Introduction

Bacterial infections are a frequent and common complication of cirrhosis and are responsible for a significant morbidity and mortality.
The presence of acute kidney injury (AKI) is often considered a poor prognostic factor.

Aims & Methods

The aim of our study is to evaluate the prevalence of AKI during bacterial infections in cirrhotic patients and to determine its prognostic value.
We conducted a retrospective and analytical study over a period of 3 years, including all patients followed for cirrhosis who were hospitalized for management of a bacterial infection. The different clinical, biological, and therapeutic data were collected.

Results

We included 80 patients (38 men and 42 women). The mean age was 62 years [26 - 93 ].
The main comorbidities noted were type 2 diabetes mellitus in 38% of cases and arterial hypertension in 10% of cases.
The etiologies of cirrhosis were dominated by viral (38.8%), autoimmune (18%) and metabolic (11.3%) causes.
Cirrhosis was Child-Pugh A, B and C in 25%, 68.8% and 6.3% of cases respectively.
The clinical signs were mainly represented by oedemato-ascitic decompensation in 56.3% of cases, hepatic encephalopathy in 22.5% of cases and only 30 % of patients had fever.
The identified infections were mainly urinary infection (35.3%), Spontaneous bacterial peritonitis (35.3%) and pulmonary infection (23.3%).
The prevalence of AKI was 35% (n = 28), classified as Stage I, II and III in 42%, 22% and 36% of cases respectively.
The presence of AKI was statistically associated with an initial Child-Pugh's score ≥ B7 (3% vs 21%, p = 0.001) , refractory ascites ( 40% vs 22% , p = 0.001) and the presence of a documented spontaneous bacterial peritonitis ( 58 vs 9% , p = 0.001) .
The analytical study found a statistically significant correlation between AKI and 15 days mortality (24.2% vs 4.3%, p=0.01).
When analyzing the receiver operating characteristic (ROC) curve, AUC of serum creatinine in predicting 15 days mortality was 0.781 (p=0.03).

Conclusion

In our study AKI is associated with a poor prognosis and higher mortality rates. Therefore serum creatinine is a valuable marker allowing better initial stratification.

Introduction

Antibiotic prophylaxis has been recommended to reduce the risk of infection and mortality in patients with cirrhosis and acute variceal bleeding (AVB). Recent data from Europe indicated that, despite antibiotic prophylaxis, bacterial infections, particularly of the respiratory tract, still occur in a subset of AVB patients, even with the administration of prophylactic antibiotics. Nonetheless, evidence concerning infections in AVB patients in Asia is limited and may differ from that in Western countries.

Aims & Methods

This retrospective study aimed to determine the incidence of bacterial infections among patients with AVB and to identify characteristics correlated with the occurrence of infection. Data from consecutive cirrhotic patients with AVB admitted to a tertiary care center, Rajavithi Hospital, Bangkok, between January 1, 2018, and October 31, 2024 were reviewed and analyzed. Patients with clinical signs of infections on admission were excluded.

Results

A total of 77 patients were included, with 67 (87%) being male. The average age was 52.88 ± 12.16 years. The predominant causes of cirrhosis were alcohol (66.2%), hepatitis C virus (27.3%), and hepatitis B virus (16.9%). The severity of cirrhosis was categorized as Child-Pugh A, B, and C in 31.2%, 24.2%, and 24.6% of patients, respectively. All patients were administered intravenous ceftriaxone as prophylactic antibiotic upon admission and underwent esophagogastroduodenoscopy within 48 hours, with 82% receiving endoscopic variceal ligation. Bacterial infections were identified in 12 patients (15.6%). The observed infection types included pneumonia (41.6%), primary bacteremia (25%), spontaneous bacterial peritonitis (16.7%), and urinary tract infection (16.7%). The median time to infection commencement was 2 (1-15) days, and the median duration of hospitalization was 5 (2-6) days, with a mortality rate of 6%. In univariate analysis, significant predictors of infections included Child-Pugh class B/C (p=0.004), BMI (p=0.037), histoacryl glue injection (p=0.044), and serum albumin (p=0.003). A multivariate analysis revealed a statistically significant link between low serum albumin levels and the occurrence of bacterial infection, with an adjusted odds ratio of 0.13 (95% CI: 0.02 - 0.94); p=0.043.

Conclusion

Bacterial infections, especially pneumonia, remain a significant concern in cirrhotic patients with AVB despite the use of prophylactic antibiotic, particularly in individuals with hypoalbuminemia.

Introduction

Iodinated contrast (IC) is one of the leading causes of acute kidney injury (AKI). Nephrotoxicity of IC in cirrhosis is a debated issue due to low-quality evidence.

Aims & Methods

This study aims to evaluate the association between exposition to IC in cirrhotic patients and the development of AKI. We performed a systematic review in PubMed, Embase and Cochrane databases, searching for studies conducted in cirrhotic patients exposed to IC. The primary outcomes were: 1) AKI development in cirrhotic patients exposed or not to IC; and 2) AKI development in cirrhotic and health patients exposed to IC. The odds ratio (OR) was used for binary outcomes with their respective 95% confidence interval (CI). Heterogeneity was assessed using the Cochran Q test and I² statistics.

Results

The meta-analyses included 4 studies and 1,055 patients. Three studies (911 patients) evaluated cirrhotic patients exposed or not exposed to IC. There was a significant increase in AKI in cirrhotic patients exposed to IC (OR 3.10; 95% CI 1.45 to 6.61, p=0.003; I2=0%). Three studies (654 patients) evaluated cirrhotic and health patients exposed to IC. There was no difference in AKI comparing both groups (OR 1.61; 95% CI 0.63 to 4.16, p=0.322; I2=0%).

Conclusion

Patients with cirrhosis exposed to IC showed higher incidence of AKI compared with those not exposed, but when compared with health individuals also exposed to IC the incidence of AKI seems to be the same.

References

1. Campion D, Rizzo M, Ponzo P, Risso A, Giovo I, Rizzi F, et al. Risk of contrast-induced acute kidney injury in cirrhotic patients undergoing computed tomography: myth or reality? J Hepatol. 2020;73:S702.
2. Campion D, Ponzo P, Risso A, Caropreso P, Caviglia GP, Sanavia T, et al. A prospective, multicenter, three-cohort study evaluating contrast-induced acute kidney injury (CI-AKI) in patients with cirrhosis. J Hepatol. 2024;80(1):62–72.
3. Filomia R, Maimone S, Caccamo G, Saitta C, Visconti L, Alibrandi A, et al. Acute kidney injury in cirrhotic patients undergoing contrast-enhanced computed tomography. Medicine (Baltimore). 2016 Sep;95(38):e4836.
4. Safi W, Rauscher I, Umgelter A. Contrast-induced acute kidney injury in cirrhotic patients. A retrospective analysis. Ann Hepatol. 2015 Nov;14(6):895–901.
5. Visconti L, Filomia R, Maimone S, Montuori F, Ricciardi CA, Di Mauro E, et al. SP211ACUTE KIDNEY INJURY IN CIRRHOTIC PATIENTS UNDERGOING CONTRAST-ENHANCED COMPUTED TOMOGRAPHY. Nephrol Dial Transplant. 2015 May;30(suppl_3):iii448–iii448.

Introduction

Acute kidney injury (AKI) represents a complication associated with high morbidity and mortality, as well as progression to chronic kidney disease. Early recognition is critical for targeted treatment to reverse AKI. A high percentage of patients have been shown to experience volume overload and pulmonary edema, as volume re-expansion is systematically performed in all patients without prior evaluation of their volume status. A relationship between volume overload and mortality has been demonstrated. The VExUS protocol enables the identification and stratification of systemic venous congestion, complementing inferior vena cava diameter assessment with pulsed Doppler of the suprahepatic veins, portal vein, and interlobar renal veins, evaluating altered flow patterns observed in venous congestion.

Aims & Methods

General Objective: To evaluate the impact of volume overload measured by VExUS on mortality and morbidity in patients with hepatic cirrhosis and acute kidney injury.
Materials and Methods: A prospective, observational, and analytical cohort study was conducted in patients diagnosed with hepatic cirrhosis who developed AKI as a complication and required hospitalization at the Centro Médico Nacional de Occidente. These patients received intravenous albumin at a dose of 1 g/kg/day for 48 hours, followed by an evaluation of their response to treatment. Prior to albumin administration, ultrasound was performed with the VExUS protocol to determine the patients' venous congestion status. The study was carried out between July 2022 and August 2024. No sample size calculation was performed; instead, all patients meeting the inclusion criteria during the study period were included to encompass the entire population affected by this condition.

Results

A total of 38 patients treated at the Centro Médico Nacional de Occidente were included. Patients were classified according to the VExUS index into three levels: 0 (60.5%), 1 (23.7%), and 2 (15.8%). Clinical, biochemical, and outcome variables such as response to albumin, hospital mortality, and survival time were recorded.
The results showed that hospital mortality was 39.5%, with higher rates in patients with higher VExUS levels. Survival analysis revealed that patients with VExUS 0 had an average survival time of 497 days, compared to 207 days in VExUS 1 and 237 days in VExUS 2. Although the Chi-square analysis did not show a statistically significant association between VExUS and mortality (p = 0.361), a trend was observed suggesting a relationship between higher VExUS levels and worse outcomes. The CLIF-SOFA score emerged as a significant predictor of mortality, with a 10.5% increase in risk for each additional unit.

Conclusion

The VExUS index is positioned as a useful tool to evaluate volume overload and its impact on clinical outcomes, highlighting its potential to guide therapeutic decisions in patients with hepatic cirrhosis and AKI. Prospective and multicenter studies with larger sample sizes are recommended to confirm these findings and evaluate the impact of VExUS-guided interventions on personalized clinical management.

References

1. Velez JC et al. Point-of-Care Echocardiography Unveils Misclassification of Acute Kidney Injury as Hepatorenal Syndrome. Am J Nephrol. 2019;50(3):204-211. doi: 10.1159/000501299.
2. Koratala A et al. Point of Care Ultrasound in Cirrhosis-Associated Acute Kidney Injury: Beyond Inferior Vena Cava. Kidney360. 2022 Oct 5;3(11):1965-1968. doi: 10.34067/KID.0005522022.
3. Abhilash Koratala, Claudio Ronco, Amir Kazory. Albumin Infusion in Patients with Cirrhosis: Time for POCUS-Enhanced Physical Examination. Cardiorenal Med 2021;11:161–165.
4. David Jury and Andrew D. Shaw. Utility of bedside ultrasound derived hepatic and renal parenchymal flow patterns to guide management of acute kidney injury. Curr Opin Crit Care 2021, 27:587 – 592.
5. Bhardwaj V, et al. Combination of Inferior Vena Cava Diameter, Hepatic Venous Flow, and Portal Vein Pulsatility Index: Venous Excess Ultrasound Score (VEXUS Score) in Predicting Acute Kidney Injury in Patients with Cardiorenal Syndrome: A Prospective Cohort Study. Indian J Crit Care Med 2020;24(9): 783–789.
6. Koratala A, et al. Nephrologist-performed point-of-care venous excess Doppler ultrasound (VExUS) in the management of acute kidney injury. J Ultrasound. 2023 Mar;26(1):301-306. doi: 10.1007/s40477-022-00760-6
7. Banegas-Deras EJ, et al. Acute kidney injury and point-of-care ultrasound in liver cirrhosis: redefining hepatorenal syndrome. Clin Kidney J. 2024 Apr 15;17(5):sfae112. doi: 10.1093/ckj/sfae

Introduction

Cirrhotic patients undergo intricate changes in their haemostatic system, resulting in a ‘rebalanced haemostasis’. In patients with acute decompensation (AD) and acute-on-chronic liver failure (ACLF), this delicate balance is particularly susceptible to disruption by external stressors such as infections or acute kidney injury (AKI) rendering them more vulnerable to haemostatic complications than individuals with stable cirrhosis [1,2].

Aims & Methods

This case-control study evaluated coagulation profiles (INR, aPTT, PT, fibrinogen, coagulation factors and inhibitors, rotational thromboelastometry (ROTEM), and thrombin generation assay (TGA) [BleedScreen/ (BS) ThromboScreen (TS) ± thrombomodulin (TM)]) in 215 cirrhotic patients, comparing subgroups with/without AKI or bacterial infection to assess haemostatic impact.

Results

The cohort included 215 patients, with 37 (17.2%) having AKI and 31 (14.4%) bacterial infections. AKI patients had higher median Child-Pugh (11 vs 7, P<0.001) and MELD-Na scores (25 vs 11, P<0.001) than non-AKI patients, with more AD (32.4% vs 23%) and ACLF (59.5% vs 10.1%, P<0.001). Infected patients also showed higher CP (9 vs 7) and MELD-Na scores (33 vs 12, P<0.001), with more ACLF (51.6% vs 13%, P<0.001).
In the overall cohort, AD and ACLF patients have more hypocoagulability on ROTEM than SC. TG was preserved in AD compared to SC but showed more hypocoagulable features in ACLF, which were offset after TM addition. Both TG and ROTEM abnormalities correlated with liver disease severity.
Bacterial infection was linked to increased TG capacity (endogenous thrombin potential (ETP)-TM: 928.15 vs. 770.10 nm·min, P=0.030) and significantly less ETP suppression by TM (11.07% vs. 30.33%, P<0.001). Despite a greater prevalence of ACLF, ROTEM profiles did not differ between infected and non-infected patients. Standard coagulation assays revealed a hypocoagulable state, with lower levels of FII, VII, X, IX, and XI, while fibrinogen and platelet counts remained similar. Hypercoagulable features included increased FVIII and decreased protein S, (PS) and C (PC), and antithrombin (AT).
In the AKI group, TGA showed significantly accelerated TG in BS and TS with reduced TG capacity in TS. After TM addition, no differences in TG speed or total TG capacity were noted. Patients with AKI showed a significantly lower ETP inhibition by TM. ROTEM showed prolonged clotting times in INTEM and EXTEM and reduced maximum clot firmness in FIBTEM, with overall more hypocoagulability (21.2% vs. 4.2%, P=0.003). Standard coagulation assays showed mixed features in AKI, with increased INR, prolonged aPTT and reduced fibrinogen, FII, V, VII, X, IX, and XI levels, along with elevated FVIII and reduced AT and PC. Platelet counts were similar.

Conclusion

Global coagulation assays (TGA and ROTEM) showed similar profiles in infected vs non-infected cirrhotic patients, with some hypercoagulable features on TGA in infection, despite high ACLF prevalence (>50%). In contrast, AKI showed accelerated TG but reduced TG capacity, more hypocoagulable ROTEM features, and lower coagulation factors and inhibitors.
Although ACLF rates were comparable in AKI and infection groups, hypocoagulability was more pronounced in AKI, where in the infection group coagulation status was preserved or showed even some hypercoagulable features. This indicated that these coagulation abnormalities reflect the effects of these destabilizing factors rather than disease severity alone.

References

1. Zanetto A, Northup P, Roberts L, Senzolo M. Haemostasis in cirrhosis: Understanding destabilising factors during acute decompensation. Vol. 78, Journal of Hepatology. Elsevier B.V.; 2023. p. 1037–47.
2. Intagliata NM, Davis JPE, Lafond J, Erdbruegger U, Greenberg CS, Northup PG, Caldwell SH. Acute kidney injury is associated with low factor XIII in decompensated cirrhosis. Dig Liver Dis. 2019 Oct;51(10):1409-1415.

Disclosure

The reagents for the ROTEM analyses were sponsored by Werfen. This study received a Gilead fellowship, and K.F. received a BSTH-CSL Behring encouragement award.

Introduction

Acute kidney injury (AKI) in cirrhosis manifests as pre-renal azotemia (PRA), hepatorenal syndrome (HRS), or acute tubular necrosis (ATN), each with distinct prognosis ⁽¹⁾. Early subtype classification and outcome prediction are critical. In Decompensated Cirrhosis patients with AKI, urine NGAL (UNGAL) and urine IL-18 (UIL-18) have been evaluated for differentiating between ATN and non-ATN AKI (PRA and HRS) with conflicting results ^(2,3). The present study compared the diagnostic accuracy of UNGAL and UIL-18 for predicting ATN AKI, AKI resolution and in-hospital mortality.

Aims & Methods

Present study was conducted at a tertiary care hospital (GIPMER, India) from July 1, 2023 to December 31, 2024. Patients with Decompensated Cirrhosis having AKI stage IB or higher were included, while advanced chronic kidney disease, Hepatocellular carcinoma prior liver transplant were excluded. The AKI was diagnosed as per International Club of Ascites Consensus (2015) and classified as per clinical adjudication after volume expansion with injection Human Albumin (20%, 1 g/kg body weight) on day 3 ⁽⁴⁾. Urine NGAL (sandwich ELISA) and IL-18 (sandwich ELISA) were measured after 48 hours of volume expansion, that is on day 3 of AKI diagnosis. The primary outcome was prediction of ATN-AKI on day 3 and secondary outcomes were prediction of AKI resolution at discharge and in-hospital mortality. The Receiver-operator curve (ROC) and multivariate logistic regression were used for analysis and p value <0.05 considered statistically significant.

Results

Total of 81 Decompensated Cirrhosis patients with AKI were enrolled in study. The aetiology of AKI was 24 (29.5%) PRA, 37 (45.7%) HRS and 20 (24.7%) ATN respectively. Mean MELD Na score was 28.4+7.3 and majority (82.7%) were CTP-C. Mean Serum Creatinine was 2.85+0.95 mg/dl. Mean UNGAL was 109.7 (PRA), 206.6 (HRS) and 396.4 (ATN) ug/g Creatinine (p<0.001). Mean UIL-18 was 39.8 (PRA), 85.6 (HRS) and 139.3 (ATN) pg/ml (p<0.001). AUROC for differentiation of ATN from non-ATN for urine NGAL was 0.9 (best cut-off 236.3 ug/g Creat) and urine IL-18 was 0.88 (best cut-off 108.75 pg/ml). AKI resolution occurred in 95.8% (PRA), 81% (HRS), and 40% (ATN). Mortality was highest in ATN (50%), vs PRA (16.7%) and HRS (8.1%). AUROC of UNGAL was 0.211 and UIL-18 was 0.185 for predicting AKI resolution. AUROC of UNGAL was 0.654 and UIL-18 was 0.641 for predicting in-hospital mortality (AUROC: NGAL 0.654, IL-18 0.641). Urine NGAL ( and urine IL-18 failed to predict AKI resolution (p 0.14 and 0.27) and in-hospital mortality (p 0.06 and 0.07) in multivariate regression analysis.

Conclusion

Urine NGAL and IL-18 had good diagnostic accuracy in predicting ATN-AKI in patients with Decompensated Cirrhosis, however do not independently predict resolution of AKI and in-hospital mortality.

References

1. Tariq R, Hadi Y, Chahal K, Reddy S, Salameh H, Singal AK. Incidence, mortality and predictors of acute kidney injury in patients with cirrhosis: A systematic review and meta-analysis. J Clin Transl Hepatol. 2020;8(2):135.
2. Puthumana J, Ariza X, Belcher JM, Graupera I, Ginès P, Parikh CR. Urine interleukin 18 and lipocalin 2 are biomarkers of acute tubular necrosis in patients with cirrhosis: a systematic review and meta-analysis. Clinical Gastroenterology and Hepatology. 2017;15(7):1003-13.
3. Huelin P, Solà E, Elia C, Solé C, Risso A, Moreira R, et al. Neutrophil gelatinase-associated lipocalin for assessment of acute kidney injury in cirrhosis: a prospective study. Hepatology.2019;70(1):319–33.
4. Angeli P, Ginès P, Wong F, Bernardi M, Boyer TD, Gerbes A, et al. Diagnosis and
management of acute kidney injury in patients with cirrhosis: revised consensus recommendations of the International Club of Ascites. Gut. 2015;64(4):531–7.

Introduction

Spontaneous bacterial peritonitis (SBP) is a well-recognized decompensation that significantly affects the clinical outcome of patients with liver cirrhosis. The aim of this study is to assess the factors associated with short-term mortality in this patient population.

Aims & Methods

We conducted a retrospective study (January 2022 to December 2024) on all cirrhotic patients with SBP, admitted in the Gastroenterology Department of “St. Spiridon” County Clinical Emergency Hospital Iasi, a tertiary referral center. The SBP cases were identified based on elevated ascitic fluid absolute PMN count > 250 cells/mm³, with or without positive ascitic fluid bacterial culture.

Results

Out of the 114 cirrhotic patients diagnosed with SBP for the first time, 39 (34,2%) were female and 75 (65,8%) were male, with a mean age of 57 years. Most patients had advanced liver disease according to the Child-Pugh classification: 98 patients (86%) were classified as Child C, and 16 patients (14%) as Child B. The mean MELD-Na score was 23.3 points. The overall in-hospital mortality rate was 17.5% (20 patients). According to the multivariable analysis, several factors were significantly associated with in-hospital mortality, such as: renal dysfunction (OR 8.4118 [95% CI 2.9190 to 24.2403]; P=0.0001), serum bilirubin higher than 3 mg/dl (OR 4.8571 [95% CI 1.7445 to 13.5216]; P=0.0025), serum sodium lower than 130 mmol/l (OR 4.3750 [95% CI 1.5973 to 11.9833]; P=0.0041), international normalized ration (INR) higher than 2 (OR 4.5222 [95% CI 1.6471 to 12.4161]; P=0.0034).

Conclusion

Renal dysfunction, elevated INR, hyperbilirubinemia, and hyponatremia appear to be significant factors associated with the worsening of prognosis in cirrhotic patients with SBP, influencing in-hospital mortality.