Liver transplantation (LT) is a life-saving procedure for patients with end-stage liver disease; however, with the growing shortage of organ donors, the need to identify futile transplants has become increasingly urgent. Futility in liver transplantation refers to situations where the expected post-transplant survival or quality of life is poor, making the procedure unlikely to yield a meaningful benefit. Various definitions of futility are used across different countries and transplant centers, with criteria often based on clinical factors such as age, comorbidities, MELD score, and functional status. For hepatologists and transplant surgeons, clearer guidelines are essential to make informed decisions and avoid unnecessary transplants that may place patients at risk without improving their prognosis. While some studies have proposed futility scores, there is currently no universal consensus on a standardized definition or set of criteria. This highlights the need for further prospective trials to evaluate the predictors of futility in liver transplantation, aiming to refine decision-making processes, optimize organ allocation, and improve patient outcomes. Future research should focus on the development of universally accepted futility criteria and explore interventions to mitigate the factors contributing to transplant futility.

Even after recovery of kidney function following AKI, progression to CKD may still occur, characterized by a reduction in peritubular capillaries (PTC) and subsequent kidney fibrosis. Reactive oxygen species (ROS) from uncoupled eNOS are suspected to damage endothelial cells and cause PTC rarefaction observed in AKI-CKD. Intermedin (IMD) inhibits eNOS uncoupling by activating AMPK, but its impact on AKI-CKD transition remains unclear.

We utilized IMD-deficient (IMD-/-) mice to explore its effects on AKI-CKD transition, PTC density, endothelial damage, and kidney ROS in a kidney ischemia/reperfusion injury (IRI) model. To elucidate its protective mechanism for PTCs, we subsequently investigated the effects of IMD on endothelial cells and ROS using a hypoxia/reoxygenation (HR) model with human umbilical vein endothelial cells (HUVECs). Finally, we investigated the influence of IMD on AMPK/GTPCH-I/BH4/eNOS to explore its mechanism in alleviating oxidative stress.

Compared with IMD+/+ littermate sham controls, PTC density was significantly reduced in IMD-/- sham mice, with significantly increased oxidative stress. Post-AKI, both IMD+/+ and IMD-/- mice demonstrated substantial declines in kidney function and histology, along with significant fibrosis, PTC reduction, and heightened oxidative stress. Moreover, the severity of kidney damage in IMD-/- mice following AKI was considerably more pronounced than in IMD+/+ mice. HR significantly induced eNOS uncoupling and oxidative stress in HUVECs. Treatment with IMD effectively inhibited eNOS uncoupling and ROS production, achieving levels comparable to the antioxidant N-acetylcysteine. The inhibitory effect of IMD on eNOS uncoupling was abrogated when L-NAME was introduced after HR. HR significantly impaired AMPK activation, which could be reversed by IMD. Additional experiments with inhibitors of GTPCH-I and AMPK, and exogenous BH4, confirmed that IMD protects endothelial cells by activating AMPK/GTPCH-I/BH4, thereby inhibiting eNOS uncoupling and ROS production.

We concluded that IMD inhibits AKI-CKD transition by protecting endothelial cells of PTC via AMPK/GTPCH-I/BH4/eNOS pathway.

This study aimed to evaluate the efficacy and safety of terlipressin and albumin in patients with hepatorenal syndrome.

A systematic review with meta-analysis of randomized controlled trials comparing terlipressin and albumin versus albumin with or without placebo in patients with cirrhosis and hepatorenal syndrome was performed. The study protocol was registered at the PROSPERO platform (CRD42021246684).

Nine randomized controlled trials fulfilled the selection criteria and were included in this meta-analysis. There was no evidence of a significant difference between the groups regarding mortality in 15 days [risk ratio (RR) = 0.73, 95% confidence interval (CI) = 0.47-1.13, P  = 0.16, I2  = 52%] or in 90 days (RR = 0.94, 95% CI = 0.80-1.09, P  = 0.84, I2  = 29%). Regarding hepatorenal syndrome reversal failure, a significant benefit was demonstrated in the terlipressin and albumin group (RR = 0.64, 95% CI = 0.53-0.78, P  < 0.00001, I2  = 72%). There was no evidence of a significant difference between the groups regarding adverse events (RR = 3.5, 95% CI = 0.94-13.09, P  = 0.06, I2  = 89%).

Terlipressin associated with albumin led to a significantly lower rate of hepatorenal syndrome reversal failure, but there was no evidence of a significant effect of this treatment regarding mortality or adverse events.

Together with carriers in liver and small intestine, kidney transporters function to conserve and compartmentalize bile acids in the enteronephrohepatic circulation. In patients with liver disease, systemic bile acid levels are elevated, undergo increased renal glomerular filtration, and contribute to the pathogenesis of cholemic nephropathy and acute kidney injury. In this review, we describe mechanisms for renal bile acid transport and highlight very recent discoveries that challenge current paradigms for the pathogenesis of cholemic nephropathy and renal tubule cast formation. We also discuss the therapeutic potential of inhibiting the kidney apical sodium-dependent bile acid transporter (ASBT) to redirect bile acids into urine for elimination, reduce hepatobiliary accumulation and systemic levels of bile acids, and treat cholemic nephropathy. In conclusion, a deeper understanding of the enteronephrohepatic bile acid axis is providing insights into novel strategies to protect both liver and kidney in patients with liver disease.

Liver cirrhosis is a leading cause of morbidity and mortality worldwide, with complications such as ascites, spontaneous bacterial peritonitis (SBP), and hepatorenal syndrome (HRS) significantly worsening prognosis. This paper aims to review the pathophysiology, diagnostic approaches, and management strategies for ascites and the complication of it, emphasizing the role of portal hypertension.

We conducted a comprehensive review of the literature on liver cirrhosis, portal hypertension, ascites formation, and related complications. Existing evidence was evaluated and ranked using the GRADE system: A (high) to D (verly low). Recommendation strength was graded 1 (strong) or 2 (weak).

Portal hypertension is the key factor in ascites development. Non-invasive tools such as liver stiffness measurement (LSM) have proven to be effective in identifying patients at risk for clinically significant portal hypertension (CSPH), thus guiding treatment decisions. Carvedilol, recommended over propranolol, offers superior efficacy in reducing portal pressure. Diuretics, in combination with a moderate sodium-restricted diet, are the first-line treatment for ascites. However, refractory ascites requires advanced interventions. Spontaneous bacterial peritonitis (SBP) remains a major complication in patients with ascites, while hepatorenal syndrome - acute kidney injury (HRS-AKI) demands early recognition and timely vasoconstrictor therapy.

Liver cirrhosis and the complication of it significantly impact patient quality of life and survival. Portal hypertension is a critical driver of ascites and other complications, making early identification through non-invasive diagnostic methods essential for appropriate management. Medical treatments, including non-selective beta-blockers (NSBBs), diuretics, and advanced procedures, offer substantial benefits in controlling ascites and preventing further decompensation.

Acute kidney injury (AKI) is a serious complication of cirrhosis. A systematic, global characterisation of AKI occurring in patients with cirrhosis is lacking. We therefore aimed to assess global differences in the characteristics, management, and outcomes of AKI in hospitalised patients with cirrhosis.

In this prospective, multicentre, cohort study, we enrolled adults (≥18 years) with decompensated cirrhosis who were hospitalised for a cirrhosis-related complication, with or without AKI, at 65 centres across five continents. We captured AKI prevalence, stage, phenotype, and details on AKI management and clinical course. Universal health coverage index and gross national income per capita were also collected. The primary outcome was 28-day mortality. Multivariable models including demographic and clinical variables, cirrhosis cause, cirrhosis severity, AKI severity, AKI management variables, universal health coverage, and gross national income were used to analyse independent associations with 28-day mortality. Secondary outcomes were AKI classification, progression, and resolution. This study is complete and registered with ClinicalTrials.gov (NCT05387811).

Between July 1, 2022, and May 31, 2023, we enrolled 3821 patients who were hospitalised for decompensated cirrhosis. Mean age was 57·7 years (SD 13·1), 2467 (64·6%) were men, and 1354 (35·4%) were women. Most patients were White (2128 [55·7%]). 1456 (38·1%, 95% CI 36·6-39·6) of 3821 patients had AKI (943 [64·8%] men and 513 [35·2%] women). Globally, patients presented with similar AKI stages, but patients from North America and Asia had the highest MELD-Na scores at presentation and the highest rates of peak AKI stage 3. Overall, hypovolaemic AKI was the most common phenotype (858 [58·9%] of 1456), followed by HRS-AKI (253 [17·4%]) and acute tubular necrosis (216 [14·8%]). The prevalences of hypovolaemic AKI and HRS-AKI were similar across regions, but acute tubular necrosis was more frequent in Asia (p<0·0001 across regions). Additionally, regional differences in the management of AKI (use of albumin, vasopressors, and diuretics) were found. 335 (28·6%) of 1171 patients with initial AKI stages 1 or 2 had progression to higher stages during hospitalisation. AKI resolved in 862 (59·2%) cases during hospitalisation. 333 (22·9%) patients with AKI had died by 28 days. Multivariable analyses showed that increased age, female sex, presence of ascites, presence of hepatic encephalopathy, increased white blood cell count, increased MELD-Na, hospital-acquired AKI, a lower universal health coverage index (<80), and not being in a high-income country were independently associated with an increased risk of 28-day mortality. Increased serum albumin was associated with a decreased risk of 28-day mortality.

This study found important regional differences in AKI severity, phenotype, management, and outcomes in patients with decompensated cirrhosis. Health-care coverage remains an important driver of survival in patients with cirrhosis and AKI.

European Association Study for the Study of the Liver and the Italian Society of Internal Medicine.

Major advances in managing critically ill patients with liver disease have improved their prognosis and access to intensive care facilities. Acute-on-chronic liver failure (ACLF) is now a well-defined disease and these patients can be fast-tracked for liver transplantation (LT) with good outcomes if there are no contraindications. In acute liver failure, plasma exchange has improved prognosis for patients not eligible for immediate transplant. Further advances in novel therapies and refinement of the criteria for early LT in ACLF and also clinical implementation of artificial intelligence tools will probably constitute the next major breakthroughs in critically ill patients with liver disease.

Acute kidney injury (AKI) is a critical and often fatal complication in decompensated cirrhosis, significantly affecting inpatient survival rates. Hepatorenal syndrome (HRS), a distinct subtype of AKI, develops in individuals with advanced cirrhosis and portal hypertension. It is marked by progressive kidney dysfunction, poor prognosis, and frequently causes death before liver transplantation. The pathogenesis of HRS involves vasodilation of the splanchnic vessels, leading to overactivation of the endogenous vasoactive systems, circulatory dysfunction, and reduced renal perfusion, which ultimately impairs glomerular filtration. Recent studies have highlighted the role of systemic inflammation in exacerbating renal damage. Despite these changes, renal histology in HRS usually shows no significant abnormalities, and there is typically no hematuria, proteinuria, or abnormal findings on ultrasound. Common risk factors for HRS include spontaneous bacterial peritonitis, infections, and large-volume paracentesis without albumin infusion. Diagnosing HRS is challenging, particularly in distinguishing it from acute tubular necrosis, due to the absence of specific biomarkers. Treatment primarily involves vasoconstrictors such as terlipressin and albumin, with liver transplantation being the definitive therapeutic option. This review provides an updated understanding of HRS, addressing its pathophysiology, diagnosis, management, and future challenges, based on recent expert consensus.

AKI is common in patients with liver cirrhosis (LC) affecting (30 to 50%). Our study aimed to evaluate the role of urinary biomarkers as predictors of AKI, its etiology and mortality. We performed a prospective cohort study of patients with LC during 1 year. Urine samples for biomarkers dosage were collected within 48 h of hospital admission. Diagnosis of AKI was performed according to KDIGO 2012 criteria. The results were presented using Chi-square, T test, AUC-ROC and logistic regression (p < 0.05). We included 100 patients, 58.5 ± 16.1 years, main etiologies of LC were alcohol and and metabolic disfunction associated with steatohepatitis. Infection was the main cause of LC decompensation. AKI occurred in 53% of patients and mortality was 20%. CHILD C, infectious as cause of decompensation, baseline creatinine, need for mechanical ventilation and noradrenaline use and urinary were associated with AKI. We found no association between AKI and KIM-1 and IL-18. The main etiologies of AKI were transient ischeamia (49%), renal (43.4%), and hepatorenal syndrome (HRS) (7.5%). There was difference between the groups in hematuria, proteinuria, FENa, FEUr and uNGAL which were higher in renal AKI when compared to transient ischaemia and HSR. FENa and FEUr were excellent predictors of AKI etiology (AUC-ROC > 0.80, sensitivity and specificity > 0.80), while only uNGAL was good predictor of AKI etiology (AUC-ROC, sensitivity and specificity > 0.70). Regarding death, CHILD C, baseline creatinine, KDIGO 3, septic AKI, need for mechanical ventilation and IL-18 were identified as associated variables. Only NGAL was predictor of AKI and its etiology, anticipating AKI diagnosis in 2.5 ± 1.1 days, while IL-18 was predictor of death. We highlight the importance of lower-cost biochemical tests as FENa and FEUr and clinical information as CHILD and cause of LC descompensation which were relevant in predicting AKI, its etiology and death.

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.

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.

In this review, we discuss the pathophysiology and management of acute kidney injury (AKI) in the setting of acute-on-chronic liver failure (ACLF). ACLF is characterised by the occurrence of acute hepatic and/or extrahepatic organ failure, induced by immune dysregulation and systemic inflammation in patients with chronic liver disease. Kidney involvement is common, with AKI occurring in 30% to > 95% of ACLF patients, depending on the definition used. Since there is a lack of kidney biopsy data in these patients, the underlying pathophysiological basis of AKI remains incompletely understood, and systemic inflammation is believed to be the primary driver of organ injury. The management of AKI has been largely extrapolated from studies in decompensated cirrhosis, and there is little data specifically in the ACLF setting. However, available evidence suggests that structural kidney injury is more common in ACLF than in decompensated CLD, and therefore, AKI in ACLF is less likely to respond to volume repletion and vasopressors. Treatment options remain limited for those who are non-responsive to intravenous fluids and vasopressors. Liver transplantation (LT), with or without kidney transplantation, is the definitive treatment for these patients. At present, extracorporeal therapies such as therapeutic plasma exchange and kidney replacement therapies play a supportive role in ACLF as a bridge to LT; however, the optimal timing and dosing remain unclear. While theoretically, extracorporeal therapies have the potential to reverse or halt progression of organ damage in ACLF, there is limited evidence currently.

In liver cirrhosis patients, acute kidney injury (AKI) is a common and severe complication associated with significant morbidity and mortality, often leading to chronic kidney disease (CKD). This progression reflects a complex interplay of renal and hepatic pathophysiology, with AKI acting as an initiator through maladaptive repair mechanisms. These mechanisms-such as tubular cell cycle arrest, inflammatory cascades, and fibrotic processes-are exacerbated by the hemodynamic and neurohormonal disturbances characteristic of cirrhosis. Following AKI episodes, persistent kidney dysfunction or acute kidney disease (AKD) often serves as a bridge to CKD. AKD represents a critical phase in renal deterioration, characterized by prolonged kidney injury that does not fully meet CKD criteria but exceeds the temporal scope of AKI. The progression from AKD to CKD is further influenced by recurrent AKI episodes, impaired renal autoregulation, and systemic comorbidities such as diabetes and metabolic dysfunction-associated steatotic liver disease, which compound kidney damage. The clinical management of AKI and CKD in cirrhotic patients requires a multidimensional approach that includes early identification of kidney injury, the application of novel biomarkers, and precision interventions. Recent evidence underscores the inadequacy of traditional biomarkers in predicting the AKI-to-CKD progression, necessitating novel biomarkers for early detection and intervention.

Guidelines recommended volume expansion with albumin for 48 hours for patients with cirrhosis and acute kidney injury (AKI) to correct hypovolemia and rule out prerenal AKI. A recent update in the ADQI-ICA consensus guidelines suggested shortening this duration to 24 hours, primarily based on expert opinion. This study aimed to evaluate the response rates to albumin treatment after 24 and 48 hours and to compare and assess the prognostic significance of three different definitions of response to albumin therapy.

Data from 127 prospectively recruited patients with cirrhosis and AKI from two German centers were analyzed. We examined three response definitions after 24 and 48 hours: (1) serum creatinine (SCr) decrease >0.3 mg/dl, (2) SCr decrease >25%, and (3) SCr decrease in at least one AKI stage. Follow-up was prolonged until liver transplantation, death or hemodialysis.

Overall, 30-54% of the patients responded to albumin treatment depending on the definition, and response rates were balanced across AKI stages. Notably, a relevant number of patients who responded at 48 hours did not respond within the first 24 hours. Additional responses to albumin during the second 24 hours according to definitions 1, 2, and 3 were 28%, 22%, and 18%, respectively. Response according to definition 3 was associated with higher hemodialysis- and transplantation-free survival rates.

A substantial proportion of patients require 48 hours to respond to albumin treatment. Shortening the duration of albumin therapy may lead to overtreatment with terlipressin.

This study provides valuable insights into the optimal duration of albumin treatment for patients with cirrhosis and acute kidney injury, challenging the recent recommendation to shorten the duration of albumin treatment. Furthermore, the optimal definition for response to albumin (reduction of at least one acute kidney injury stage) has been assessed. The results of this study are highly clinically relevant since shortening albumin therapy may lead to overtreatment with terlipressin, and evidence to support a specific definition of response to albumin was lacking. Clinicians can use these findings to predict treatment outcomes better, avoid fluid overload, and improve patient prognosis, while also considering the potential risks of early intervention with terlipressin.

Background Invasive procedures pose a greater risk for patients with liver cirrhosis. This study investigates the impact of cirrhosis on the outcomes of implantable cardiac defibrillator (ICD) implantation. Methods We conducted a retrospective analysis using the National Readmissions Database (NRD) from 2016 to 2020. Adult patients who received an ICD, identified by the International Statistical Classification of Diseases and Related Health Problems 10th Revision (ICD-10) codes, were included. Outcomes were compared between patients with and without underlying liver cirrhosis. The primary outcome was all-cause inpatient mortality. Secondary outcomes included ischemic cerebrovascular accidents (CVA), major bleeding (gastrointestinal, intracranial, pulmonary, and other bleeding), packed red blood cell (pRBC) transfusion, pericardial complications (pericardial effusion, hemopericardium, or pericardial tamponade), acute kidney injury (AKI), acute myocardial infarction (AMI), length of stay, and total hospital charges. Results Among 264,518 patients who underwent defibrillator implantation, 3,507 patients (1.3%) had liver cirrhosis. Patients with cirrhosis experienced significantly higher inpatient mortality (adjusted odds ratio (aOR): 2.29, 95% confidence interval (CI): 1.70-3.08, P<0.001), major bleeding (aOR: 2.40, 95% CI: 1.97-2.91, P<0.001), pRBC transfusion (aOR: 2.19, 95% CI: 1.81-2.64, P<0.001), pericardial complications (aOR: 1.37, 95% CI: 1.05-1.79, P=0.02), and AKI (aOR: 1.44, 95% CI: 1.29-1.59, P<0.001). No significant difference was observed in the incidence of ischemic CVA (aOR: 0.89, 95% CI: 0.33-2.43, p=0.83), but there was a reduced incidence of AMI (aOR: 0.69, 95% CI: 0.59-0.84, P<0.001) in patients with cirrhosis. Additionally, liver cirrhosis was associated with increased hospital stays (adjusted mean difference (aMD): 2.79 days, 95% CI: 2.20-3.37, P<0.001) and higher total charges (aMD: $35,624, 95% CI: 23,698-47,549, P<0.001). Conclusion Cirrhosis is associated with increased mortality, bleeding complications, and greater resource utilization after ICD implantation. These results emphasize the need for careful evaluation when considering this procedure in patients with liver cirrhosis.

Acute kidney injury is a severe complication of cirrhosis. However, the impact of mild decreases in renal function is controversial. This study aims to evaluate the prognosis of the different stages of acute kidney injury in cirrhosis.

This is a multicenter prospective cohort study of patients hospitalized for acute decompensation of cirrhosis, with serum creatinine values measured at least twice. Primary outcome was mortality (in-hospital, 30 days, 90 days and 12 months).

Nine hundred twenty-eight patients were included in the study. Acute kidney injury was diagnosed in 505 patients (stages 1a-21.6%, 1b-27.5%, 2-28.1%, 3-22.8%). Mortality rates of patients with acute kidney injury stage 1a were significantly higher than those of individuals without acute kidney injury (in-hospital-19.3% vs 4.7%; 30-day-21.8% vs 6.7%; 90-day-35.2% vs 17.5%; 12-month-54.1% vs 37.1%; p < 0.05 for all comparisons). Mortality rates were even higher for acute kidney injury stages 1b, 2 and 3. Survival analysis demonstrated that patients without acute kidney injury performed significantly better than those with any stage of acute kidney injury (p < 0.01). Acute kidney injury stages 1a, 1b, 2 and 3 were independently associated with survival in the multivariate analysis (p < 0.01).

Patients hospitalized for acute decompensation of cirrhosis who develop acute kidney injury have significantly higher mortality rates than those who do not develop this complication. This is true even for the mildest stages of acute kidney injury (stage 1a) and remains so at different time-points, supporting recommendations for earlier treatments.

Acute kidney injury (AKI) is commonly encountered in patients hospitalized for decompensated cirrhosis and is associated with prolonged hospital stays, increased treatment burden, and even mortality. The present study aimed to determine the prevalence of and develop a predictive nomogram for AKI in patients with decompensated cirrhosis.

This cross-sectional, double-center study involved 544 patients hospitalized with decompensated cirrhosis. Acute kidney injury was diagnosed using American Gastroenterological Association's guidelines with one more criterion: an increase in serum creatinine ≥ 0.3 mg/dL within 48 h or an increase in serum creatinine ≥ 50% compared to baseline serum creatinine or when the urine output is reduced below 0.5 mL/kg/h for > 6 h. We used the Bayesian model averaging method find the optimal model for predicting AKI. A predictive nomogram was also developed to enable risk prediction.

The overall AKI prevalence was 26.7% (95% Confidence interval [CI] 25.7-27.7). The optimal model for predicting AKI included diuretic therapy (odds ratio [OR]: 5.55; 95%CI 3.31-9.33), infection (OR: 2.06; 95%CI 1.31-3.22), ascites (OR: 3.20; 95%CT: 1.67-6.13), Child-Pugh group C (OR: 2.91; 95%CI 1.84-4.62), serum potassium (OR per 1 mmol/L increase: 1.62; 95%CI 1.25-2.1) and serum chloride (OR per 1 mmol/L decrease: 1.03; 95%CI 1.01-1.06). The area under the receiver operating characteristic curve was 0.8, with a 95%CI ranging from 0.75 to 0.84.

Acute kidney injury was relatively common among patients hospitalized for decompensated cirrhosis. A novel nomogram-including diuretic therapy, infection, ascites, Child-Pugh group C, serum potassium and, serum chloride, was helpful for the selective screening of AKI in patients with decompensated cirrhosis.

Accumulating evidence has challenged the traditional model of the liver-kidney connection in hepatorenal syndrome. Cirrhosis can significantly impact cardiac function, leading to cirrhotic cardiomyopathy. Recent understanding reveals how cardiac dysfunction plays a pivotal role in the development of renal dysfunction in this setting, suggesting that disturbances traditionally categorized under hepatorenal syndrome may actually represent a hepatic form of cardiorenal syndrome - hepatocardiorenal syndrome - where the liver affects the kidney through cardiorenal pathways.

Effective management of hepatocardiorenal syndrome and acute kidney injury in cirrhosis relies on accurately assessing a patient's hemodynamic and volume status. Point-of-care ultrasound, including lung and focused cardiac ultrasound, is a valuable diagnostic tool that provides crucial data on fluid tolerance, subclinical pulmonary congestion, and left ventricular filling pressures. This objective, bedside approach offers a comprehensive assessment that directly influences patient management and therapeutic decisions.

Point-of-care ultrasound plays an essential role in evaluating and managing hepatocardiorenal syndrome, providing insights into the underlying pathophysiology. By assessing hemodynamic parameters, it helps guide therapy and monitor patient responses, ensuring more accurate and effective treatment of patients with cirrhosis and acute kidney injury.

Acute-on-chronic liver failure (ACLF) is a condition associated with high mortality in the absence of liver transplantation. There have been various definitions proposed worldwide. The first consensus report of the working party of the Asian Pacific Association for the Study of the Liver (APASL) set in 2004 on ACLF was published in 2009, and the "APASL ACLF Research Consortium (AARC)" was formed in 2012. The AARC database has prospectively collected nearly 10,500 cases of ACLF from various countries in the Asia-Pacific region. This database has been instrumental in developing the AARC score and grade of ACLF, the concept of the 'Golden Therapeutic Window', the 'transplant window', and plasmapheresis as a treatment modality. Also, the data has been key to identifying pediatric ACLF. The European Association for the Study of Liver-Chronic Liver Failure (EASL CLIF) and the North American Association for the Study of the End Stage Liver Disease (NACSELD) from the West added the concepts of organ failure and infection as precipitants for the development of ACLF and CLIF-Sequential Organ Failure Assessment (SOFA) and NACSELD scores for prognostication. The Chinese Group on the Study of Severe Hepatitis B (COSSH) added COSSH-ACLF criteria to manage hepatitis b virus-ACLF with and without cirrhosis. The literature supports these definitions to be equally effective in their respective cohorts in identifying patients with high mortality. To overcome the differences and to develop a global consensus, APASL took the initiative and invited the global stakeholders, including opinion leaders from Asia, EASL and AASLD, and other researchers in the field of ACLF to identify the key issues and develop an evidence-based consensus document. The consensus document was presented in a hybrid format at the APASL annual meeting in Kyoto in March 2024. The 'Kyoto APASL Consensus' presented below carries the final recommendations along with the relevant background information and areas requiring future studies.