In preterm neonates, functional limits of pulmonary and/or renal regulation processes and the considerable acidload of common formulas predispose to a great risk for the development of latent metabolic acidosis, characterized by e.g.impaired mineralization and reduced growth. Furthermore, in a prospective study in very low birth weight-infants, latentmetabolic acidosis was assumed to contribute to the development of nephrocalcinosis. To obtain fundamental data of acidbaseregulation in preterm infants under different diets, we investigated 48 preterm 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 modifiedbatch with reduced acid load). Irrespective of the diet, we could not find notable differences between individual data ofacid-base status in blood samples. In contrast, dietary acid-base intake was accurately reflected in the urine, pointing to effectiveindividual compensation of alimentary acid-load by renal base saving mechanisms. Thus, in preterm infants, nutritionalacid-base challenges can be judged earlier and more safely by urinary than by blood acid-base analysis A physiologicallybased and empirically adjusted calculation model allows to estimate the impact of mineral and protein content ofa formula on the urinary ionogram and thus on the average renal net acid excretion in a regularly fed and growing preterminfant. The algorithm of this proposed calculation model could prove to be a useful tool in the design of new formulaswith adaequate base supply for preterm infants.
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