SUMMARY Eighty five 24 hour sodium balance studies and creatinine clearance measurements were performed in 70 infants of gestational age 27-40 weeks and postnatal age 3-68 days. The kidney's capacity to regulate sodium excretion was a function of conceptional age (the sum of gestational age and postnatal age) and an independent effect of postnatal age was also observed-extrauterine existence increased the maturation of this function. The sodium balance was negative in ICO% of infants of <30 weeks' gestation, in 70% at 30-32 weeks, in 46% at 33-35 weeks, and in 0% of >36 weeks, and the incidence of hyponatraemia closely paralleled that of negative sodium balance. Despite a low glomerular filtration rate (GFR) urinary sodium losses were highest in the most immature babies but fractional sodium excretion (FENa) was exponentially related to gestational age. An independent effect of postnatal age could be identified on FENa but not in GFR. These findings indicate that in infants of >33 weeks' gestation sodium conservation is possible because of a favourable balance between the GFR and tubular sodium reabsorption, but that below this age GFR exceeds the limited tubular sodium reabsorption capacity. The rapid increase in sodium reabsorption in the first few postnatal days seems to be due to maturation of distal tubular function, probably mediated by aldosterone. We suggest that the glomerulotubular imbalance for sodium is a consequence of the immaturity of the tubuloglomerular feedback mechanism, and we estimate that the minimum sodium requirement during the first 2 weeks of extrauterine life is 5 mmol (mEq)/kg/day for infants of <30 weeks' gestation and 4 mmol (mEq)/kg/day for those born between 30 and 35 weeks.

Background: The nutritional requirements of prematurely born infants are different from those of babies born at term. Inadequate or inappropriate dietary intake in the neonatal period may have long term adverse consequences on neurodevelopmental function. The late effect of neonatal sodium deficiency or repletion in the premature human infant on neurological development and function has not been examined, despite evidence in animals of a serious adverse effect of salt deprivation on growth of the central nervous system. Methods: Thirty seven of 46 children who had been born prematurely (gestational age of 33 weeks or less) and allocated to diets containing 1-1.5 mmol sodium/day (unsupplemented) or 4-5 mmol sodium/day (supplemented) from the 4th to the 14th postnatal day were recalled at the age of 10-13 years. Detailed studies of neurodevelopmental performance were made, including motor function and assessment of intelligence (IQ), memory and learning, language and executive skills, and behaviour. Sixteen of the children were found to have been in the supplemented group and 21 in the unsupplemented group. Results: Children who had been in the supplemented group performed better in all modalities tested than those from the unsupplemented group. The differences were statistically significant (analysis of variance) for motor function, performance IQ, the general memory index, and behaviour as assessed by the children's parents. The supplemented children outperformed the unsupplemented controls by 10% in all three components of the memory and learning tests (difference not significant but p < 0.1 for each) and in language function (p < 0.05 for object naming) and educational attainment (p < 0.05 for arithmetic age). Conclusions: Infants born at or before 33 weeks gestation require a higher sodium intake in the first two weeks of postnatal life than those born at or near term, and failure to provide such an intake (4-5 mmol/day) may predispose to poor neurodevelopmental outcome in the second decade of life.

SUMMARY Clinical and biochemical effects of supplementing dietary sodium intake to 4 to 5 mmol(mEq)/kg/day from days 4 to 14 of life were studied in 22 infants of gestational age 27 to 34 weeks. These infants were compared with a group of 24 unsupplemented babies. Supplemented infants lost less weight postnatally and regained birthweight more quickly: their improved weight gain continued after supplementation was stopped. Sodium balance was positive at age 5 to 11 days in supplemented babies but slightly negative in controls. Potassium balance was more strongly positive in the supplemented group. Plasma sodium concentration was higher in supplemented infants during weeks 3 and 4. Hyponatraemia was signficantly more common in unsupplemented (37-5%) than supplemented (13-6%) infants. No infant became oedematous, hypernatraemic, or showed evidence of circulatory overload. The incidence of patent ductus arteriosus and necrotising enterocolitis was not increased; no intracranial haemorrhages occurred. Urinary potassium:sodium ratio was lower in supplemented babies than controls suggesting responsiveness of the distal tubule to mineralocorticoids. Providing 4 to 5 mmol(mEq)/kg/day of sodium to infants born before 34 weeks' gestation for the first two postnatal weeks improves growth and biochemical status and causes no undesirable side effects.We have previously shown that preterm babies of less than 35 weeks' gestation have high renal and intestinal sodium losses during the first two weeks of life, leading to negative sodium balance and hyponatraemia (plasma sodium less than 130 mmol(mEq)/l) in many. 2 We concluded that increasing dietary sodium intake to 4 mmol(mEq)/ kg/day for infants of gestational age 31 to 34 weeks and 5 mmol(mEq)/kg/day for infants of less than 31