Renal aspects of neonatal sodium homeostasis

Current knowledge on renal sodium handling during the neonatal period is reviewed with particular reference to its clinical implications. It has been demonstrated that fractional sodium excretion is inversely proportional to the maturity of the neonate. The high rate of urinary sodium excretion in the low-birth-weight premature infants results in sodium depletion, hyponatraemia and hypoosmolality; evidence has been provided to indicate that it may contribute to the development of late metabolic acidosis, failure to gain weight and impaired function of the central nervous system. When challenged by salt loading, a significantly more marked natriuretic response could be seen in preterm than in full-term neonates. Acute sodium overdose may cause iatrogenic hypernatraemia and neonatal intracranial haemorrhage. Long-term high sodium intake may induce salt and water retention, peripheral oedema, increased intracranial pressure, congestive heart failure, reopening of the ductus arteriosus and hypertension in adult life. Alterations in salt balance even in the very low-birth weight premature infant result in adaptive changes in the function of the renin-angiotensin-aldosterone system, renal prostaglandin E and F2a production and plasma prolactin level. When drug therapy known to affect renal sodium handling such as indomethacin, furosemide, dopamine, aminophylline and glucocorticoid is prescribed in the perinatal period, neonatal salt and water balance should carefully be monitored.