ICCBH2013 Poster Presentations (1) (201 abstracts)
1Medical University of Bialystok, Bialystok, Poland.
Objectives: Idiopathic hypercalciuria may infer not only an increased risk of nephrolithiasis but may also be associated with reduced bone mineral density (BMD) in adults. However, little is known about relationships between hypercalciuria, oxaluria, urolithiasis, citraturia and fracture risk in children. The aim of this cross-sectional study was to evaluate associations between hypercalciuria, urinary oxalate and citrate, BMD and fractures in hypercalciuric children.
Methods: Medical records were studied to evaluate history of fractures, which were documented by X-ray examination. Dual energy X-ray absorptiometry (DXA) was used to assess body composition, bone mineral content (BMC) and BMD in total body and lumbar spine L1L4 in 40 children and adolescents (26 boys and 14 girls) aged 3.518 years (mean±S.D.: 14.9±3.3) with hypercalciuria and/or urinary calcium oxalate stones (87.5% of the sample) diagnosed using high resolution ultrasonography. Urinary calcium, phosphate, uric acid excretion, oxaluria, and citraturia were invetsigated in the 24-h urine collections.
Results: Mean Z-score for spine BMD was −1.08±1.09. Decreased BMD (Z-score below −2.0) was found in nine subjects (22.5% of the sample). Of all studied children, 13 (32.5%; boys/girls: 10/3) sustained 20 low-energy fractures in the peripheral skeleton (forearm, wrist, tibia, and ankle). Subjects with fractures had significantly lower citraturia rate (467±296 mg/g creatinine/24 h) compared with those fracture-free (484±266 mg/g creatinine/24 h) (P=0.02). Urinary citrate excretion was positively correlated with BMD (adjusted for age and lean mass) only in the fractured children (r=0.76, P=0.04), whereas no such correlation was observed in children without fractures. No associations were found between calciuria, oxaluria, uricosuria, phosphaturia and bone mass or fractures.
Conclusions: Deficits in BMD among hypercalciuric children and adolescents are common although not associated with calciuria or oxaluria. Small sample size in this study, however, limits inferences that could be drawn. Our findings suggest that prolonged hypocitraturia may be, at least partly, an independent risk factor of both reduced peak bone mass and an increased fragility during growth. Whether the life-long risk of osteoporotic fractures attributable to low citrates will be sustained in these patients is unclear.