ESPE Abstracts

Background and hypothesis: The neonatal period is characterized by high urinary sodium loss, most notably in preterm infants that questions the ability of the mineralocorticoid pathway to maintain sodium homeostasis.

Results: We have demonstrated that neonatal sodium wasting is associated with a physiological renal aldosterone resistance in relation to a low renal mineralocorticoid receptor (MR) expression at birth in full-term infants, both in humans and mice, along with a down regulation of other mineralocorticoid signaling key-players. Moreover, very preterm infants present with defective aldosterone secretion while the kidney remains sensitive to aldosterone action owing to transient MR expression in the distal tubule during this period. Conversely, high circulating cortisol/corticosterone levels along with detectable renal glucocorticoid receptor are present at birth, consistent with functional glucocorticoid-signaling pathway both in preterm and full-term newborns.

Conclusion: Thus, the neonatal period is characterized by defective mineralocorticoid signaling from two different mechanisms in preterm and full-term newborns, whereas renal glucocorticoid signaling is functional and very likely implicated in fetal programming. These results open new therapeutic possibilities for preterm infants in order to prevent from sodium wasting.