Persistent hypercalciuria and elevated 25-hydroxyvitamin D3 in children with infantile hypercalcaemia

• Published in: Pediatric nephrology (Berlin, West) Vol. 11; no. 1; pp. 2 - 6
• Main Authors: Pronicka, E, Rowińska, E, Kulczycka, H, Lukaszkiewicz, J, Lorenc, R, Janas, R
• Format: Journal Article
• Language: English
• Published: Germany Springer Nature B.V 01.02.1997
• Subjects: Adolescent; Calcifediol - urine; Calcitonin - blood; Calcium - blood; Calcium - metabolism; Calcium Metabolism Disorders - urine; Child; Child, Preschool; Female; Humans; Hypercalcemia - urine; Infant; Kidney Function Tests; Male; Nephrocalcinosis - urine; Parathyroid Hormone - blood; Phosphorus - blood; Phosphorus - metabolism
• ISSN: 0931-041X; 1432-198X
• DOI: 10.1007/s004670050221

The aim of the study was to characterize abnormalities of calcium-phosphate and vitamin D3 metabolism in children with a past history of "mild" Lightwood-type idiopathic infantile hypercalcaemia. Seventeen seemingly healthy children aged 2-12 years, with long-term idiopathic hypercalcaemic syndrome since infancy were studied. Two reference groups were also included (vitamin D3 intoxication/healthy and Williams groups). Despite a long-term milk-restricted diet and a restricted vitamin D3 intake, urinary calcium excretion in the study group was 0.117 +/- 0.07 mumol/kg per 24 h. Compared with the reference groups (0.047 +/- 0.029 and 0.067 +/- 0.06 mumol/kg per 24 h, P < 0.05), there was significant hypercalciuria in the children with idiopathic hypercalcaemia since infancy. Serum concentrations of 25-hydroxyvitamin D3 in the study 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-Dihydroxyvitamin D3 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 disturbances of vitamin D3 and calcium-phosphate metabolism persistent in the normocalcaemic phase of idiopathic infantile hypercalcaemia may be a primary metabolic defect of the condition. The mechanisms leading to elevation of metabolites of 1,25-dihydroxy- and 25-hydroxyvitamin D3 and the relationship between this and persistent hypercalciuria and nephrocalcinosis need pathophysiological explanation.