Amino acid metabolism and the liver in renal failure.
The study of amino acid metabolism across the splanchnic organs can be useful for investigating derangements in nitrogen metabolism in chronic renal insufficiency. For this purpose, arterial-hepatic venous differences for 19 free amino acids, ammonia and urea, determined in whole blood, were measured in six patients with chronic renal insufficiency and in six subjects with normal renal function. In normal conditions, the hepatosplanchnic bed significantly extracts glutamine, alanine, glycine, serine, threonine, lysine, arginine, phenylalanine, valine, tyrosine, histidine, leucine, and ammonia, and releases glutamate, citrulline, and urea. In chronic renal insufficiency, glutamine uptake decreases, serine, valine and ammonia uptake disappears, proline extraction becomes present, citrulline output is no longer detectable and glutamate release falls slightly. Furthermore, the splanchnic uptake of ammonia and the output of urea into the hepatic veins are markedly reduced. Since glutamine and ammonia are major substrates for urea synthesis, their lower uptakes, as observed in renal insufficiency, may be consistent with the reduced urea output. The changes in splanchnic metabolism observed in chronic renal insufficiency have a minor effect on the abnormalities in circulating amino acids. Finally, the splanchnic metabolism shows an important role in the homeostasis of circulating tyrosine and proline.
D000328:Adult; D000596:Amino Acids / Q000097:blood*; D000641:Ammonia / Q000097:blood; D001158:Arteries; D005260:Female; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism*; D008099:Liver / Q000378:metabolism*; D008297:Male; D008875:Middle Aged; D014508:Urea / Q000097:blood; D014680:Veins
D000596:Amino Acids; D000641:Ammonia; D014508:Urea