mpMRI and HVPG measurement, with an average interval of 32 ± 31 days. The mpMRI protocol included 2D/3D MR elastography (MRE), T 1 /proprietary iron‐compensated T 1 (cT 1 )/T 1ρ mapping, gadoxetate‐enhanced dynamic contrast‐enhanced MRI (DCE‐MRI) of the liver and spleen, SWE and blood tests. Statistical analyses included Mann–Whitney U tests, ROC analysis, logistic regression and Cox proportional hazards models. Results CSPH was present in 13 patients (22%). Several MRI parameters showed high diagnostic performance for CSPH (AUC ≥ 0.8), with spleen stiffness‐2D MRE (AUC 0.88, 95% confidence interval (CI) 0.78–0.98) and liver uptake on DCE‐MRI (AUC 0.83, 95% CI 0.70–0.96) performing best, while SWE had AUCs of 0.63 (95% CI 0.45–0.81) for liver and 0.67 (95% CI 0.44–0.89) for spleen. Combining spleen stiffness‐2D MRE and liver uptake achieved an AUC of 0.93 (95% CI 0.86–1.00) for diagnosing CSPH. For predicting decompensation, spleen stiffness‐3D MRE and liver uptake rate had AUCs of 0.83 (95% CI 0.68–0.99) and 0.83 (95% CI 0.70–0.95), respectively, outperforming SWE. Conclusions Spleen stiffness measured with MRE combined with gadoxetate liver uptake (measured with DCE‐MRI) can diagnose CSPH and predict liver decompensation, with superior performance compared to SWE. Trial Registration ClinicalTrials.gov identifier: NCT03436550

AbstractBackgroundPatients with end‐stage heart failure frequently have significant congestive hepatopathy requiring hepatology assessment prior to heart transplantation listing. An elevated Model for End‐stage Liver Disease score with modification to exclude INR (MELD‐XI) has been associated with increased mortality following heart transplantation (HT). This study's primary aim was to examine whether Child‐Turcotte‐Pugh (CTP) classification is associated with post‐transplant mortality in patients bridged to transplant with left ventricular assist devices.Methods and ResultsWe conducted a retrospective analysis of 134 patients from our center. Age, CTP class, and MELD‐XI at HT were included in the multivariate model for the primary outcome, which demonstrated a significant association between 1‐year mortality and CTP class (CTP‐A HR: .08, CI .01–.46, P < .01; CTP‐B HR: .25, CI .05–1.2, P = .08; reference group CTP‐C), and MELD‐XI (HR: 1.15; CI: 1.03–1.28; P = .01), but no significant difference for age (HR: .97; CI: .93–1.01; P = .15). Only 13/33 patients with CTP improvement after assist device also had improvement in MELD‐XI.ConclusionsPatients with relatively low MELD‐XI scores with discordantly high CTP classification may be a distinct subset for whom MELD‐XI underestimates the risk of mortality after heart transplantation compared to CTP.

Surgical innovation and multidisciplinary management have allowed children born with univentricular physiology congenital heart disease to survive into adulthood. An estimated global population of 70 000 patients have undergone the Fontan procedure and are alive today, most of whom are <25 years of age. Several unexpected consequences of the Fontan circulation include Fontan-associated liver disease. Surveillance biopsies have demonstrated that virtually 100% of these patients develop clinically silent fibrosis by adolescence. As they mature, there are increasing reports of combined heart-liver transplantation resulting from advanced liver disease, including bridging fibrosis, cirrhosis, and hepatocellular carcinoma, in this population. In the absence of a transplantation option, these young patients face a poor quality of life and overall survival. Acknowledging that there are no consensus guidelines for diagnosing and monitoring Fontan-associated liver disease or when to consider heart transplantation versus combined heart-liver transplantation in these patients, a multidisciplinary working group reviewed the literature surrounding Fontan-associated liver disease, with a specific focus on considerations for transplantation.

Background and Aims A high proportion of patients develop chronic kidney disease (CKD) after liver transplantation (LT). We aimed to develop clinical/protein models to predict future glomerular filtration rate (GFR) deterioration in this population. Approach and Results In independent multicenter discovery (CTOT14) and single‐center validation (BUMC) cohorts, we analyzed kidney injury proteins in serum/plasma samples at month 3 after LT in recipients with preserved GFR who demonstrated subsequent GFR deterioration versus preservation by year 1 and year 5 in the BUMC cohort. In CTOT14, we also examined correlations between serial protein levels and GFR over the first year. A month 3 predictive model was constructed from clinical and protein level variables using the CTOT14 cohort (n = 60). Levels of β‐2 microglobulin and CD40 antigen and presence of hepatitis C virus (HCV) infection predicted early (year 1) GFR deterioration (area under the curve [AUC], 0.814). We observed excellent validation of this model (AUC, 0.801) in the BUMC cohort (n = 50) who had both early and late (year 5) GFR deterioration. At an optimal threshold, the model had the following performance characteristics in CTOT14 and BUMC, respectively: accuracy (0.75, 0.8), sensitivity (0.71, 0.67), specificity (0.78, 0.88), positive predictive value (0.74, 0.75), and negative predictive value (0.76, 0.82). In the serial CTOT14 analysis, several proteins, including β‐2 microglobulin and CD40, correlated with GFR changes over the first year. Conclusions We have validated a clinical/protein model (PRESERVE) that early after LT can predict future renal deterioration versus preservation with high accuracy. This model may help select recipients at higher risk for subsequent CKD for early, proactive renal sparing strategies.