E. Pronicka et al., PERSISTENT HYPERCALCIURIA AND ELEVATED 25-HYDROXYVITAMIN D-3 IN CHILDREN WITH INFANTILE HYPERCALCEMIA, Pediatric nephrology, 11(1), 1997, pp. 2-6
The aim of the study was to characterize abnormalities of calcium-phos
phate and vitamin D-3 metabolism in children with a past history of ''
mild'' Lightwood-type idiopathic infantile hypercalcaemia. Seventeen s
eemingly healthy children aged 2-12 years, with long-term idiopathic h
ypercalcaemic syndrome since infancy were studied. Two reference group
s were also included (vitamin D-3 intoxication/healthy and Williams gr
oups). Despite a long-term milk-restricted diet and a restricted vitam
in D-3 intake, urinary calcium excretion in the study group was 0.117
+/- 0.07 mmol/kg per 24 h. Compared with the reference groups (0.047 /- 0.029 and 0.067 +/- 0.06 mmol/kg per 24 h, P<0.05), there was signi
ficant hypercalciuria in the children with idiopathic hypercalcaemia s
ince infancy. Serum concentrations of 25-hydroxyvitamin D-3 in the stu
dy group were also elevated compared with the reference groups (57.4 /- 15.5 vs. 34.6 +/- 9.3 and 22.7 +/- 10.5 ng/ml). 1,25-Dihydroxyvitam
in D-3 levels were at the upper limit of normal (45.9 +/- 13.1 vs. 35.
0 +/- 8.1 and 30.0 +/- 13.7 pg/ml). Non-progressive, clinically silent
nephrocalcinosis was visible on ultrasound examinations. The disturba
nces of vitamin Dg and calcium-phosphate metabolism persistent in the
normocalcaemic phase of idiopathic infantile hypercalcaemia may be a p
rimary metabolic defect of the condition. The mechanisms leading to el
evation of metabolites of 1,25-dihydroxy- and 25-hydroxyvitamin D-3 an
d the relationship between this and persistent hypercalciuria and neph
rocalcinosis need pathophysiological explanation.