RENAL RESPONSE OF PREMATURE INFANTS TO ADMINISTRATION OF BICARBONATE AND POTASSIUM

THE OBSERVATIONS to be described were undertaken in an attempt to answer the following questions: 1. Does renal immaturity play a role in the "physiologic" acidosis of the premature infant? 2. Can this acidosis be corrected by the administration of bicarbonate? 3. Is the premature infant able to excrete potassium as readily as the adult? The answers to these questions possess both physiologic and clinical interest. The acidosis of the premature infant has been attributed to increased production of organic acids. However, immaturity of renal functions involving hydrogen ion excretion could be responsible for failure of the infant to correct the acidosis completely. In addition, a decreased maximum rate of tubular reabsorption of bicarbonate due to decreased hydrogen ion excretion would in itself result in a continuous drain on bicarbonate stores. In regard to the second question, it is generally agreed that correction of the "physiologic" acidosis of the premature infant is not indicated. However, further knowledge may reveal circumstances where it is desirable to increase serum bicarbonate. If so, it would be of clinical importance to known whether the serum bicarbonate concentration of the premature infant can be raised to normal adult values by the administration of bicarbonate. If the maximum rate of tubular reabsorption of bicarbonate is decreased, bicarbonate administration would result not in increased serum bicarbonate concentrations but only in increased rate of excretion. The third question has very clear clinical application. Safe treatment of potassium deficiency by the administration of potassium is dependent in large part upon the ability of the kidney to excrete potassium rapidly.