glutaminase and Nephrosis

The erythrocyte enzymes of glutamic acid metabolism (glutaminase I, glutaminase II, glutamic acid decarboxylase, glutamine synthetase, and transaminases) and related amino acids (glutamine, glutamic acid, aspartic acid, alanine, and gamma-aminobutyric acid) were estimated in 69 children with protein-energy malnutrition, 13 with nephrosis, and 10 with Indian childhood cirrhosis. Twenty-one apparently healthy children served as controls. There was a significant increase in the activities of erythrocytic glutaminase I, glutaminase II, glutamic acid decarboxylase, and glutamine synthetase in all the three hypoproteinemic states, while the activities of the transaminases showed a decrease in all the conditions. The concentrations of all the amino acids were significantly increased in both the varieties of protein-energy malnutrition (edematous and nonedematous). In nephrosis and Indian childhood cirrhosis, aspartic acid, alanine, and gamma-aminobutyric acid showed a significant rise. The concentration of glutamic acid was also significantly increased in nephrosis. The observations of the present study suggest an increase in intracellular production of glutamic acid in hypoproteinemia.

Topics: Alanine Transaminase; Amino Acids; Aspartate Aminotransferases; Child, Preschool; Erythrocytes; Glutamate Decarboxylase; Glutamate-Ammonia Ligase; Glutamates; Glutaminase; Humans; Infant; Liver Cirrhosis; Nephrosis; Protein-Energy Malnutrition; Proteins

Topics: Acidosis, Renal Tubular; Aldosterone; Ammonia; Animals; Carbon Dioxide; Glutaminase; Hydrogen-Ion Concentration; Hyperaldosteronism; Kidney; Male; Nephrosis; Potassium; Rats; Sodium