In Ethiopia, cirrhosis is the 6th leading cause of death and is responsible for high hospitalization and mortality rates. However, until now, factors affecting in-hospital mortality of patients with liver cirrhosis are poorly understood. This study assessed the predictors of in-hospital mortality among cirrhotic patients in Ethiopia.

A retrospective cross-sectional study using data collected from the electronic medical records of patients who were admitted for complications of liver cirrhosis between January 1, 2023, and March 31, 2024, in the medical wards of Adera Medical Center, St. Paul's Hospital Millennium Medical College, and Tikur Anbessa Specialized Hospital. Frequency and cross-tabulation were used for descriptive statistics. Predictor variables with a p-value <0.25 in bivariate analyses were included in the logistic regression.

Of the 299 patients included in the final analysis, the majority (79.6%) were males, and the median age of the study participants was 45 (IQR, 36-56) years. Hepatitis B virus (32.1%) was the most common etiology, followed by alcohol (30.1%) and hepatitis C virus (13.4%). Ascites (69.2%), upper gastrointestinal bleeding (50.5%), and hepatic encephalopathy (44.8%) were the most common forms of presentation. The in-hospital mortality rate was 25.4%. West Haven grade III or IV hepatic encephalopathy (AOR: 12.0; 95% CI 2.33-61.63; P < 0.01), hepatocellular carcinoma (AOR: 9.05; 95% CI 2.18-37.14; P: 0.01), history of previous admission within one year period (AOR: 6.80; 95% CI 2.18-21.18; P < 0.01), acute kidney injury (AOR: 6.47; 95% CI 1.77-23.64; P < 0.01), and model for end-stage liver disease - sodium score (AOR: 1.17; 95% CI 1.05-1.30; P: 0.02), were found to be predictors of in-hospital mortality.

In-hospital mortality of cirrhotic patients is high in Ethiopia. West Haven grade III or IV hepatic encephalopathy is the leading cause of mortality. Hence, prompt identification and management of hepatic encephalopathy and its precipitant at an earlier stage is crucial for better treatment outcomes and survival.

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.

Polymyxin B, a last resort for carbapenem-resistant gram-negative bacteria (CRGNB) infections, has infection site-specific pharmacokinetic/pharmacodynamic (PK/PD) properties. However, there is little clinical evidence to support optimal exposures of polymyxin B for different site infections. We performed a prospective, observational, multicenter study to evaluate the clinical outcomes and PK/PD of intravenous polymyxin B treatment for various site CRGNB infections. The main clinical outcomes were 14-day all-cause mortality and nephrotoxicity, and the secondary outcomes were 28-day mortality and clinical response. The area under curves (AUCs) of polymyxin B were determined, and their associations with clinical outcomes were analyzed by stratification based on the infection site. A total of 312 patients were ultimately enrolled from 10 research centers. The overall 14-day mortality was 29.5%, and those of patients with lower respiratory tract infection (LRTI), intra-abdominal infection (IAI), and bloodstream infection (BSI) were 32.3%, 19.7%, and 30.3%, respectively. The 28-day mortality rate was 38.1%, while LRTI patients had the highest mortality (41.4%) and IAI patients lowest (34.8%). The clinical response rate was 46.2%, which was similar among the subgroups. The overall AKI rate was 60.9%. An AUC greater than 50 mg∙h/L was related to lower mortality in IAI patients but not in LRTI patients, which led to a lower but not significant difference in the overall analysis. The AUC of polymyxin B was an independent risk factor for 14-day mortality in IAI patients, and the cutoff value was 76 mg∙h/L. The results would be helpful for personalized dosing and monitoring of polymyxin B.CLINICAL TRIALSThis study is registered with the Chinese Clinical Trial Registry as ChiCTR2200056667.

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 Acute Disease Quality Initiative (ADQI)-International Club of Ascites (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 (HD).

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 response to albumin during the second 24 hours were 38 %, 24 %, and 25 % (definitions 1, 2, and 3, respectively). Response according to definition 3 was associated with a better HD- and transplantation-free survival.

A substantial proportion of patients requires 48 hours to respond to albumin treatment. Shortening time 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 (AKI), challenging the recent recommendation of shortening the treatment period with albumin. Furthermore, the optimal definition for response to albumin (reduction of at least one AKI 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 the choice of the 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 (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.

The presence of acute kidney injury (AKI) significantly increases in-hospital mortality risk for cirrhotic patients. Early prognosis prediction for these patients is crucial. We aimed to develop and validate a machine learning model for in-hospital mortality prediction for cirrhotic patients with AKI.

Data from cirrhotic patients with AKI hospitalized at the First Affiliated Hospital of Zhejiang University between January 1, 2013, and December 31, 2020 were used to train and validate an extreme Gradient Boosting model to predict in-hospital mortality risk. The Boruta algorithm was used for variable selection. The optimal model was selected and named as PHM-CPA (Prediction of in-Hospital Mortality for Cirrhotic Patients with AKI). The PHM-CPA model was then externally validated in patients from eICU Collaborative Research Database (eICU-CRD) and Medical Information Mart for Intensive Care III dataset (MIMIC). The predictive performance of PHM-CPA model was compared with that of logistic regression (LR) model and 25 previously reported models.

A total of 519 cirrhotic patients with AKI were enrolled in model training cohort, of whom 118 (23%) died during hospitalization. Fifteen variables from common laboratory tests were selected to develop the PHM-CPA model. The PHM-CPA model achieved an AUROC of 0.816 (95% CI, 0.763-0.861) in the internal validation cohort and 0.787 (95% CI, 0.745-0.830) in the external validation cohort. The PHM-CPA model consistently outperformed the LR model and 25 previously reported models.

We developed and validated the PHM-CPA model, comprising readily available clinical variables, which demonstrated superior performance and calibration in predicting in-hospital mortality for cirrhotic patients with AKI.

Acute kidney injury (AKI) is a frequent complication of chronic liver disease (CLD) contributing to high morbidity and mortality worldwide. While liver transplantation (LT) has shown favorable outcomes, early identification and management of AKI is imperative for survival. This review aims to highlight the epidemiology, pathophysiology, management, and prognosis of AKI in CLD.

An extensive literature search was performed using PubMed, Medline, and Google Scholar to identify literature related to epidemiology, burden, clinical presentations, prognosis, and management of AKI in CLD.

The identified studies highlighted a wide range of prevalence of AKI in hospitalized patients with CLD. The etiology and pathophysiology are multifactorial and include prerenal AKI, acute tubular injury, sepsis, gastrointestinal bleeding, bacterial translocation from the gut, and hepatorenal syndrome (HRS). AKI is associated with a higher risk of morbidity and mortality and progression to chronic kidney disease following LT. Management of AKI in CLD varies based on the underlying etiology. While vasoconstrictors like terlipressin have shown great potential in the treatment of HRS-AKI and is widely used in Europe and United States, LT remains the definitive therapy of choice. In most cases, kidney replacement therapy serves as a bridge to liver transplant.

AKI is a serious complication of CLD and early identification is essential. Diagnosis and management, particularly HRS is challenging and requires a high index of suspicion. More research is required to identify novel therapies to improve outcomes of AKI in patients with CLD.

Chronic kidney disease (CKD) frequency is increasing in patients with cirrhosis and these individuals often experience acute kidney injury (AKI). Direct comparisons of outcomes between AKI-only versus AKI on CKD (AoCKD) among patients with cirrhosis are not well described.

A total of 2057 patients with cirrhosis and AKI across 11 hospital networks from the HRS-HARMONY consortium were analyzed (70% AKI-only and 30% AoCKD). The primary outcome was unadjusted and adjusted 90-day mortality, with transplant as a competing risk, using Fine and Gray analysis.

Compared with patients with AKI-only, patients with AoCKD had higher median admission creatinine (2.25 [interquartile range, 1.7-3.2] vs 1.83 [1.38-2.58] mg/dL) and peak creatinine (2.79 [2.12-4] vs 2.42 [1.85-3.50] mg/dL) but better liver function parameters (total bilirubin 1.5 [interquartile range, 0.7-3.1] vs 3.4 [1.5-9.3] mg/dL; and international normalized ratio 1.4 [interquartile range, 1.2-1.8] vs 1.7 [1.39-2.2]; P < .001 for all). Patients with AoCKD were more likely to have metabolic dysfunction associated steatotic liver disease cirrhosis (31% vs 17%) and less likely to have alcohol-associated liver disease (26% vs 45%; P < .001 for both). Patients with AKI-only had higher unadjusted mortality (39% vs 30%), rate of intensive care unit admission (52% vs 35%; P < .001 for both), and use of renal-replacement therapy (20% vs 15%; P = .005). After adjusting for age, race, sex, transplant listing status, and Model for End-Stage Liver Disease-Sodium score, AoCKD was associated with a lower 90-day mortality compared with AKI-only (subhazard ratio, 0.72; 95% confidence interval, 0.61-0.87).

In hospitalized patients with AKI and cirrhosis, AoCKD was associated with lower 90-day mortality compared with AKI-only. This may be caused by the impact of worse liver function parameters in the AKI-only group on short-term outcomes. Further study of the complicated interplay between acute and chronic kidney disease in cirrhosis is needed.

In various disease contexts, magnesium abnormalities are associated with acute kidney injury (AKI) incidence. However, this association remains unclear and has not been systematically investigated in patients with cirrhosis. Hence, we aimed to elucidate the association between admission serum magnesium levels and AKI incidence in intensive care unit (ICU)-admitted cirrhotic patients.

A retrospective cohort study was conducted using MIMIC-IV2.2 data, focusing on critically ill patients with cirrhosis. We employed univariable and multivariable logistic regression and restricted cubic spline analyses to robustly address our research objectives. To further substantiate the findings, subgroup and sensitivity analyses were also conducted.

Among the 3,228 enrolled ICU-admitted cirrhotic patients, 34.4% were female, and the overall AKI incidence was 68.6% (2,213/3,228). Multivariable logistic regression analysis revealed an independent relationship between elevated serum magnesium levels and increased AKI risk (OR = 1.55 [95% CI = 1.15-2.09], p = 0.004). Compared with individuals with serum magnesium levels < 1.6 mg/dL, individuals with serum magnesium levels in Q2 (1.6-2.6 mg/dL) and Q3 (≥2.6 mg/dL) had adjusted ORs for AKI of 1.89 (95% CI = 1.34-2.65, p < 0.001) and 2.19 (95% CI = 1.27-3.75, p = 0.005), respectively. The restricted cubic spline analysis revealed that AKI risk increased linearly with increasing serum magnesium levels. Subgroup analysis revealed that the association between serum magnesium levels and AKI incidence was remarkably stable in subgroup analysis (all Pinteraction >0.05).

High serum magnesium concentrations were significantly associated with an increased AKI risk in ICU-admitted patients with cirrhosis. Further randomized trials are needed to confirm this association.

Acute kidney injury (AKI) is one of the most common complications for critically ill patients with cirrhosis, but it has remained unclear whether urine output fluctuations are associated with the risk of AKI in such patients. Thus, we explored the influence of 24-h urine-output trajectory on AKI in patients with cirrhosis through latent category trajectory modeling.

This retrospective cohort study examined patients with cirrhosis using the MIMIC-IV database. Changes in the trajectories of urine output within 24 h after admission to the intensive care unit (ICU) were categorized using latent category trajectory modeling. The outcome examined was the occurrence of AKI during ICU hospitalization. The risk of AKI in patients with different trajectory classes was explored using the cumulative incidence function (CIF) and the Fine-Gray model with the sub-distribution hazard ratio (SHR) and the 95% confidence interval (CI) as size effects.

The study included 3,562 critically ill patients with cirrhosis, of which 2,467 (69.26%) developed AKI during ICU hospitalization. The 24-h urine-output trajectories were split into five classes (Classes 1-5). The CIF curves demonstrated that patients with continuously low urine output (Class 2), a rapid decline in urine output after initially high levels (Class 3), and urine output that decreased slowly and then stabilized at a lower level (Class 4) were at higher risk for AKI than those with consistently moderate urine output (Class 1). After fully adjusting for various confounders, Classes 2, 3, and 4 were associated with a higher risk of AKI compared with Class 1, and the respective SHRs (95% CIs) were 2.56 (1.87-3.51), 1.86 (1.34-2.59), and 1.83 1.29-2.59).

The 24-h urine-output trajectory is significantly associated with the risk of AKI in critically ill patients with cirrhosis. More attention should be paid to the dynamic nature of urine-output changes over time, which may help guide early intervention and improve patients' prognoses.

Acute-on-chronic liver failure (ACLF) is a syndrome characterized by the acute decompensation of chronic liver disease, resulting in organ failure and high short-term mortality. The progression of ACLF is dynamic and reversible in a considerable proportion of patients during hospitalization. Early detection and accurate assessment of ACLF are essential; however, ideal methods for this purpose are still lacking. Therefore, this study aimed to develop a new score for predicting the onset of ACLF in patients with various chronic liver diseases.A total of 6,188 patients with various chronic liver diseases were included in the study. Clinical and laboratory data were collected, and the occurrence of ACLF within 28 days was recorded. The Lasso-Cox regression method was employed to develop prediction models for the onset of ACLF at 7, 14, and 28 days. Among 5,221 patients without ACLF, 477 progressed to ACLF within 28 days. Seven predictors were identified as significantly associated with the occurrence of ACLF at 7, 14, and 28 days. A new scoring system was developed as follows: [NEUT ≥ 7, 109/L; 1 or 0] × 0.49 + [PLT < 100, 109/L; 1 or 0] × 0.44 + [TBIL ≥ 35, µmol/L; 1 or 0] × 0.05 + [HDL-C < 0.5, mmol/L; 1 or 0] × 1.04 - Ln[Hb, g/L] × 0.89 + [BUN > 7, mmol/L; 1 or 0] × 0.51 + Ln[INR] × 0.87 + 3.40. This new score demonstrated superior discrimination, with the C-indexes of 0.958, 0.944, and 0.938 at 7, 14, and 28 days, respectively, outperforming those of four other scores (CLIF-C-ACLF-Ds, MELD, MELD-Na, and CLIF-C-ADs score; all P < 0.001). Additionally, the new score improved in predictive accuracy, time-dependent receiver operating characteristics, probability density function evaluations, and calibration curves, making it highly predictive for the onset of ACLF at all time points. The optimal cut-off value of 9.6 effectively distinguished between high- and low-risk patients for ACLF onset. These findings were further validated in a separate cohort of patients. A new progressive score, based on seven predictors, has been developed to accurately forecast the occurrence of ACLF within 7, 14, and 28 days in patients with various chronic liver diseases. This tool may be utilized to identify high-risk patients, tailor follow-up management, and guide the escalation of care, prognostication, and transplant evaluation.

Acute kidney injury (AKI) frequently complicates the course of hospitalized patients with cirrhosis and negatively affects their prognosis. How AKI response influences the timing of liver transplantation (LT) remains unclear. We sought to assess the impact of AKI response to treatment on survival and LT rates in patients with cirrhosis awaiting LT. This was a retrospective multicenter study of cirrhosis patients waitlisted for LT and hospitalized with AKI in 2019. The exposure was AKI response versus no response during hospitalization. Outcomes were 90-day overall and transplant-free survival, and rates of LT with time to transplant. We adjusted for age, sex, race, cirrhosis etiology, site, and Model for End-Stage Liver Disease-Sodium (MELD-Na) score. Among the 317 patients in this study, 170 had an AKI response (53.6%), and 147 had no response (46.4%). Compared to nonresponders, responders had better 90-day overall survival (89.4% vs. 76.2%, adjusted subhazard ratio for mortality 0.34, p =0.001), and transplant-free survival (63.5% vs. 25.2%, aHR for probability of death or transplant 0.35, p <0.001). The LT rate was lower in responders (45.9% vs. 61.2%, adjusted subhazard ratio 0.55, p =0.005); 79% of transplants in responders occurred after discharge, at a median of 103 days, while 62% of transplants in nonresponders occurred during hospitalization, with the remainder occurring postdischarge at a median of 58 days. In patients with cirrhosis waitlisted for LT who are hospitalized with AKI, AKI response to therapy is associated with improved 90-day survival, despite a reduced LT rate and longer time to LT.

Background: Acute kidney injury (AKI) is one of the common complications of liver cirrhosis. It occurs in nearly 20% of patients with cirrhosis who are hospitalized. Prior literature demonstrated that the AKI occurrence in patients with cirrhosis is independently associated with higher mortality. However, there are data assessing predictors and outcomes of AKI resolution in hospitalized patients with cirrhosis. Therefore, the aim of the current study was to identify clinical predictors of AKI resolution among inpatients with cirrhosis that are easily obtained and to evaluate the clinical outcomes of those patients. Methods: The current study is a retrospective cohort of patients with cirrhosis who were hospitalized and had AKI between 2012 and 2020 at a tertiary referral center. Patients included in this study were identified using the International Classification of Diseases 9 codes and then they were manually verified by two independent chart reviewers. AKI was classified according to the AKI Network (AKIN) serum creatinine (Cr) criteria, with AKIN resolution defined as AKIN stage 1 or lower at the time of discharge, while unresolved AKIN was defined as AKIN stage 2 or 3 at the time of discharge. For univariate analysis, Fisher's exact and the two-sample T-test were utilized. For multivariable analysis, stepwise logistic regression was performed to evaluate variables associated with AKIN resolution. Survival curves were estimated and compared using the Kaplan-Meier method and Log-Rank Test. A p-value cutoff of 0.05 was used for statistical significance. Results: Between 2012 and 2020, there were 140 patients who were included (59% males). The majority of patients had viral hepatitis (54%) as the cirrhosis etiology with 80% of them having hepatitis C virus. Most patients had fluid-responsive AKI (49%), and stage 1 AKIN (69%). In terms of outcomes, the majority of patients (117 patients; 84%) had AKIN resolution at the time of discharge. In the multivariable analysis, after adjusting for clinical meaningful variables, our study shows that higher albumin value at the time of admission (adjusted Odds Ratio "aOR" = 3.28; p = 0.01) and non-metabolic dysfunction-associated steatotic liver disease (non-MASLD) cirrhosis (aOR = 9.43; p < 0.01) were variables associated with higher odds of AKIN resolution at the time of discharge. Conversely, we show that a higher Cr value at the time of admission was associated with lower odds of AKIN resolution at the time of discharge (aOR = 0.31; p < 0.01). When evaluating mortality, patients with unresolved AKIN at the time of discharge had higher rates of in-hospital mortality (p < 0.01) compared to those with resolved AKIN. Survival curve analyses using the Kaplan-Meier method indicated that patients with resolved AKIN experienced higher 90-day survival rates (p < 0.01). Additionally, those with resolved AKIN demonstrated greater transplant-free survival compared to patients with unresolved AKIN at both the 1-year (p = 0.04) and 3-year (p < 0.01) follow-ups. Conclusions: When evaluating clinical predictors of AKIN resolution in admitted patients with cirrhosis, our study showed that a higher admission albumin value and non-MASLD etiology of cirrhosis were associated with higher odds of AKIN resolution at the time of discharge. Conversely, a higher admission Cr value was associated with lower odds of AKIN resolution at the time of discharge. We also demonstrate that AKIN resolution during index admission was associated with improved short- and long-term transplant-free survival (up to 3 years). Our findings warrant external validation in larger cohorts to further evaluate the impact of inpatient AKI resolution on cirrhosis outcomes. Our findings can help clinicians predict AKIN outcomes and encourage more aggressive management of AKI, especially in high-risk patients, which can improve mortality.

Kidney injury is a significant complication in end-stage liver disease (ESLD), leading to increased morbidity and mortality. While liver transplant alone (LTA) can promote kidney recovery (KR), non-recovery associates with adverse outcomes, but the underlying pathophysiology is still unclear. We studied 10 LTA recipients with or without kidney failure (KF) and measured serum levels of OPN and TIMP-1 (previously identified predictors of KR), 92 proinflammatory proteins (Olink), and urinary cell populations. Our findings revealed elevated OPN and TIMP-1 levels in KF patients, strongly correlated with tubular epithelial cells in urine. Proteomic analysis showed distinct profiles in KF, non-KF, and healthy donors, indicating an ongoing proinflammatory signature in KF. Cytokines correlated with OPN and TIMP-1 levels. We propose that high pre-LTA OPN and TIMP-1 levels are crucial for tubular regeneration and normalize with kidney recovery. Insufficient pre-LTA OPN levels may lead to persistent kidney failure. Our present data also newly indicate that kidney failure post-LTA is an active condition, in which tubular cells are persistently shed in the urine. The strict association between systemic inflammation and tubular cell loss suggests a pathogenic link that could offer therapeutic opportunities to promote kidney recovery.

Data to guide dialysis decision-making for transplant-ineligible patients with cirrhosis are lacking.

We aimed to describe the processes, predictors, and outcomes of renal replacement therapy (RRT) initiation for transplant-ineligible patients with cirrhosis at a single liver transplantation center.

We conducted a mixed-methods study of a retrospective cohort of 372 transplant-ineligible inpatients with cirrhosis with acute kidney injury (AKI) due to hepatorenal syndrome (HRS-AKI) or acute tubular necrosis (ATN) between 2008 and 2015. We performed survival analyses to evaluate 6-month survival and renal recovery and examined end-of-life care outcomes. We used a consensus-driven medical record review to characterize processes leading to RRT initiation.

We identified 266 (71.5%) patients who received RRT and 106 (28.5%) who did not receive RRT (non-RRT). Median survival was 12.5 days (RRT) vs. 2.0 days (non-RRT) (HR 0.36, 95%CI 0.28-0.46); 6-month survival was 15% (RRT) vs. 0% (non-RRT). RRT patients were more likely to die in the intensive care unit (88% vs. 32%, p < 0.001). HRS-AKI patients were more likely to be RRT dependent at 6 months than ATN patients (86% vs. 27%, p = 0.007). The most common reasons for RRT initiation were unclear etiology of AKI on presentation (32%) and belief of likely reversibility of ATN (82%).

Most transplant-ineligible patients who were initiated on RRT experienced very short-term mortality and received intensive end-of-life care. However, approximately 1 in 6 were alive at 6 months. Our findings underscore the critical need for structured clinical processes to support high-quality serious illness communication and RRT decision-making for this population.

Acute kidney injury (AKI) manifests as a clinical syndrome characterised by the rapid accumulation of metabolic wastes, such as blood creatinine and urea nitrogen, leading to a sudden decline in renal function. Currently, there is a lack of specific therapeutic drugs for AKI. Previously, we identified gastrin-releasing peptide receptor (GRPR) as a pathogenic factor in AKI. In this study, we investigated the therapeutic potential of a novel Chinese medicine monomer, aurantiamide (AA), which exhibits structural similarities to our previously reported GRPR antagonist, RH-1402. We compared the therapeutic efficacy of AA with RH-1402 both in vitro and in vivo using various AKI models. Our results demonstrated that, in vitro, AA attenuated injury, necroptosis, and inflammatory responses in human renal tubular epithelial cells subjected to repeated hypoxia/reoxygenation and lipopolysaccharide stimulation. In vivo, AA ameliorated renal tubular injury and inflammation in mouse models of ischemia/reperfusion and cecum ligation puncture-induced AKI, surpassing the efficacy of RH-1402. Furthermore, molecular docking and cellular thermal shift assay confirmed GRPR as a direct target of AA, which was further validated in primary cells. Notably, in GRPR-silenced HK-2 cells and GRPR systemic knockout mice, AA failed to mitigate renal inflammation and injury, underscoring the importance of GRPR in AA's mechanism of action. In conclusion, our study has demonstrated that AA serve as a novel antagonist of GRPR and a promising clinical candidate for AKI treatment.

The development of acute kidney injury (AKI) in the setting of alcohol-associated hepatitis (AH) portends a poor prognosis. Whether the presence of AH itself drives worse outcomes in patients with cirrhosis and AKI is unknown.

Retrospective cohort study of 11 hospital networks of consecutive adult patients admitted in 2019 with cirrhosis and AKI. AKI phenotypes, clinical course, and outcomes were compared between AH and non-AH groups.

A total of 2062 patients were included, of which 303 (15%) had AH, as defined by National Institute on Alcohol Abuse and Alcoholism (NIAAA) criteria. Patients with AH, compared to those without, were younger and had higher Model for End-stage Liver Disease-Sodium (MELD-Na) scores on admission. AKI phenotypes significantly differed between groups (p < 0.001) with acute tubular necrosis occurring more frequently in patients with AH. Patients with AH reached more severe peak AKI stage, required more renal replacement therapy, and had higher 90-day cumulative incidence of death (45% [95% CI: 39%-51%] vs. 38% [95% CI: 35%-40%], p = 0.026). Using no AH as reference, the unadjusted sHR for 90-day mortality was higher for AH (sHR: 1.24 [95% CI: 1.03-1.50], p = 0.024), but was not significant when adjusting for MELD-Na, age and sex. However, in patients with hepatorenal syndrome, AH was an independent predictor of 90-day mortality (sHR: 1.82 [95% CI: 1.16-2.86], p = 0.009).

Hospitalised patients with cirrhosis and AKI presenting with AH had higher 90-day mortality than those without AH, but this may have been driven by higher MELD-Na rather than AH itself. However, in patients with hepatorenal syndrome, AH was an independent predictor of mortality.

Acute kidney injury (AKI) occurs frequently in patients with end-stage liver disease and cirrhosis and is associated with increased short-term mortality. This study aims to study the prevalence and risk factors associated with AKI development and mortality in cirrhosis of liver patients.

In the current prospective study, hospitalized patients with liver cirrhosis from October 2021 to March 2023 were recruited. Demographic, clinical, and laboratory data were collected, which included, the etiology of cirrhosis, comorbidities, severity of liver disease, and relevant biochemical parameters. The patient was followed up for 90 days to record the clinical outcome. The statistical software SPSS was utilized to conduct the analysis.

Of 364 liver cirrhosis patients, 25.2% (n, 92) had AKI and belonged to an average age of 51.54 ± 11.82 years. The majority of individuals in the study were males (90.4%), and alcohol (63.4%) was the most common etiology of liver cirrhosis. The present study showed that higher level of direct bilirubin (p = 0.011) and MELD score (p = 0.0001) were identified as significant risk factors for AKI development in patients with liver cirrhosis. Regarding mortality, the significant risk factors were the presence of AKI (p = 0.045) and MELD score (p = 0.025). Among AKI patients, 90-day mortality rates were higher in patients with acute tubular necrosis (p value = 0.010) and stage 3 AKI (p value = 0.001).

AKI is common in cirrhosis of liver patients. Elevated levels of direct bilirubin and MELD score emerged as significant factors associated with AKI development. Furthermore, AKI and MELD scores were identified as independent risk factors for mortality at both 30 and 90 days. Survival rates were influenced by both the type and stage of AKI; AKI stage 3 and ATN patients had significantly higher mortality rate. Early AKI detection and management are crucial for reducing mortality risk in liver cirrhosis patients.

Acute kidney injury (AKI) is a common complication among patients with decompensated cirrhosis and its development is associated with worse prognosis in terms of survival. Patients with decompensated cirrhosis may develop a unique type of AKI, known as hepatorenal syndrome (HRS-AKI), characterized by marked impairment of kidney function due to haemodynamic changes that occur in late stages of liver cirrhosis. Besides, patients with cirrhosis also may develop chronic alterations of kidney function (chronic kidney disease, CKD), the incidence of which is increasing markedly and may be associated with clinical complications. The aim of this review is to provide the reader with an update of the most relevant aspects of alterations of kidney function in patients with cirrhossi that may be useful for theri clinical practice.

Patients with cirrhosis are susceptible to development of acute kidney injury (AKI), which leads to poor outcome. We conducted a study to evaluate the spectrum of AKI in patients with cirrhosis.

This study was conducted in consecutive cirrhotic patients with AKI admitted in a tertiary care center of India from April 2020 to December 2022. Details including history, examination findings, and results of laboratory investigations were recorded.

A total of 243 patients were enrolled in this study. The majority (91.3%) of the patients were males. The most common etiology of cirrhosis was alcohol in 58.4% (n = 142) followed by hepatitis B in 10.3% (n = 25) of patients. Pre-renal form of AKI was present in 54.4% (n = 132) of patients and hepatorenal syndrome (HRS) in 21.8% (n = 53) of patients. IgA nephropathy was the commonest (n = 6) glomerular pathology in nonresponders with intrinsic renal disease. Majority of the patients belonged to stage II (46.9%) and stage I AKI (37%), while only 16.1% had stage III AKI. Various stages of AKI showed a significant correlation (P < 0.05) with Child-Turcotte-Pugh (CTP) score and Model for End-stage Liver Disease (MELD)-Na score. The overall in-hospital mortality rate was found to be 18.5% (n = 45).

Renal dysfunction is a frequent complication among cirrhotic patients. Pre-renal factors were the most common cause of AKI in cirrhotics. Stages of AKI showed significant correlation with liver prognostic scores. Renal biopsy should be considered in patients not responding to treatment, to guide further management.

The hemodynamic alterations seen in liver cirrhosis lead to renal vasoconstriction, ultimately causing acute kidney injury (AKI). The renal resistive index (RRI) is the most common Doppler ultrasound variable for measuring intrarenal vascular resistance.

To evaluate the association of the RRI with AKI in patients with liver cirrhosis and to identify risk factors for high RRI.

This was a prospective observational study, where RRI was measured using Doppler ultrasound in 200 consecutive hospitalized patients with cirrhosis. The association of RRI with AKI was studied. The receiver operating characteristic (ROC) curve analysis was utilized to determine discriminatory cut-offs of RRI for various AKI phenotypes. Multivariate analysis was conducted to determine the predictors of high RRI.

The mean patient age was 49.08 ± 11.68 years, with the majority (79.5%) being male; the predominant etiology of cirrhosis was alcohol (39%). The mean RRI for the study cohort was 0.68 ± 0.09, showing a progressive increase with higher Child-Pugh class of cirrhosis. Overall, AKI was present in 129 (64.5%) patients. The mean RRI was significantly higher in patients with AKI compared to those without it (0.72 ± 0.06 vs 0.60 ± 0.08; P < 0.001). A total of 82 patients (41%) had hepatorenal syndrome (HRS)-AKI, 29 (22.4%) had prerenal AKI (PRA), and 18 (13.9%) had acute tubular necrosis (ATN)-AKI. The mean RRI was significantly higher in the ATN-AKI (0.80 ± 0.02) and HRS-AKI (0.73 ± 0.03) groups than in the PRA (0.63 ± 0.07) and non-AKI (0.60 ± 0.07) groups. RRI demonstrated excellent discriminatory ability in distinguishing ATN-AKI from non-ATN-AKI (area under ROC curve: 93.9%). AKI emerged as an independent predictor of high RRI (adjusted odds ratio [OR]: 11.52), and high RRI independently predicted mortality among AKI patients (adjusted OR: 3.18).

In cirrhosis patients, RRI exhibited a significant association with AKI, effectively differentiated between AKI phenotypes, and predicted AKI mortality.

Hepatitis C virus (HCV) can cause a range of kidney diseases. HCV is the primary cause of mixed cryoglobulinaemia, which leads to cryoglobulinaemic vasculitis and cryoglobulinaemic glomerulonephritis (GN). Patients with acute cryoglobulinaemic vasculitis often exhibit acute kidney disease due to HCV infection, which typically progresses to acute kidney injury (AKI). HCV also increases the risk of chronic kidney disease (CKD) and the likelihood of developing end-stage renal disease (ESRD). Currently, direct-acting antiviral agents (DAAs) can be used to treat kidney disease at different stages. This review focuses on key findings regarding HCV and kidney disease, discusses the impact of DAAs, and highlights the need for further research and treatment.

This article delves into the intricate challenges of acute kidney injury (AKI) in cirrhosis, a condition fraught with high morbidity and mortality. The complexities arise from distinguishing between various causes of AKI, particularly hemodynamic AKI, in cirrhotic patients, who experience hemodynamic changes due to portal hypertension. The term "hepatocardiorenal syndrome" is introduced to encapsulate the intricate interplay among the liver, heart, and kidneys. The narrative emphasizes the often-overlooked aspect of cardiac function in AKI assessments in cirrhosis, unveiling the prevalence of cirrhotic cardiomyopathy marked by impaired diastolic function. The conventional empiric approach involving volume expansion and vasopressors for hepatorenal syndrome is critically analyzed, highlighting potential risks and variable patient responses. We advocate for a nuanced algorithm for AKI evaluation in cirrhosis, prominently featuring point-of-care ultrasonography (POCUS). POCUS applications encompass assessing fluid tolerance, detecting venous congestion, and evaluating cardiac function.

Acute-on-chronic liver failure (ACLF) is a severe clinical entity associated with elevated short-term mortality. We aimed to characterize patients with decompensated cirrhosis according to presence of ACLF, their association with active alcohol intake, and long-term survival in Latin America.

Retrospective cohort study of decompensated cirrhotic in three Chilean university centers (2017-2019). ACLF was diagnosed according EASL-CLIF criteria. We assessed survival using competing-risk and time-to-event analyses. We evaluated the time to death using accelerated failure time (AFT) models.

We included 320 patients, median age of 65.3±11.7 years old, and 48.4% were women. 92 (28.7%) patients met ACLF criteria (ACLF-1: 29.3%, ACLF-2: 27.1%, and ACLF-3: 43.4%). The most common precipitants were infections (39.1%), and the leading organ failure was kidney (59.8%). Active alcohol consumption was frequent (27.7%), even in patients with a prior diagnosis of non-alcoholic fatty liver disease (NAFLD) (16.2%). Ninety-two (28.7%) patients had ACLF (ACLF-1: 8.4%, ACLF-2: 7.8%, and ACLF-3: 12.5%). ACLF patients had a higher MELD-Na score at admission (27 [22-31] versus 16 [12-21], p<0.0001), a higher frequency of alcohol-associated liver disease (36.7% versus 24.9%, p=0.039), and a more frequent active alcohol intake (37.2% versus 23.8%, p=0.019). In a multivariate model, ACLF was associated with higher mortality (subdistribution hazard ratio 1.735, 95%CI: 1.153-2.609; p<0.008). In the AFT models, the presence of ACLF during hospitalization correlated with a shorter time to death: ACLF-1 shortens the time to death by 4.7 times (time ratio [TR] 0.214, 95%CI: 0.075-0.615; p<0.004), ACLF-2 by 4.4 times (TR 0.224, 95%CI: 0.070-0.713; p<0.011), and ACLF-3 by 37 times (TR 0.027, 95%CI: 0.006-0.129; p<0.001).

Patients with decompensated cirrhosis and ACLF exhibited a high frequency ofactive alcohol consumption. Patients with ACLF showed higher mortality and shorter time todeath than those without ACLF.

Kidney dysfunction is challenging in liver transplant candidates to determine whether it is reversible or not. This review focuses on the pertinent data on how to best approach liver transplant candidates with kidney dysfunction in the current era after implementing the simultaneous liver kidney (SLK) allocation policy and safety net.

The implementation of the SLK policy inverted the steady rise in SLK transplants and improved the utilization of high-quality kidneys. Access to kidney transplantation following liver transplant alone (LTA) increased with favorable outcomes. Estimating GFR in liver transplant candidates remains challenging, and innovative methods are needed. SLK provided superior patient and graft survival compared to LTA only for patients with advanced CKD and dialysis at least 3 months. SLK can provide immunological protection against kidney rejection in highly sensitized candidates. Post-SLK transplant care is complex, with an increased risk of complications and hospitalization.

The SLK policy improved kidney access and utilization. Transplant centers are encouraged, under the safety net, to reserve SLK for liver transplant candidates with advanced CKD or dialysis at least 3 months while allowing lower thresholds for highly sensitized patients. Herein, we propose a practical approach to liver transplant candidates with kidney dysfunction.

Acute kidney injury (AKI) in patients with cirrhosis is a diagnostic challenge due to multiple and sometimes overlapping possible etiologies. Many times, diagnosis cannot be made based on case history, physical examination or laboratory data, especially when the nephrologist is faced with AKI with a hemodynamic basis, such as hepatorenal syndrome. In addition, the guidelines still include generalized recommendations regarding withdrawal of diuretics and plasma volume expansion with albumin for 48 h, which may be ineffective and counterproductive and may have iatrogenic effects, such as fluid overload and acute cardiogenic pulmonary edema. For this reason, the use of new tools, such as hemodynamic point-of-care ultrasound (PoCUS), allows us to phenotype volume status more accurately and ultimately guide medical treatment in a noninvasive, rapid and individualized manner.

Hepatorenal syndrome (HRS) is a form of kidney dysfunction that characteristically occurs in liver cirrhosis. It is characterized by a marked impairment of kidney function in response to circulatory and hemodynamic alterations that occur in advanced stages of liver cirrhosis, aggravated by systemic inflammation and bacterial translocation. The classical definitions of the types of HRS have been recently revisited and 2 forms of HRS have been redefined: the acute form, referred to as acute kidney injury (HRS-AKI), and the chronic form, referred to as chronic kidney disease. HRS-AKI is one of the most severe forms of AKI in patients with cirrhosis and it consists of an abrupt impairment of kidney function, frequently triggered by an infection, appearing in the setting of advanced decompensated cirrhosis. Differential diagnosis with other causes of AKI is crucial because HRS-AKI requires a specific treatment. Differential diagnosis with AKI-acute tubular necrosis may be challenging and kidney biomarkers may be useful in this setting. Treatment of HRS-AKI is based on the administration of vasoconstrictor drugs in combination with volume expansion with albumin. Prognosis of HRS-AKI is poor, and the ideal definitive treatment consists of liver transplantation or simultaneous liver-kidney transplantation. HRS-AKI has a big impact on patients' quality of life. Management of HRS-AKI remains challenging in specific situations such as alcohol-associated hepatitis or metabolic-associated steatotic liver disease cirrhosis. Developing preventive measures for HRS-AKI, improving its early identification, discovering new biomarkers for differential diagnosis, and improving the response to therapy are some of the unmet needs in the field of HRS-AKI.

Hepatorenal syndrome (HRS) is a feared complication in patients with advanced cirrhosis and is associated with significant morbidity and mortality. While recognized as a distinct physiologic condition for well over one hundred years, a lack of objective diagnostic tests has made the diagnosis one of exclusion. Since 1979, multiple sets of diagnostic criteria have been proposed. Though varying in detail, the principal intent of these criteria is to identify patients with severe, functional acute kidney injury that is unresponsive to volume resuscitation and exclude those with structural injury. However, accurate differential diagnosis remains challenging. Recently, multiple urinary biomarkers of kidney injury, including neutrophil gelatinase-associated lipocalin, have been studied as a means of objectively phenotyping etiologies of acute kidney injury in patients with cirrhosis. Along with markers reflecting tubular functional integrity, including the fractional excretion of sodium, injury markers will likely be incorporated into future diagnostic criteria. Making an accurate diagnosis is critical, as therapeutic options exist for HRS but must be given in a timely manner and only to those patients likely to benefit. Terlipressin, an analog of vasopressin, is the first line of therapy for HRS in much of the world and has recently been approved for use in the United States. Significant questions remain regarding the optimal dosing strategy, metrics for titration, and the potential role of point-of-care ultrasound to help guide concurrent albumin administration.

The concept of structural kidney damage and renal dysfunction as a result of jaundice attracted attention in the medical community in the early and mid-20th century. The postulated doctrine of the time was that the excretion of elevated concentrations of bile results in bile-stained casts occupying collecting and distal convoluted tubules, degeneration of tubular epithelium, and decreased renal function. Compared to the hepatorenal syndrome, the poster child of hepatology and nephrology collaboration, the notion of structural kidney damage and renal dysfunction as a result of cholemia lost its traction and has almost disappeared from modern textbooks. Today, cholemic nephropathy is experiencing a renaissance, with multiple case reports and case series of jaundiced patients with kidney dysfunction and evidence of bile acid casts upon histologic examination. Published cases include acute hepatitis, chronic liver injury, cirrhosis, and obstructive etiologies. Diagnosis of cholemic nephropathy is based on histological examination, typically showing intraluminal bile casts predominantly located in the distal tubules. In common bile duct-ligated mice, the histomorphological and functional alterations of cholemic nephropathy mimic those seen in humans. Some argue against the concept of cholemic nephropathy and postulate that bile casts are a secondary phenomenon. What we need are carefully designed trials to establish diagnostic criteria and subsequently translate this knowledge into evidence-based therapies.

Hepatorenal syndrome (HRS) is a rare and highly morbid form of kidney injury unique to patients with decompensated cirrhosis. HRS is a physiologic consequence of portal hypertension, leading to a functional kidney injury that can be reversed by restoring effective circulating volume and renal perfusion. While liver transplantation is the only definitive "cure" for HRS, medical management with vasoconstrictors and i.v. albumin is a cornerstone of supportive care. Terlipressin, a V1a receptor agonist that acts on the splanchnic circulation, has been used for many years outside the United States for the treatment of HRS. However, its recent Food and Drug Administration approval has generated new interest in this population, as a new base of prescribers now work to incorporate the drug into clinical practice. In this article, we review HRS pathophysiology and diagnostic criteria, the clinical use of terlipressin and alternative therapies, and identify areas of future research in the space of HRS and kidney injury in cirrhosis.

Acute kidney injury (AKI) increases mortality in cirrhosis. Early identification of the cause of AKI helps in planning appropriate management. We aimed to find whether neutrophil gelatinase-associated lipocalin (NGAL) can be used to differentiate between different types of AKI in cirrhosis and predict short-term outcomes in patients with decompensated cirrhosis and AKI.

This was a time-bound study in which consecutive hospitalized patients with cirrhosis and AKI were prospectively recruited and managed as per standard care. Acute on chronic liver failure (ACLF) was diagnosed as per the EASL-CLIF Acute-on-Chronic Liver Failure in Cirrhosis (CANONIC) criteria. Urine NGAL was measured by enzyme-linked immunosorbent assay (ELISA) by Epitope Diagnostics Inc. kit (San Diego, USA.) in all patients on admission, and patients were followed up until hospital discharge or death.

A total of 110 consecutive patients (median [range] age: 44 [28-81] years;87.3%were male; ACLF: 71.8%; acute decompensation 28.2%; Model for end-stage liver disease (MELD) 27 [13-46]; Child-Turcotte-Pugh (CTP) 11 [7-15]) with cirrhosis and AKI were recruited. Alcohol was the most common etiology of cirrhosis(64.5%)). Pre-renal azotemia (PRA) was the most common cause of AKI (n = 56). Urine NGAL was significantly elevated in acute tubular necrosis (ATN) (1747 [6-6141] ng/ml than in hepatorenal syndrome (HRS) (379 [33.5-2320] ng/ml; P < 0.0001) and PRA (167 ng/ml [3.34-660]; P < 0.0001). Sixty-four percent patients with ATN, 27.6% patients with HRS, and none with PRA required dialysis. A total of 79.31% patients with HRS and 76% with ATN died. Urine NGAL was significantly higher in patients who required hemodialysis than in those who did not (1733 [243-6141] ng/ml vs 235 [3.34-2320] ng/ml; P < 0.0001). Both urine NGAL (n = 110) and plasma NGAL (n = 90) were significantly higher in patients who died (urine NGAL: -475 [6-6141] ng/ml vs 247 [3.34-2320] ng/ml; P = 0.002;plasma NGAL-950 [94-4859] ng/ml vs 608 [18-3300)]g/ml; P < 0.001). On multivariate analysis, urine NGAL and INR could predict mortality.

NGAL can differentiate between different types of AKI in cirrhosis and predict the need for hemodialysis and mortality in decompensated cirrhosis with AKI.

Acute kidney injury (AKI) significantly contributes to the mortality and morbidity rates among pediatric liver transplant (LT) recipients.

Our study aimed to assess the potential factors contributing to AKI in pediatric LT patients and to analyze the impact of AKI on postoperative mortality and hospitalization duration.

About 235 pediatric LT patients under the age of 18 between the years 2015 and 2021 were evaluated retrospectively. The relationship between preoperative and intraoperative variables of the patients and AKI developed when the early postoperatıve period was assessed.

A correlation was found between the patients' preoperative age, albumin levels, and AKI. AKI was found to be associated with the duration of surgery and intraoperative blood transfusion.

Our findings revealed that the severity of AKI in pediatric LT patients is linked to extended surgical durations and increased blood transfusions resulting from hemodynamically compromised blood loss. Furthermore, independent risk factors for AKI were identified as prolonged warm ischemia and the overall duration of the operation.

Demiroz D, Colak YZ, Ozdes OO, Ucar M, Ali Erdogan M, Toprak HI, et al. Incidence and Risk Factors of Acute Kidney İnjury in Pediatric Liver Transplant Patients: A Retrospective Study. Indian J Crit Care Med 2024;28(1):75-79.

Hepatorenal syndrome (HRS) is a disorder associated with cirrhosis and renal impairment, with portal hypertension as its major underlying cause. Moreover, HRS is the third most common cause of acute kidney injury, thus creating a major public health concern. This review summarizes the available information on the pathophysiological implications of HRS. We discuss pathogenesis associated with HRS. Mechanisms such as dysfunction of the circulatory system, bacterial infection, inflammation, impaired renal autoregulation, circulatory, and others, which have been identified as critical pathways for development of HRS, have become easier to diagnose in recent years. Additionally, relatively recently, renal dysfunction biomarkers have been found indicating renal injury, which are involved in the pathophysiology of HRS. This review also summarizes the available information on the management of HRS, focusing on vasoconstrictive drugs, renal replacement therapy, and liver transplant together with currently being investigated novel therapies. Analyzing new discoveries for the underlying causes of this condition assists the general research to improve understanding of the mechanism of pathophysiology and thus prevention of HRS.