Food mineral composition and acid-base balance in preterm infants.

BACKGROUND: Due to a transient age-related low renal capacity for net acid excretion, preterm infants fed formula are at a considerable risk of spontaneously developing incipient late metabolic acidosis, clinically characterized by e.g., disturbed bone mineralization and impaired growth. AIM OF THE STUDY: From acid-base data in blood and urine under different diets of modified human milk or preterm formulas is attempted to explore the impact of food mineral (and protein) composition on renal regulation and systemic acid-base balance in preterm infants. PATIENTS AND METHODS: Data were collected from 48 infants fed their own mother's milk (28 native human milk, 20 enriched with fortifier) and 34 patients on formula (23 on a standard batch, 11 on a modified batch with reduced acid load). Intake of food was measured and acid-base data were determined in blood and timed-urine (8-12 h) samples. RESULTS: Differences in mineral composition of the diets led to considerable differences of daily "alkali-intake", without significant effects on non-respiratory (base excess, BE) and respiratory (PCO(2)) acid-base data in the blood. In contrast, a highly significant proportionality between individual dietary alkali intake and daily renal base (Na(+) + K(+)-Cl(-)) excretion was observed (y = 0.32x-0.70, n = 80, r = 0.77, P < 0.0001), irrespective of the type of the diet. CONCLUSION: Renal base saving mechanisms are normally effective in preterm infants to compensate for differences in dietary acid-base load. Generally, nutritional acid-base challenges can be judged much earlier and more safely by urinary than by blood acid-base analysis. Taking into account the age specific low capacity for renal NAE, the relatively high nutritional acid load of preterm standard formula should be reduced.

Development of nephrocalcinosis in very low birth weight infants.

Premature infants undergo intensive growth during the postnatal period. Adequate mineralization is dependent on sufficient intake of calcium (Ca) and phosphorus (P). However, Ca and P supplementation can be associated with some risks, for example development of nephrocalcinosis. We investigated pathophysiological risk factors in premature very low birth weight (VLBW) infants associated with the development of nephrocalcinosis. From June 1994 to September 1995 all preterm neonates with a birth weight below 1,500 g were screened prospectively. At regular intervals of 2 weeks, ultrasonography (US) of the kidneys was performed and parameters of mineral metabolism were assessed in blood and spot urine samples. For analysis, premature infants with nephrocalcinosis (group N) were compared with infants without nephrocalcinosis (group R) and with a retrospectively pair-matched subgroup of premature infants without nephrocalcinosis (control group C) taken from the same study. Nephrocalcinosis was detected in 20 of 114 preterm neonates (group N, 17.5%). Of these 20 infants with nephrocalcinosis, 16 presented with a tendency towards systemic acidosis (pH<7.25) on day 2-7, compared with only 4 of 20 premature infants of the control group. Premature infants of group N had a lower serum P at 2 weeks of life and 5 (versus 0 patients of the control group C) had transient hypophosphatemia (serum P<1.6 mmol/l). Moreover, the Ca/creatinine ratio in spot urine specimens tended to be higher (P<0.1) in patients developing nephrocalcinosis. There were no significant differences in the duration of ventilation, the length of stay in the intensive care unit, and duration and frequency of furosemide and steroid treatment between the groups N and C. VLBW premature infants developing nephrocalcinosis frequently presented with slightly impaired acid-base homoeostasis within the 1st week, followed by signs of impaired mineralization (and immature or impaired renal function) within 2 weeks. In VLBW premature infants, close observation of acid-base status and regular analysis of spot urine specimens (Ca, P, creatinine) during the first weeks of life may help to identify those premature infants at risk for nephrocalcinosis.