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ISSN 1001-5256 (Print)
ISSN 2097-3497 (Online)
CN 22-1108/R
Issue 1
Jan.  2014
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Analysis of endotoxin and endothelin-1 levels in patients with type 1 hepatorenal syndrome

DOI: 10.3969/j.issn.1001-5256.2014.01.016
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  • Received Date: 2013-05-13
  • Published Date: 2014-01-20
  • 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.

     

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