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

The intake of dietary protein has been associated with increased arterial ammonia levels. However, the origin of this rise in ammonia levels is unknown. This study was designed to examine whether this increase is caused by ammonia formed by the gut escaping hepatic clearance, or ammonia formed by the kidney and subsequently released into the circulation.

Splanchnic and renal fluxes of ammonia and amino acids were studied 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 an iso-osmolar NaCl solution (n = 6).

After the protein meal, and less pronounced after the amino acid meal, arterial ammonia levels increased from approximately 25 to 75 micromol/l. Arterial pH changes and splanchnic ammonia release were negligible. The renal vein ammonia efflux increased after the protein meal (0.67+/-0.10 to 1.94+/-0.35 micromol/kg bw/min) and to a lesser degree after the amino acid meal (to 1.20+/-0.39 micromol/kg bw/ min). Renal uptake of alanine, and not glutamine, increased stoichiometrically, paralleling the enhanced renal vein ammonia efflux.

Arterial ammonia increases after a meal in pigs, coinciding with a negligible splanchnic ammonia release, but increased renal vein ammonia efflux. Thus, post-prandial plasma ammonia levels appear to be mainly related to renal ammoniagenesis. Alanine appears to be the main precursor for this renal ammoniagenesis in the pig.