# Bone Metabolism Defects in Children With Idiopathic Hypercalciuria: An Update

## TL;DR

This review discusses bone metabolism issues in children with idiopathic hypercalciuria and how they may lead to osteopenia and fractures in adulthood.

## Contribution

The paper provides an updated summary of bone metabolism defects, diagnostic methods, and treatment options in children with idiopathic hypercalciuria.

## Key findings

- Up to one-third of children with idiopathic hypercalciuria have lower bone mineral density.
- Biochemical bone turnover markers can complement DXA scans in monitoring these patients.
- Treatment options include dietary changes, potassium citrate, thiazide diuretics, and bisphosphonates.

## Abstract

Idiopathic hypercalciuria (IH) in adults is considered to be the most common identifiable metabolic risk factor for calcium nephrolithiasis, also contributing to osteopenia and osteoporosis. Data on children and adolescents associating IH with bone metabolism show that up to one-third of such patients present with lower bone mineral density (BMD), increasing the risk of osteopenia, osteoporosis, and bone fractures in adulthood. Several factors, such as the degree of hypercalciuria and the presence of calcium urolithiasis, seem to affect the severity of bone metabolism abnormalities in children with IH. In order to follow these patients, BMD has traditionally been estimated by dual-energy X-ray absorptiometry (DXA) scan. In children, chronological age should be taken into account when measuring BMD, as well as weight, height, and BMI. In addition, biochemical bone turnover markers provide surrogate indices of bone turnover and complement the static measurements of BMD. They respond rapidly to changes in bone physiology, and their measurement can be repeated more frequently. However, since children’s bone mass increases constantly until after puberty, age, sex, and pubertal stage have to be taken into consideration when assessing these markers. In addition, relevant studies in children and adolescents have shown conflicting results. Regarding the management of patients with IH, identification and appropriate treatment are of great importance in order to prevent the formation of kidney stones, as well as to improve bone metabolism defects and decrease fracture risk. Such treatment measures include dietary interventions, potassium citrate supplementation and/or thiazide diuretics, and bisphosphonates in resistant cases. This review summarizes the latest data on bone metabolism defects in children and adolescents with IH, the possible pathomechanisms involved, the biochemical markers that could be used together with DXA to follow these patients, and the available treatment options.