title: [Effect of hypoproteic diets enriched with essential and non-essential amino acids on the uninephrectomized rat ].
abstract: Hyperalimentation solutions, with low protein content but rich in amino acids, have been more frequently used as a dietary treatment for renal terminal patients, with the purpose to increase their survival. However, the literature in this respect is contradictory. Some authors justify the use of amino acids due to the fact that they seem to regenerate damaged tubular cells (glycine, for example). Other authors, on the contrary, do not agree with this position, since some amino acids, like L-Serine and Lysine, are nephrotoxic. In 1977, it was demostrated that Lysine and Arginine inhibited protein tubular reabsorption, inducing proteinuria, while Glycine, Alanine, Asparagine and Glutamic Acid did not. In order to clarify this issue, we carried out a controlled animal study using uninephrectomized rats fed during nine weeks, with different hypoproteinic diets (4% protein content), enriched individually with five different amino acids. The hypoproteinic diets were enriched with Lysine and Arginine (essential amino acids) and Proline, Glutamic Acid and Asparagine (non essential amino acids). Assays for serum biochemical markers and renal function were carried-out pre-nephrectomy, two weeks after nephrectomy (post-nephrectomy control) and nine weeks post-diet for all the animals, no matter the diet to which they were subjected, the serum biochemistry results showed that all the hypoproteinic diets, enriched with amino acids, affected the renal function. The nephrotoxicity of the tested amino acids, followed this decreasing order: Glutamic Acid > Proline > Lysine > Asparagine > Arginine. hypoproteinic diets enriched with Lysine, Asparagine and Arginine, produced glomerular hyperfiltration, without proteinuria. In summary, our results point towards the idea that, contrarily to what has been described in the literature by some authors: enrichment of hypoproteinic diets with certain amino acids does not seem to protect against progression of renal disease in physiologically compromised kidneys.
authors.affiliation: Universidad Central de Venezuela, Sección de Investigaciones Cardio-Renales, Instituto de Medicina Experimental, Facultad de Medicina, Apartado Postal 50587, Caracas 1050, Venezuela.
authors.forename: Virginia Leticia
authors.initials: VL
authors.lastname: Colina
authors.forename: Margarita
authors.initials: M
authors.lastname: Pérez-Gonzalez
authors.forename: Jacobo
authors.initials: J
authors.lastname: Villalobos
authors.forename: Vito
authors.initials: V
authors.lastname: Lamanna
mesh_terms: D000596:Amino Acids / Q000378:metabolism / Q000494:pharmacology; D000601:Amino Acids, Essential / Q000378:metabolism; D000818:Animals; D018753:Diet, Protein-Restricted; D005527:Food, Fortified; D005919:Glomerular Filtration Rate; D007668:Kidney / Q000187:drug effects / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000378:metabolism / Q000628:therapy; D008297:Male; D023421:Models, Animal; D009392:Nephrectomy; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000596:Amino Acids; D000601:Amino Acids, Essential