Abstract
Conclusions
Glycosuria resulting from ACTH administration in premature infants is due to an imbalance of glomerulotubular function demonstrated by a rise in GFR/TmG ratio. The cause of the rise in this ratio varied and was due either to a disproportionate rise in glomerular nitration rate or fall in glucose Tm. The nonglycosuric ACTH-treated infants did not show this rise in the GFR/TmG ratio.
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