Food mineral composition and acid–base balance in preterm infants
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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.
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 (PCO2) 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.
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.