Abstract
Intrauterine bone mineral accretion can be achieved in VLBW infants when Ca and P are administered in sufficient quantities to result in an urinary excretion of both elements(1). We observed three ELBW infants (650g/26weeks; 780/26; 580/27) who developed serial rib fractures and general severe bone demineralization inspite of an individual Ca/P supplementation monitored by urine Ca/P concentrations(1). Retrospective comparison of all Ca and P concentrations in simultaneously taken plasma and urine samples showed P-excretion at low plasma P concentrations (1.1-1.9 μM), i.e. an DTPR. Renal threshold for P was 2.4-2.8 μM in age-matched controlls. Demineralization was a result of renal P wasting. In one severely growth retarded infant who was born after recording silent CTG this tubular defect was present shortly after birth. Two infants developed DTPR during combined antibiotic treatment for sepsis. Fosfomycin was suspected to have impaired tubular function. Conclusion: DTPR causes severe bone demineralization in preterm infants and interferes with monitoring the P supplementation by measuring urinary P concentrations. (l)Assessment of Ca and P requirements and prevention of osteopenia in VLBW infants. Pediatr. Res. 20:1050(1986).
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