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The intrauterine bone mineral accretion rate can be achieved in preterm infants by supplementation with calcium (Ca) and phosphorus (Pi) up to the point where both ions are simultaneously

excreted with urine. We report on a female preterm infant (birth weight 1030g, gestational age 29 weeks) who unexpectedly developed bone mineral deficieny, measured by single photon

absorption densitometry at right mid humerus (67 mg cm−1 at 1530 g body weight on day 60), in spite of rather high plasma concentrations of Ca (2.6-2.9 mmol/l) and Pi (2.2-3.0 mmol/l) as

well as constant urinary excretion of Ca and Pi. The explanation was found to be an unusual high plasma total protein concentration (82 g/l at birth decreasing to 74 on day 54) leading to

low ionized Ca (0.85-0.95 mmol/l). This subsequently caused secondary hyperparathyroidism (330 pg/ml, 1-84 assay, on day 50) and osteopenia. Oral Ca gluconate (1-2 mmol kg−1 day−1) increased

ionized Ca (1.1 M), normalized plasma PTH (27 pg/l) and allowed good bone mineralization (27 mg cm−1 per 520 g weight gain), which equaled to the intrauterine rate (4.4 mg cm−1 per 100 g

weight gain). Conclusion: Ionized, not total, plasma Ca is relevant to mineralization. In case of high protein concentration calciuria does not reliably indicate calcium surplus as usually

and Ca supplementation should be increased until ionized Ca is normal to achieve normal mineralization.

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