Abstract
After acute administration of ammonium chloride, infants 1 to 16 months of age were similar to older children in their capacity to acidify their urine. The infants had a higher rate of excretion of titratable acid and a lower rate of excretion of ammonium but were similar in their rate of excretion of total hydrogen ion.Bicarbonate titrations performed in infants during the first year of life demonstrated a threshold ranging from 21.5 to 22.5 mmoles per L, maximal rate of reabsorption from 2.6 to 2.9 mmoles per 100 ml glomerular filtrate, and marked titration splay. A nephronic frequency distribution curve of the ratio of glomerular filtration rate to tubular reabsorptive capacity demonstrated both heterogeneity and skewing to the right, suggesting the presence of significant numbers of nephrons with low tubular transport capacity relative to filtration rate.It is suggested that the "physiologic acidosis" of the infant is due neither to a limited renal capacity to excrete hydrogen ion nor to a reduced capacity for reabsorption of bicarbonate, but rather to a low renal plasma bicarbonate threshold. Although the level of the threshold may relate to the kinetics of bicarbonate reabsorption during this period, it appears to be due at least in part to functional and morphologic heterogeneity of nephrons.