Urinary hyperexcretion of proline, hydroxyproline and glycine is a defined component of the transient impairment in tubular absorption of amino acids after birth in man and rat. In both species, loss of iminoaciduria precedes reduction of hyper-glycinuria. This coincides with in vitro evidence in rat for phased “activation” of substrate-specific membrane carriers, the one for proline appearing early, that for glycine, late. “Activation” apparently involves appearance of new carrier proteins rather than gain in energy coupling to existing carriers, since studies of amino acid interaction during influx, heteroexchange and inhibition of energy metabolism indicate a specific initial lack of relevant carriers. However “maturation” of total amino acid transport in kidney also involves another component. By comparing Vmax for uptake in vitro of proline, glycine and α-amino isobutyric acid on carriers present from birth, we found their relative capacities to increase synchronously after birth. This is compatible either with increasing membrane area or with more efficient coupling of energy to transport. Thus changes both in specific activity of carriers and in total membrane activity characterize ontogeny of amino acid transport in kidney.