Enhanced renal vein ammonia efflux after a protein meal in the pig

Background/Aims: The intake of dietary protein has been associated with inc reased arterial ammonia levels. However, the origin of this rise in ammonia levels is unknown. This study was designed to examine whether this increas e is caused by ammonia formed by the gut escaping hepatic clearance, or amm onia formed by the kidney and subsequently released into the circulation. Methods: Splanchnic and renal fluxes of ammonia and amino acids were studie d in 10 pigs that were fed in a randomized cross-over design with a protein meal (n=8), a meal with an equimolar amount of free amino acids (n=8) or a n iso-osmolar NaCl solution (n=6), Results: After the protein meal, and less pronounced after the amino acid m eal, arterial ammonia levels increased from approximately 25 to 75 mu mol/l . Arterial pH changes and splanchnic ammonia release were negligible, The r enal vein ammonia efflux increased after the protein meal (0.67 +/- 0.10 to 1.91 +/- 0.35 pmol/kg bw/min) and to a lesser degree after the amino acid meal (to 1.20 +/- 0.39 mu mol/kg bw/min). Renal uptake of alanine, and not glutamine, increased stoichiometrically, paralleling the enhanced renal vei n ammonia efflux. Conclusions: Arterial ammonia increases after a meal in pigs, coinciding wi th a negligible splanchnic ammonia release, but increased renal vein ammoni a efflux. Thus, post-prandial plasma ammonia levels appear to be mainly rel ated to renal ammoniagenesis, Alanine appears to be the main precursor for this renal ammoniagenesis in the pig.