Analysis of endotoxin and endothelin-1 levels in patients with type 1 hepatorenal syndrome

• Main Author: GAO Baoxiu
• Format: Article
• Language: zho
• Published: Editorial Department of Journal of Clinical Hepatology 2014-01-01
• Series: Linchuang Gandanbing Zazhi
• Subjects: hepatorenal syndrome; liver cirrhosis; endotoxins; endothelin-1
• Online Access: http://www.lcgdbzz.org/qk_content.asp?id=5601&ClassID=112814475
• ISSN: 1001-5256; 1001-5256

ObjectiveTo analyze the clinical data, laboratory parameters, infection rate, and serum procalcitonin (PCT) and ET-1 levels of patients with cirrhotic ascites and type 1 hepatorenal syndrome (HRS) and to investigate the roles of endotoxin and ET-1 in the development of HRS. MethodsBetween January 2009 and October 2012, 56 inpatients with cirrhotic ascites and type 1 HRS (HRS group) and 60 inpatients with cirrhotic ascites who had normal renal function (non-HRS group) were included in the study. Their general data, causes of liver cirrhosis, infection rates and types, Child-Pugh classification, systemic inflammatory response syndrome (SIRS) score, and mean arterial pressure (MAP) were recorded; blood samples were collected to evaluate liver and renal function and measure serum electrolyte, PCT, and ET-1 levels. The clinical data and laboratory parameters were compared between the two groups. Categorical data were analyzed by chi-square test; comparison of normally distributed continuous data between the two groups was made by independent-samples t test, and comparison of non-normally distributed continuous data between the two groups was made by Wilcoxon rank sum test. ResultsThe infection rate of HRS group (75.0%) was significantly higher than that of non-HRS group (28.4%) (χ2=11.91, P＜0.05). The PCT and ET-1 levels and SIRS score of HRS group ［8.72 (3.14, 31.68) ng/L, 13.04±2.82 pg/ml, and 2.1±1.1］ were significantly higher than those of non-HRS group ［0.11 (0.04, 0.45) ng/L, 5.76±1.68 pg/ml, and 0.6±0.6］ (P＜0.05). In addition, the HRS group had significantly higher serum urea, creatine, cystatin C, and K levels than the non-HRS group (P＜0.05), while the HRS group had significantly lower Na and Cl levels than the non-HRS group (P＜0.05). There were no significant differences in ALT and AST levels between the two groups (P＞005). ConclusionEndotoxin causes elevated expression of ET-1, and ET-1 induces renal perfusion deficiency by intense renal vasoconstriction, thus leading to type 1 HRS. Endotoxin and ET-1 are closely associated with the development of type 1 HRS.