[Nitrogen metabolism and renal amino acid excretion during total parenteral feeding of hypermetabolic patients with various carbohydrate regimes].
During an investigative study about the utilization of parenterally administered amino-acids (AA) in severe catabolic states nitrogen balances, urea production rates and catabolic nitrogen as well as urinary losses of amino-acids were determined in six adult polytraumatized patients treated in an intensive care unit. In addition to 19 g nitrogen (0.3 g N/kg/day) 3,000 kcal (12.5 MJ) were given simultaneously as carbohydrates. Either a mixture of laevulose 20%, glucose 10%, xylitol 10% (LGX) or glucose 50% were infused alternatively for four days in a randomized cross-over scheme. Another group of three patients received the LGX-regime alone for six days altogether. Higher urinary N-losses, increased urea production rates corresponding to a rise in the s.c. catabolic nitrogen were obtained on days where the LGX-mixture was infused; there was also an increased excretion of alpha-amino-N due to a distinct aminoaciduria. Not all amino-acids did react in the same manner. When comparing excretion to supply higher losses (greater than 20%) were observed for: THR greater than TRY greater than VAL greater than ILE greater than PHE. Methionine and alanine were also excreted in higher amounts, whereas under glucose an elevated excretion was especially noted with glutamine and alpha-aminobutyric acid. The increased urea production rate associated with a reduced incorporation of amino-acids as well as the accentuated renal AA-losses under LGX may be ascribed to a slight increase in protein catabolism connected with some impairment of AA-utilization due to a temporary metabolic hepatic 'block'. Under glucose an intensified endogenous mobilization as well as the higher exogenous supply of insulin might be responsible for a somewhat better AA-utilization. Amino-acid clearances under the carbohydrate mixture in the second group were - with the exception of lysine and leucine - raised distinctly similar to values seen in aminoaciduria of other origin. This leads to the assumption that the AA-overflow might result from a partial insufficiency or overload of renal transport ('carrier') systems being responsible for amino-acid reabsorption. The question of an adequate supply - concerning essential amino acids in particular - taking into consideration the relatively high losses under one of the nutritional regimes investigated is shortly touched upon. Finally the possibility of adapting AA-mixtures to the respective carbohydrate solutions in order to improve nitrogen balances and utilization is discussed.