Edward L. Pratt

Observations on the urinary amino acid excretion in man : the influence of age and diet.

Abstract Using the Dowex 50 column chromatographic technique of Moore and Stein, studies have been made of free amino acid excretion in 12 infants and two older children in order to evaluate the influence of age and of diet. Consideration has been given to various stand ards of reference for evaluating amino acid excretion, and it is concluded that it is best expressed in terms of creatinine excretion. In terms of creatinine excretion it was found that premature infants excrete roughly ten times as much free amino acid as do subjects ten or more years old, and that full-term infants excrete roughly three times as much as the older subjects. Our data on 10-year-olds reveal values virtually identical with those reported for adults. The pattern of individual amino acid excretion was found to differ in early life from that seen in older children and adults. A number of amino acids are present in greater amount and several are found only at that time of life. Hydroxyproline has been identified in the urine of premature and newborn infants. An unidentified ninhydrin reactant, designated as peak No. 9 is described which has not been observed in subjects more than 5 months old. The anomalous behavior of taurine is described, being present in large quantities in the neonatal period, virtually disappearing thereafter, and reappearing again in quantity by the tenth year. Certain late effects of prematurity are described. The effects of diet on amino aciduria are considered, the indications being that the amino acid output in the urine is influenced to some extent by the diet. Comparisons were made of free amino aciduria on a diet of whole protein (milk) and on a synthetic diet supplying nitrogen as a mixture of natural amino acids. Certain differences were encountered the significance of which is discussed. The disappearance of peak No. 9 on the amino acid diet was particularly striking. Some preliminary attempts to identify it are reported.

Retention of water and electrolyte during recovery in a patient with diabetic acidosis.

Summary The retentions during recovery in apatient with severe diabetic acidosis were 114 Gm. of water, 9 meq. of chloride, 13 meq. of sodium, and 6 meq. of potassium per kilogram of body weight. In the light of this and previousstudies, the significance of losses of water and electrolytes was discussed. It is pointed out that the acidosis is due in large part to accumulation of organic acids and that the loss of Na in relation to chloride is little if any in excess of their ratio in extracellular fluids. The magnitude of the deficits of Na, Cl, and water indicate that about 80 c.c. per kilogram of a fluid containing Na and Cl in the ratio found in extracellular fluids suffices to replace most of the deficits of water and all the deficits of Na and Cl. As long as all fluids are given parenterally, provision for water without electrolyte in glucose solutions must be given to cover the obligatory expenditure of water in urine and as insensible loss. Although potassium deficits are moderate, the effects of insulin are likely to produce a rapid and dangerous decrease in serum potassium concentration. Potassium should therefore be administered as soon as insulin begins to reduce blood sugar (two to six hours). The amount to be given is apparently 2 to 4 meq. per kilogram during the first twenty-four hours.

Idiopathic hyperchloremic renal acidosis

Summary Two cases of idiopathic hyperchloremic renal acidosis are presented. One was diagnosed when the patient was 8 weeks of age by chemical investigation of persistent acidosis. Appropriate treatment, consisting of the addition of sodium citrate to his dietary intake for 20 months, resulted in apparently complete recovery. The other case was diagnosed when the child was 51/2 years of age, when renal calcifications were radiographically visualized. Continued alkali therapy corrected the acidosis and had a favorable effect on the physical development of this patient. The natural course of this disease is presented. The disturbance of the electrolyte metabolism is described, with emphasis on its importance in early detection of this disease and on the elimination of other illnesses which clinically may simulate this condition.