Renal acid excretion in infants with the respiratory distress syndrome.

Abstract

Extract: Acid-base balance in blood and hydrogen ion, phosphorus concentrations, and acid-base excretion in urine were measured in 10 infants with respiratory distress syndrome (RDS), in 8 control full term infants, and in 7 control premature infants on days 1, 2, and 3 of life. Infants with RDS were acidemic in comparison with full term and premature control infants. Hydrogen ion concentrations in urine were similar for premature control subjects and acidemic infants with RDS but lower in comparison with those of full term control infants. The inability of infants with RDS, in the face of acidemia, to create an appreciable urine to plasma hydrogen ion concentration gradient provided evidence for a renal tubular deficiency in hydrogen ion secretion. Phosphate levels in urine and, as a result, titratable acid were usually low in the three groups of infants. Relative phosphaturia did occur in some infants with RDS, but, because of the deficiency in hydrogen ion secretion, urinary phosphate was often not utilized as titratable acid. At high urinary concentrations of hydrogen ion (above 400 μmEq/liter), control premature infants and acidemic infants with RDS excreted urine having lower ammonium concentration than that found in control full term infants. The inability of infants with RDS with acidemia to excrete ammonium when hydrogen ion concentrations in urine were high was evidence of a renal tubular deficiency in ammonia production. Infants with RDS differed from control premature infants by having high hydrogen ion and bicarbonate concentrations in blood in relation to higher blood PCO2 values. In addition, at low hydrogen ion concentrations in urine, infants with RDS excreted urine that contained higher concentrations of bicarbonate than that found in control premature infants. Because infants with RDS did not excrete ammonium, they could not compensate for the increased acid load and bicarbonate excretion associated with respiratory acidemia. In addition, they could not compensate for the low titratable acid, which resulted from decreased excretion of phosphate, characteristic of the newborn period. Infants with RDS did not respond to acidemia by increasing net acid excretion in urine beyond that excreted by control infants. Indeed, some infants with RDS inappropriately excreted base, thereby aggravating their already existing acidemia. Speculation: Low gestational and postnatal age is the likely etiologic factor responsible for the decreased capacity for urinary acid excretion seen in infants with RDS. The apparent improvement in renal tubula hydrogen ion secretion with increasing gestational age may be associated with maturation of an enzyme system such as carbonic anhydrase. Likewise, the apparent improvement in renal tubular ammonia production with increasing gestational age may occur in relation to maturation of an enzyme system such as glutaminase.