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Published on: January 29, 2018
Bone alterations in children with idiopathic hypercalciuria at the time of diagnosis
Maria-Goretti Moreira Guimarães Penido1, Eleonora Moreira Lima, Viviane Santuari Parizotto Marino
1Pediatric Nephrology Unit, University Hospital, Federal University of Minas Gerais, Belo Horizonte, Brazil.
Insights
Children with idiopathic hypercalciuria (IH) show altered bone metabolism and osteopenia at diagnosis. Bone resorption markers like N telopeptide are key for early detection and preventing future bone issues.
Area of Science:
- Pediatric Nephrology
- Pediatric Endocrinology
- Bone Metabolism
Background:
- Idiopathic hypercalciuria (IH) can lead to bone alterations in children.
- Early identification of bone metabolism changes is crucial for managing IH.
Purpose of the Study:
- To evaluate bone mass in children with IH at diagnosis.
- To compare bone metabolism markers and bone mineral density (BMD) between children with IH and healthy controls.
Main Methods:
- Recruited 88 children with IH and 29 healthy controls.
- Measured serum and urinary markers of kidney and bone metabolism.
- Performed bone densitometry (BMD, BMC, Z scores) on lumbar spine, whole body, and femoral neck.
Main Results:
- Children with IH had higher serum alkaline phosphatase, PTH, urinary calcium, and uric acid.
- Lower urinary volume and citrate excretion were observed in children with IH.
- Significantly reduced BMD, BMC, and Z scores at the lumbar spine, whole body, and femoral neck in children with IH.
- Osteopenia (reduced BMDvol) found in 35% of children with IH.
- Higher urinary N telopeptide (bone resorption marker) correlated with lower BMD.
Conclusions:
- Altered bone metabolism and osteopenia are present at diagnosis in children with IH.
- Urinary N telopeptide is a valuable early marker for bone alterations in IH.
- Bone metabolism assessment is essential in IH to prevent osteoporosis and fractures.
Abstract:
Some children with idiopathic hypercalciuria (IH) develop bone alterations at some stage of the disease. The aims of this study were to evaluate bone mass in 88 children with IH (G1) at the time of diagnosis and to compare the findings with data for a control group of 29 normal children (G2). Kidney and bone metabolism markers were measured in both groups, and bone densitometry was performed. Serum alkaline phosphatase, intact parathyroid hormone, urinary calcium and uric acid were significantly higher in G1, whereas urinary volume and urinary citrate excretion were lower. The following densitometric parameters were significantly lower in G1: (1) lumbar spine (L(2)-L(4)) bone mineral density (BMD), bone mineral content (BMC), BMC corrected for height and for width of the vertebra, volumetric BMD (BMDvol), and Z score; (2) whole-body BMD; (3) femoral neck BMD. Lumbar spine BMDvol was reduced (osteopenia) in 35% of the patients compared with G2. N telopeptide, a urinary marker of bone resorption, was significantly higher in G1 than in G2, and was negatively correlated with lumbar spine BMD and BMDvol. Children with urinary lithiasis or idiopathic hyperuricosuria associated with IH showed no significant differences in bone metabolism compared with children without these associations. We conclude that (1) there is an altered bone metabolism in IH, with osteopenia already present at diagnosis in 35% of the patients; (2) N telopeptide is one of the most useful markers of bone alterations in IH, especially at an early stage of the disease; (3) investigation of bone metabolism is necessary in IH to prevent future serious consequences such as osteoporosis and bone fractures.
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