title: Which amino-acids do serum and hemofiltrate of critically ill patients with acute renal failure contain?
abstract: The removal of amino acids during continuous renal replacement therapies induces clinical problems. Previous studies on animals have shown nephroprotective (glycine, alanine) or negative effects (lysine) on renal function in occurrence of acute renal failure. Disturbed metabolism in acute renal failure needs adequate parenteral nutrition. On the other hand, experience with continuous renal replacement therapies of metabolic crises in inborn errors of metabolism indicate a good control of disturbed amino acid metabolism. The aim of our study was to find amino acids, that might play an important role in the pathogenesis, prognosis and detection of acute renal failure and severe illness, so far only estimated by lactic acid. Thirty-three probes (serum and hemofiltrate) were taken from patients, suffering with acute renal failure caused by septic shock, severe pancreatitis and hepatorenal syndrome, one hour after the beginning of extracorporal circulation, the conditions of treatment were standardized. The material was deproteinized and studied by the amino acid analyzer LBK 4251 Apha Plus (Pharmacia, Stockholm, Sweden), while the lactic acid concentration was determined in a standard laboratory. Proline, glycine, alanine, methionine and histidine showed a close relationship to the lactic acid levels, but these amino acids were an essential part of parenteral nutrition. A statistical relationship was also established in (amino acids with amide groups) asparagine, glutamine, citrulline, cystathionine and phosphoethanolamine. The mean values of most of the amino acids were higher than normal, but standard deviations were increased. The presence of these amino acids in hemofiltrate and the good sieving coefficients could mean that the better prognosis of critically ill patients in continuous renal replacement therapies may also be due to continuous control of amino acid levels (especially with amide groups).
authors.affiliation: Department of Internal Medicine A, Ernst-Moritz-Arndt-University Greifswald, Germany.
authors.forename: H J
authors.initials: HJ
authors.lastname: Guth
authors.forename: M
authors.initials: M
authors.lastname: Wiersbitzky
authors.forename: M
authors.initials: M
authors.lastname: Ziesche
authors.forename: H J
authors.initials: HJ
authors.lastname: Rose
authors.forename: G
authors.initials: G
authors.lastname: Kraatz
mesh_terms: D000409:Alanine / Q000097:blood; D000596:Amino Acids / Q000097:blood* / Q000378:metabolism; D001216:Asparagine / Q000097:blood; D002956:Citrulline / Q000097:blood; D003540:Cystathionine / Q000097:blood; D004983:Ethanolamines / Q000097:blood; D005112:Extracorporeal Circulation; D005973:Glutamine / Q000097:blood; D005998:Glycine / Q000097:blood; D006440:Hemofiltration; D006639:Histidine / Q000097:blood; D006801:Humans; D007676:Kidney Failure, Chronic / Q000378:metabolism* / Q000628:therapy; D019344:Lactic Acid / Q000097:blood; D008715:Methionine / Q000097:blood; D011392:Proline / Q000097:blood
chemical_list: D000596:Amino Acids; D004983:Ethanolamines; D005973:Glutamine; D002956:Citrulline; D019344:Lactic Acid; D003540:Cystathionine; D006639:Histidine; D001216:Asparagine; C005448:phosphorylethanolamine; D011392:Proline; D008715:Methionine; D000409:Alanine; D005998:Glycine