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

Abstract

Objective To 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. Methods Between 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. Results The 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). Conclusion Endotoxin 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.