Effects of high-volume plasmapheresis on ammonia, urea, and amino acids in patients with acute liver failure

Abstract

OBJECTIVE: In acute liver failure (ALF), urea production is severely impaired, and detoxification of ammonia by glutamine synthesis plays an important protective role. The aim of this study was to examine the effects of therapeutic high-volume plasmapheresis (HVP) on arterial concentrations and splanchnic exchange rates of ammonia, urea, and amino acids—in particular, glutamine. METHODS: A quantity of 8 L of plasma was exchanged over the course of 7 h in 11 patients with ALF after development of hepatic encephalopathy grade III–IV. Splanchnic exchange rates of ammonia, urea, and amino acids were measured by use of liver vein catheterization. RESULTS: HVP removed ammonia and glutamine at a rate of 1 μmol/min and 27 μmol/min, respectively. Arterial ammonia decreased from 160 ± 65 to 114 ± 50 μmol/L ( p < 0.001). In contrast, arterial glutamine was only minimally changed from 1791 ± 1655 to 1764 ± 1875 μmol/L (NS). This implied that the rate of systemic glutamine synthesis was increased by 27 μmol/min. Splanchnic exchange rates (before vs after HVP) were as follows: for ammonia, −93 ± 101 versus −70 ± 80 μmol/min (NS); urea-nitrogen, 0.08 ± 1.64 versus −0.31 ± 0.45 mmol/min (NS); alanine, −73 ± 151 versus 12 ± 83 μmol/min ( p < 0.05); and glutamine: 132 ± 246 versus 186 ± 285 μmol/min (NS), with negative values denoting release. CONCLUSIONS: Arterial ammonia decreased during HVP in patients with ALF. The data suggest that this effect of HVP could be explained by increased hepatic urea synthesis and possibly by increased glutamine synthesis in muscle tissue.