Jalan, R and Hayes, PC (2000) Sodium handling in patients with well compensated cirrhosis is dependent on the severity of liver disease and portal pressure. GUT , 46 (4) 527 - 533.
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Background and aims-To test the contribution of portal pressure gradient (PPG) and neurohumoral factors to sodium handling in cirrhotic patients without ascites, by comparing preascitic cirrhotic patients with patients with transjugular intrahepatic portosystemic stent shunt (TIPSS) and previous ascites.Patients-Ten patients with TIPSS and 10 preascitic cirrhotic patients.Methods-Changes in glomerular filtration, renal plasma flow, urinary sodium excretion (UNaV), and neurohumoral factors were measured before and for two hours after infusion of one litre of 0.9% saline over one hour.Results-Glomerular filtration rate and renal plasma flow were significantly higher in patients with TIPSS compared with preascitic cirrhotic patients. Following saline infusion both parameters increased significantly; this increase was significantly greater in patients with TIPSS. UNaV increased significantly in both groups following saline infusion. The increase in UNaV was significantly greater in the TIPSS group. Plasma renin activity and angiotensin II decreased significantly in both groups. Basal UNaV was independently correlated with angiotensin II concentration and PPG and the change in UNaV correlated with the PPG,Conclusions-Results suggest that patients with advanced liver disease and low portal pressure handle sodium as well as patients with compensated liver disease and high portal pressure. These results are consistent with the notion that in addition to peripheral vasodilatation and severity of liver disease, the severity of portal hypertension contributes to the abnormalities of sodium retention in cirrhosis.
|Title:||Sodium handling in patients with well compensated cirrhosis is dependent on the severity of liver disease and portal pressure|
|Keywords:||cirrhosis, transjugular intrahepatic portosystemic stent shunt, TIPSS, angiotensin, sodium handling, peripheral vasodilatation, INTRAHEPATIC PORTOSYSTEMIC SHUNT, RENIN-ANGIOTENSIN, ALCOHOLIC CIRRHOSIS, REFRACTORY ASCITES, NITRIC-OXIDE, ARTERIAL VASODILATION, ARGININE VASOPRESSIN, HEPATORENAL REFLEX, PLASMA ENDOTHELIN, WATER-EXCRETION|
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