Background/Aims: Acute kidney injury (AKI) is frequent in cirrhotic patients and is associated with a poor prognosis. Recently, the Kidney Disease: Improving Global Outcomes (KDIGO) organization recommended new criteria for the diagnosis and staging for AKI. The aim of this study was to evaluate the presence of AKI according to KDIGO criteria in cirrhotic patients admitted to the hospital and to determine its association with hospital mortality. Materials and Methods: This retrospective study included 277 cirrhotic patients admitted to the intensive care unit and gastroenterology service of a tertiary referral hospital from January 2008 to January 2012. AKI was diagnosed and classified according to the KDIGO criteria. Results: The overall incidence of AKI in cirrhotic patients was 39%, and the overall hospital mortality was 15.5%. Patients without AKI had a hospital mortality rate of 2.4%, whereas the mortality rate for patients with AKI was 36.1%. The peak AKI stage detected during hospitalization was stage 1 for 58 patients (53.7%), stage 2 for 20 patients (18.5%), and stage 3 for 30 patients (27.7%). Mortality was found to be associated with the presence, stage, and progression of AKI. Multivariate analysis showed that AKI was an independent factor significantly associated with mortality (odds ratio: 9.1; 95% confidence interval: 2.89–29.1; p<0.001). Conclusion: KDIGO criteria can be used to evaluate AKI in cirrhotic patients. The prevalence of AKI in patients with cirrhosis is high, and AKI is associated with mortality. If early preventive measures are taken, it may be possible to prevent AKI progression and thus mortality.

Introduction: There is limited research about HBV reactivation (HBVr) due to direct-acting antivirals (DAA) for HCV and most are limited by short duration of follow-up, small sample size, and absence of baseline HBV DNA. We aimed to determine the incidence and clinical course of HBVr in HBsAg and/or anti-HBcIgG positive patients treated with DAA for HCV. Methods: Seven centers retrospectively analyzed their database on HCV patients treated with DAA between 2015 and 2019. Patients with HBV coinfection or resolved HBV infection were enrolled. Serum transaminases, HBsAg, HBeAg, and HBV DNA were followed every 4 weeks during DAA treatment and every 12 weeks 1 year after treatment. Entecavir or tenofovir disoproxil fumarate was started in case of HBVr. The development of HBVr, HBV flare, liver failure, and mortality were determined. Results: 852 patients received DAA treatment for HCV. Among them, 35 (4.1%) had HBV coinfection and 246 (28.9%) had resolved HBV infection. 257 patients (53.3% male, mean age: 63 ± 9) constituted the study group (29 with coinfection and 228 with resolved infection). Three patients with coinfection were HBV DNA positive. HBVr developed in 10 (34.5%) HBsAg positive patients, either during (n = 3) or 12–48 weeks after finishing DAA treatment. HBV flare and acute liver failure developed in 1 patient (3.4%), each. Two patients with resolved infection developed HBVr (0.87%) and one (0.44%) had HBV flare. Overall, none of the patients died or underwent liver transplantation due to HBVr. Conclusion: Patients with HBV/HCV coinfection have a high risk of HBVr after DAA treatment and should receive antiviral prophylaxis. Patients with resolved infection have a low risk of HBVr and can be monitored by serial ALT measurements.

Background/aim: Albumin is the most important protein synthesized by the liver. Posttranscriptional changes occur in the molecular structure of albumin due to various factors and isoforms arise. Ischemic modified albumin (IMA) is one such isoform. This study was conducted to evaluate serum IMA concentrations in patients with hepatitis B virus (HBV)-related chronic liver diseases. Materials and methods: This study included 74 treatment-naive chronic hepatitis B patients, 25 patients with HBV-related cirrhosis, and 49 healthy controls. Serum IMA concentration was measured spectrophotometrically using the albumin cobalt binding test. Results: The mean IMA concentrations in the chronic hepatitis B group and healthy controls were 0.33 +/- 0.11 ABSU and 0.27 +/- 0.70 ABSU, respectively, and the difference was statistically significant (P < 0.001). Mean IMA/albumin ratios (IMAR) in the chronic hepatitis B and control groups were 0.08 +/- 0.04 and 0.06 +/- 0.17, respectively, and the difference was also statistically significant (P < 0.001). Higher serum IMA concentrations and IMAR were detected in patients with advanced fibrosis. Conclusion: Serum IMA concentration and IMAR are increased in patients with HBV-related chronic liver diseases and IMA and IMAR are associated with the degree of liver fibrosis. IMA and IMAR may have potential use as noninvasive markers of fibrosis in chronic hepatitis B patients.

Background/aim: Thiol-disulfide homeostasis is an important antioxidant defense mechanism. This study was conducted to investigate dynamic thiol-disulfide homeostasis in patients with hepatitis B virus-related chronic hepatitis and liver cirrhosis. Materials and methods: Seventy-one treatment-naive patients with chronic hepatitis B (CHB), 50 patients with hepatitis B virus-associated liver cirrhosis, and 45 healthy controls were included in the study. Serum total and native thiol concentrations and serum disulfide concentrations were measured using an automated method. Results: Mean serum total thiol concentrations in the control, CHB, and cirrhosis groups were 481.64 +/- 37.87 mu mol/L, 438.50 +/- 71.35 mu mol/L, and 358.07 +/- 80.47 mu mol/L, respectively (P < 0.001), and mean serum native thiol concentrations in the control, CHB, and cirrhosis groups were 452.92 +/- 36.43 mu mol/L, 400.16 +/- 65.92 mu mol/L, and 328.15 +/- 74.91 mu mol/L, respectively (P < 0.001). Mean serum disulfide concentrations in the control, CHB, and cirrhosis groups were 14.38 +/- 3.38 mu mol/L, 19.19 +/- 6.16 mu mol/L, and 14.98 +/- 5.53 mu mol/L, respectively (P < 0.001). There was a progressive decrease in both mean serum native and total thiol concentrations parallel to the liver fibrosis stage. Conclusion: Thiol-disulfide homeostasis is disturbed in patients with hepatitis B virus-related chronic hepatitis and liver cirrhosis.

Background/aim: Ultrasonographic measurements of inferior vena cava (IVC) diameters and right ventricle (RV) volumes are important tools for the evaluation of intravascular volume. The current study investigates the association of IVC diameters and RV volumes before colonoscopy in prediction of postanesthesia hypotension. Materials and methods: Seventy patients scheduled for colonoscopy were included in the study. Preoperatively, expirium (dIVC tnax) and inspirium (dIVC min) IVC diameters were measured using M-mode ultrasonography and the collapsibility index (IVC-CI) was calculated. Ventricular volumes and areas were also measured using transthoracic echocardiography. Postanesthesia hypotension was defined as mean arterial blood pressure of 30% in the mean arterial pressure after sedation. Results: Minimum and maximum IVC diameters were significantly lower (P = 0.005 and P < 0.001, respectively) and IVC-CI was significantly higher (P < 0.001) in patients who developed hypotension. Similarly, right ventricular end-diastolic area (RV-EDA), right ventricular end-systolic area (RV-ESA), right ventricular end-diastolic volume (RV-EDV), right ventricular end-systolic volume ( RVESV), and left ventricular end-systolic volume (LV-ESV) values were significantly lower in patients with hypotension (P < 0.05). Logistic regression analysis showed that dIVC min and RV-ESA were independent predictors of hypotension. Conclusion: IVC diameters and RV-ESA, RV-EDA, RV-ESV, and RV-EDV are good indicators of preoperative volume status and can be used to predict the patients at risk of developing hypotension.