Abstract
There are maturational changes in renal sodium handling in all nephron segments. The very premature infant has renal sodium wasting that can lead to volume depletion and hyponatremia. The term neonate must be in positive sodium balance for growth, which is reflected by the fact that the neonate has a decreased ability to excrete a sodium load compared with the adult. The maturation of sodium transport during renal development is due to changes in both paracellular and transcellular transport. There is a developmental increase in a number of transporters along the nephron during postnatal maturation as well as isoform changes of some important sodium transport proteins such as the Na+/H+ exchanger on the apical membrane of the proximal tubule. Finally, there are mechanisms to increase sodium reabsorption during volume depletion, as well as to promote sodium excretion with volume expansion. There are maturational changes that occur in these homeostatic mechanisms that are essential for survival.
Published Version
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