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Abstract
As ammonia has a central role of hepatic encephalopathy and since dehydration proved to be a potent predisposing factor for developing hepatic encephalopathy, the present work has been conducted aimming for studying the effect of volume expansion on renal ammonia excretion in patients with well compensated liver cirrhosis Thirty subjects were included in the work classified into: * group I: comprised 10 healthy volunteers . * group II: comprised 20 patients with well compensated liver cirrhosis. All subject were submitted to the following: - Thorough history taking & full clinical examination. - Calculation of mean arterial blood pressure and redial pulse rate before & following volume expansion. -Laboratory investigations include, CBC, liver function tests, kidney function tests, complete urine analysis, fasting & P.P. blood glucose level, creatinine clearance, arterial blood gases, serum Na+& k+, resting ECG, abdominal ultrasonography, upper G.I. endoscopy & sonar guided biopsy. - Calculation of renal plasma flow, plasma ammonia levels & calculation of urinary ammonia excretion before & following volume expansion by 1 litre 0.9% saline intravenous infusion. The results were: -The basal plasma ammonia level in patients with compensated liver cirrhosis were higher than those of control group where there was no significant difference as regard the blood urea levels. - The renal plasma flow in patients with compensated liver cirrhosis were significant lower than those of contral group, however they were more than expected. -Volume expansion by 1 litre saline 0.9% intravenous infusion in all subjects resulted in the following: •Significant increase in renal plasma flow in patients with well compensated liver cirrhosis without increase in mean arterial blood pressures, heart rates. This could be attributed to decrease in the level of circulating Angiotensin II (ANG II)& Plasma Rennin Activity (PRA). •Significant decrease in plasma ammonia level in both groups of the study. •Significant increase in urinary ammonia excretion in well compensated cirrhotic patients without significant increase in healthy volunteers. This could be attributed to one or both of the following mechanisms: 1- Increase in renal perfusion and hence luminal flow rate 2- Reduction in Renal ammoniogenesis. -There was significant correlation between blood PH in well compensated liver cirrhotic patients and both basal plasma ammonia levels, changes of plasma ammonia levels, and changes of urinary ammonia excretion following volume expansion. -Significant correlation were detected between serum K+ of well compensated liver cirrhosis and both basal plasma ammonia, changes of plasma ammonia levels & changes of urinary ammonia excretion before and after volume expansion by 1 litre 0.9% saline intravenous infusion. -There was significant correlation between basal plasma ammonia in well compensated cirrhotic patients & changes of plasma ammonia levels, & changes of urinary ammonia excretion following volume expansion. -Significant correlations were detected between changes of renal plasma flow in well compensated cirrhotic patients and both changes of plasma ammonia levels & changes of urinary ammonia excretion.