Abstract
Nephrocalcinosis is not uncommon in preterm infants, and elevated urinary oxalate excretion is known to be one of the main risk factors. When oxalate excretion was found to be higher in formula-fed than in human milk-fed infants, the formulas' oxalate content was thought to be responsible. The oxalate concentration in human milk (21 samples obtained during lactogenesis; 17 samples obtained during established lactation) and of 16 formula preparations was examined. Citrate and sulfate concentrations were also measured, because both anions influence urinary saturation. The mean (+/- SE) oxalate content of human milk increased approximately 27% from early lactogenesis (70.4 +/- 6.4 micromol/1) to established lactation (96.4 +/- 9.5 micromol/l; p < 0.05). The latter was not different from the mean oxalate concentration of formula (98.2 +/- 11.4 micromol/l), however a fourfold range of measurements was recorded in both groups. The mean citrate content of human milk increased only slightly after early lactogenesis (2.66 +/- 0.22 mmol/l), but remained significantly lower than in formula (3.34 +/- 0.23 mmol/l; p < 0.05). The mean sulfate concentration did not increase and was 13 times lower in human milk (52.1 +/- 9.5 micromol/l) than in formula (688.7 +/- 95.4 micromol/l; p < 0.0001). The higher oxalate excretion in formula-fed infants is not because of the milk's oxalate concentration. Urinary citrate and sulfate excretion may be influenced by their higher concentrations in formula preparations, which may be of clinical importance in the population that is at risk for development of nephrocalcinosis. Nephrocalcinosis is not uncommon in preterm infants, and elevated urinary oxalate excretion is known to be one of the main risk factors. When oxalate excretion was found to be higher in formula-fed than in human milk-fed infants, the formulas' oxalate content was thought to be responsible. The oxalate concentration in human milk (21 samples obtained during lactogenesis; 17 samples obtained during established lactation) and of 16 formula preparations was examined. Citrate and sulfate concentrations were also measured, because both anions influence urinary saturation. The mean (+/- SE) oxalate content of human milk increased approximately 27% from early lactogenesis (70.4 +/- 6.4 micromol/1) to established lactation (96.4 +/- 9.5 micromol/l; p < 0.05). The latter was not different from the mean oxalate concentration of formula (98.2 +/- 11.4 micromol/l), however a fourfold range of measurements was recorded in both groups. The mean citrate content of human milk increased only slightly after early lactogenesis (2.66 +/- 0.22 mmol/l), but remained significantly lower than in formula (3.34 +/- 0.23 mmol/l; p < 0.05). The mean sulfate concentration did not increase and was 13 times lower in human milk (52.1 +/- 9.5 micromol/l) than in formula (688.7 +/- 95.4 micromol/l; p < 0.0001). The higher oxalate excretion in formula-fed infants is not because of the milk's oxalate concentration. Urinary citrate and sulfate excretion may be influenced by their higher concentrations in formula preparations, which may be of clinical importance in the population that is at risk for development of nephrocalcinosis.
