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GAD activity and GABA, the product of GAD action on L-glutamate, are both prominent in mature human renal cortex. GAD activity is low in fetal kidney but rises several fold preterm to establish the characteristic post-term specific activity. The ontogeny of the initial step in the GABA pathway parallels the need for kidney to accommodate acid-base regulation after birth. PLP coenzyme is required for GAD holoenzyme integrity. Fetal renal GAD was frequently undersaturated with PLP in our series of observations, raising the suggestion that maternal vitamin B6 nutrition is not always adequate.

Ontogeny of L-Glutamic Acid Decarboxylase and γ-Aminobutyric Acid Concentration in Human Kidney