Search

Whether tubular injury develops in patients with acute kidney injury owing to hepatorenal syndrome (AKI‐HRS) is controversial. We performed repeated measurements of biomarkers of tubular injury during a 14‐day period in 60 patients with cirrhosis and AKI (34 with AKI‐HRS meeting the classical definition of type 1 HRS and 26 with AKI owing to acute tubular necrosis, AKI‐ATN). Nineteen of 34 patients had resolution of AKI‐HRS, while the remainder had persistent AKI‐HRS. The persistence of AKI‐HRS was associated with remarkably high short‐term mortality. There were no significant differences in urinary NGAL or IL‐18 between patients with resolution vs those with persistent AKI‐HRS throughout the 14‐day period. By contrast, biomarker levels were significantly lower in AKI‐HRS, even if persistent, compared to AKI‐ATN. These findings are highly suggestive of lack of significant tubular injury in AKI‐HRS and could be of value in the clinical decision between combined liver–kidney or liver transplantation alone in patients with cirrhosis and AKI candidates to transplantation. [ABSTRACT FROM AUTHOR]

Background and aims: Alcohol and metabolic syndrome (MS) coexist frequently as cofactors of liver disease. Previous studies suggest a deleterious effect of MS in advanced alcohol‐related liver disease (ArLD). However, it is unknow whether MS can increase the risk of liver fibrosis in early stages of ArLD. The aim of this study was to investigate the effect of MS on liver fibrosis in subjects with alcohol consumption from a population‐based cohort. Methods: The number of subjects include 1760(58%) of 3014 who were randomly selected from the community consumed alcohol and were classified as current drinkers, divided in moderate (n = 1222) or high‐risk drinkers (n = 275) (>21 units/week men, >14 units/week women for high‐risk drinkers), or former drinkers (n = 263). Liver fibrosis was estimated by measuring liver stiffness(LS) with transient elastography (TE). Results: Prevalence of significant LS using cutoff values of TE of 8 and 9.1kPa was increased in high‐risk compared with moderate or former drinkers and lifetime abstainers. In subjects with alcohol consumption, LS was associated with male gender, AST, ALT, years of consumption, and MS. In high‐risk drinkers, MS and intensity of consumption were the only factors associated with significant LS (OR 3.7 and 4.6 for LS ≥ 8 kPa and 3.9 and 9.2 kPa for LS ≥ 9.1 kPa, respectively). Presence of significant liver fibrosis in the liver biopsy was higher among high‐risk as compared with moderate or former drinkers. Conclusion: MS increases the risk of liver fibrosis in subjects with alcohol consumption. Among high‐risk drinkers, only MS and consumption of high amount of alcohol are associated with risk of liver fibrosis. [ABSTRACT FROM AUTHOR]