Metabolism of 15 N –Ammonia in Patients With Cirrhosis: A Three–Compartmental Analysis

Open Access
Publisher Website
Google Scholar
Abstract
Urinary 15 N–ammonia and 15 N–urea were measured by gas chromatography–mass spectrometry after the intravenous administration of 15 N–ammonia (0.2 μmol/kg/hr) to 6 volunteers and 11 patients with cirrhosis. Urinary 15 N–nitrogen excretion as ammonia and urea was measured during the 210–min infusion period, and urea synthesis and ammonia conversion to amino acids were analyzed with a three–compartment model using the nonlinear least–squares method. The rate of urea synthesis in control subjects was 14.1 ± 1.2 mg/kg/hr (mean ± S.E.M.), and in cirrhotic patients it was 11.0 ± 3.2 mg/kg/hr. The cirrhotic group was divided into those with compensated cirrhosis (Child class A patients) and those with decompensated cirrhosis (Child classes B and C patients), and the rates of urea synthesis for these groups were 14.5 ± 1.5 and 8.9 ± 1.6 mg/kg/hr, respectively. The difference between decompensated cirrhotic patients and control subjects was statistically significant (p < 0.001). The percentage of ammonia reutilization of a given dose of 15 N–ammonia was 75.9% ± 2.4% in compensated cirrhotic patients and 82.9% ± 3.6% in decompensated cirrhotic patients (p < 0.05). Fasting venous ammonia levels correlated inversely with urea synthesis (p < 0.001) and correlated positively with ammonia reutilization (p < 0.05). These results are consistent with a decreased capacity to synthesize urea and an increased capacity to convert ammonia to amino acids in chronic liver failure. (Hepatology 1992;16:347-352.)

This publication has 22 references indexed in Scilit: