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Assessment of mineral and bone biomarkers highlights a high frequency of hypercalciuria in asymptomatic healthy teenagers
Author(s) -
Bacchetta Justine,
Ginhoux Tiphanie,
Bernoux Delphine,
Dubourg Laurence,
Ranchin Bruno,
Roger Christelle
Publication year - 2019
Publication title -
acta paediatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/apa.14907
Subject(s) - medicine , hypercalciuria , asymptomatic , bone mineral , physiology , pediatrics , calcium , osteoporosis
Aim Assessment of mineral metabolism is complex in paediatrics. Methods We assessed the evolution of the main mineral and bone biomarkers (total/bone alkaline phosphatase ALP/BAP, β‐crosslaps, osteocalcin, sclerostin, C‐terminal and intact FGF23) in 100 healthy teenagers (10‐18 years, 50 boys). Results At a mean age of 13.7 ± 2.2 years, phosphatemia, tubular phosphate reabsorption, ALP and BAP significantly decreased along puberty in both genders, whilst parathyroid hormone (PTH), 25‐vitamin D (25D), FGF23, plasma calcium and urinary calcium were not modified. In girls, osteocalcin, β‐crosslaps and sclerostin significantly decreased at the end of puberty. Calciuria above the crystallisation threshold (>3.8 mmol/L) and urinary calcium/creatinine ratio >0.7 mmol/mmol were found in 39% and 6% of subjects, respectively. Multivariable analyses showed that renal function and PTH were significant predictors of calciuria and urinary calcium/creatinine, whilst 25D remained a predictor only of urinary calcium/creatinine ratio. Conclusion Using the most recent assays, this study provides data for mineral/bone biomarkers across puberty and highlights the risk of hyper‐calciuria in apparent asymptomatic healthy teenagers, not related to calcium intake but rather to 25D. Future studies are required to dissect the underlying mechanisms increasing calciuria and prevent nephrolithiasis as early as during childhood.