Ontogeny of aldosterone glucuronidation by the human newborn.
We studied urine excretion of free aldosterone and aldosterone-18-glucuronide by well preterm and fullterm infants during the first week after birth. Total urine aldosterone excretion (UAE) was not influenced by gestational age, but preterm infants excreted a lower percentage of total aldosterone as glucuronide. Mean +/- 2%, 74 +/- 2% and 77 +/- 3% on Day 1 (P less than 0.01); 88 +/- 2%, 74 +/- 2% and 72 +/- 3% on Day 4 (P less than 0.01); and 86 +/- 4%, 76 +/- 3% and 72 +/- 4% on Day 7 (P less than 0.10). Total UAE increased from Day 1 to Day 7 for infants less than 33 wk (P less than 0.05), but not for more mature infants. Percentage excreted as conjugate did not alter during the first week for any group. For infants less than 33 wk, total UAE by those who received prenatal glucocorticoids was higher than by those who did not on Day 1 (0.96 +/- 0.15 vs 0.45 +/- 0.15 nmol/kg per day; P less than 0.025). Percentage excreted as conjugate was not influenced by prenatal glucocorticoids at any postnatal age. Sodium balance was positive for all groups by 1 wk, and did not correlate with either free, conjugated or total UAE for any of the groups in this study. These data suggest that the ability to conjugate aldosterone is related to gestational maturity, and is not altered by prenatal glucocorticoids in infants less than 33 wk gestation. This aspect of aldosterone metabolism does not appear to relate to early postnatal sodium balance.
D000450:Aldosterone / Q000031:analogs & derivatives* / Q000652:urine*; D005260:Female; D005865:Gestational Age; D005965:Glucuronates / Q000494:pharmacology; D006801:Humans; D007231:Infant, Newborn / Q000652:urine*; D007234:Infant, Premature / Q000652:urine*; D008297:Male; D011188:Potassium / Q000652:urine; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D012964:Sodium / Q000652:urine
D005965:Glucuronates; C018447:aldosterone 18-glucuronide; D000450:Aldosterone; D012964:Sodium; D011188:Potassium