Nephrocalcinosis in premature infants: variability in ultrasound detection.

OBJECTIVE: To measure variability among radiologists in the ultrasound diagnosis of nephrocalcinosis in premature infants. METHODOLOGY: In this prospective multicenter study, renal ultrasounds were performed on 54 very low birth weight infants using a 5.0- and 7.5-MHz transducer, and these ultrasounds were read independently by three radiologists. kappa coefficients were calculated to assess variability in identification of nephrocalcinosis among the radiologists. RESULTS: The kappa coefficient (+/- confidence intervals) using a 5.0-MHz transducer was 0.143 (0.108, 0.178); using the 7.5-MHz transducer, the kappa coefficient was 0.268 (0.243, 0.293). All three radiologists agreed in their identification of nephrocalcinosis on 3 of 54 ultrasounds using a 5.0-MHz transducer; a total of 6 of 54 ultrasounds obtained using a 7.5-MHz transducer were read as positive by all three radiologists. CONCLUSION: There is significant variability among radiologists in the ultrasound identification of nephrocalcinosis in premature infants; a 7.5-MHz ultrasound transducer is associated with less variability in recognizing this lesion.

Effect of diuretics on urinary oxalate, calcium, and sodium excretion in very low birth weight infants.

OBJECTIVE: To study the effect of diuretic drugs on urinary oxalate excretion in premature infants, and to examine the relationship between urinary calcium and sodium excretion in premature infants. METHODOLOGY: We measured urinary oxalate, calcium, and sodium excretion in 32 premature infants at approximately 34 weeks gestational age. Seven infants were receiving furosemide, 5 infants were receiving thiazide, 8 infants were receiving furosemide plus thiazide, and 12 infants who were not receiving diuretics served as controls. RESULTS: Urinary oxalate to creatinine ratios in infants receiving furosemide (0.48 +/- .26), thiazide (0.54 +/- .20), furosemide plus thiazide (0.44 +/- .19), and control infants (0.51 +/- .43) were similar by analysis of variance (ANOVA). Data expressed as oxalate concentration gave similar results. Urinary calcium to creatinine ratios in infants receiving furosemide (0.81 +/- .30), thiazide (0.54 +/- .25), furosemide plus thiazide (0.75 +/- .49), and control infants (0.37 +/- .25) were similar by ANOVA. The urinary calcium concentration in infants receiving furosemide plus thiazide (0.085 +/- 0.042 mg/mL) was different from control infants (0.044 +/- .023) by ANOVA and Student-Newman-Keuls test. Urinary calcium to creatinine ratio was correlated with sodium to creatinine ratio (r = .751). CONCLUSION: Urinary oxalate excretion in premature infants is not affected by diuretic drugs. Urinary sodium and calcium excretion are closely linked in sodium supplemented premature infants receiving diuretics. The calciuric effect of furosemide is not decreased by the addition of thiazide in premature infants receiving sodium supplements.

Urinary oxalate excretion in premature infants: effect of human milk versus formula feeding.

OBJECTIVE: To study urinary oxalate excretion in infants fed human milk versus formula, and to compare urinary calcium oxalate and calcium phosphate saturation in premature infants with term infants and adults. METHODOLOGY: We measured urinary oxalate-to-creatinine ratio and urinary oxalate concentration in 15 premature infants fed human milk compared to 16 formula-fed premature infants, and in eight human milk-fed term infants compared to 17 formula-fed term infants. We then studied urinary calcium oxalate and calcium phosphate saturations based on our observations of elevated urinary oxalate excretion in premature infants. Urinary calcium oxalate and calcium phosphate saturations were calculated from urinary concentrations of oxalate, calcium, sodium, potassium, chloride, uric acid, magnesium, phosphorus, and urinary pH. We calculated urinary calcium oxalate and calcium phosphate saturations in nine healthy adults and nine formula-fed term infants to establish control values for urinary saturation. Urinary calcium oxalate and calcium phosphate saturations were determined in nine premature infants receiving a glucose and electrolyte solution, 11 premature infants receiving parenteral nutrition, nine formula-fed premature infants, and 11 human milk-fed premature infants. RESULTS: Urinary oxalate excretion was higher in formula-fed compared to human milk-fed premature infants whether expressed as oxalate-to-creatinine ratio (0.32 +/- 0.04 versus 0.18 +/- 0.03, P < .01) or urinary oxalate concentration (0.047 +/- 0.007 versus 0.022 +/- 0.002 mg/mL, P < .01). Urinary oxalate excretion was higher in formula-fed term infants than in human milk-fed term infants whether expressed as oxalate-to-creatinine ratio (0.14 +/- 0.01 versus 0.07 +/- 0.01, P < .01) or urinary oxalate concentration (0.022 +/- 0.002 versus 0.012 +/- 0.002 mg/mL, P < .01). The urinary calcium oxalate saturation in healthy adults was 2.84 +/- 0.79; the value in formula-fed term infants was 2.12 +/- 0.31. The urinary calcium oxalate saturation was significantly higher in premature infants receiving formula (15.68 +/- 3.15), human milk (15.02 +/- 2.27), or parenteral nutrition (11.38 +/- 2.56) compared to adults or term infants (P < .01). Urinary calcium oxalate saturation in premature infants receiving a glucose and electrolyte solution (2.45 +/- 0.36) was not significantly different from that in adults or term infants. In contrast, urinary calcium phosphate saturation in premature infants as well as term infants and adults was less than 1; precipitation of calcium phosphate is not likely to occur under these conditions. CONCLUSION: Formula-fed infants have higher urinary oxalate excretion than human milk-fed infants. Premature infants receiving standard nutritional regimens may have urinary calcium oxalate saturation levels at which dissolved calcium oxalate may form nuclei of its solid phase.