ABSTRACT. Preterm infants are more prone to bone BMA, bone mineral accretion mineral deficiency the lower their birth weight. To achieve BMC, bone mineral content the intrauterine bone mineral accretion rate postnatally, 74Pi, inorganic phosphorus low-birth-weight infants (median birth weight, 980 g; range VLBW, very low-birth-weight 430-1.580 g) were each supplemented enterally and/or parenterally with calcium and/or phosphorus in gradually increased amounts. The aim was to yield a simultaneous urinary excretion of Ca and inorganic phosphorus (Pi) at low c o n c e n~t i o n s (1-2 mmol/L) in spot urine specimens Postnatal bone mineral deficiency is a condition that is well taken twice weekly. The hypothesis was that the intrauter-known (1-6) in preterm infants and that has gained in imporine mineralization rate (4.5 mg cm-l/lOO weight gain) tance clinically since the rate of survival of VLBW infants has would be achieved postnatally in very low-birth-weight SO greatly improved. Various factors were held to be responsible infants, if they were supplemented with enough ca and/or for bone mineral deficiency, such as deficiencies of vitamin D pi to effect at least a low (1-2 mmol/L) simultaneous (7,8), Ca (7,9), Pi (10-1 3), Ca + Pi (14, 19, as well as parented urinary excretion of both ions, as compared with infants nutrition (16-20), metabolic disease, physiotherapy, long-term ventilation and, finally, treatment with furosemide. both ions and accrete the bone &hilling and co-workers (2 1) described the pivotal biochemiat a lower rate' The in bone miner?1 cal changes in breast milk-and formula-fed preterm infants and was sing1e P~~~~~~ densl-we have the findings many times (22): feeding with tome@ and lo weight gain during perids lo breast milk resulted in the phosp~openic type of rickets with wk. Infants who simuluneously excreted (>Iq2 mmolt severe hypophosphatemia and an absence of urinary Pi, together L, + Pi (' Oe4 mmol/L) in more than Of the urine with hypercalciuria. In contrast, formula-fed infants were charsamples retrospectively showed the highest bone mineral acterized by marginal hypocalcemia, no detectable urinary Ca, accretio~ 5.1 mg cm-'/loo g weight gain, which Was and showed secondary hyperparathyroidism together with hyequivalent to the fetal mineralization rate (4.5). In this perphosphaturia, i.e. the calcipenic type of rickets. The absence group the bone mineral status significantly contributed to of Pi or Ca, respectively, from the urine, is explained by maximal the variance of the bone mineral accretion rate; severely tubular reabsorption of these ions, indicating a deficiency of Ca demineralized infants showed a catch-up mineralization. A and Pi, respectively. The inorganic bone material is the crystalline significantly lower rate (2.4) was Observed in infants who mineral apatite, with the formula Ca5(P04),(0H,F) (23). Owing excreted Ca + Pi in less than half of the urinary samples. to the different amounts and ratios of Ca and Pi in breast milk Supplementation with Ca and Pi UP to the point...