Thisstudywasconductedon12cirrhoticnon—asciticpatients,10cirrhotic asciticpatients withpreservedkidneyfunction, 15cirrhoticpatients withhepatorenalsyndrome(was)aswellas 10well— matched
healthyvolunteersservingascontrob.
Theaimofthisworkwastostudyplasmaendothelin-l{ET-I)levelin
livercirrhosisandtoshedlightoni.tspossibleroleinthepathogenesisof
HRS.
Thefollowinginvestigationswereperformedtoeverysubjectbiochemicalliverfunctiontests,senirncreatinine,urinecreatinine,serumNa+,24
hoursurineNa+andplasmaET-llevel.
DiagnosisofHRSwasmadewhenserumcreatinineishighandfraclionexcretionofthefilteredsodiumislessthanI .
PlasmaET—1 level wassignificantly elevated in allpatientgroups
whencomparedwithcontrols. However,plasmaET-llevelwassignificantly higherin cirrhotic ascitic1patients thancirrhotic non-asciticpatients.PatientswithHRSexhibitedthehighestplasmaET-llevelPlasma
ET-Ishowedsignificantnegativecorrelationwithserumalbumin,serum
&urinaryNa+,whereasitshowedsignificantpositivecorrelation with
seru.mtransarninases.alkalinephosphatase,serumbilirubinandserum
creatinine: |
