• DXA
• disorders of calcium/phosphate metabolism
• osteoporosis
• type 1 diabetes

• Humans
• Adolescent
• Diabetes Mellitus, Type 1/urine
• Diabetes Mellitus, Type 1/complications
• Diabetes Mellitus, Type 1/metabolism
• Male
• Female
• Child
• Calcium/urine
• Young Adult
• Bone Density/physiology
• Longitudinal Studies
• Cross-Sectional Studies
• Biomarkers/urine
• Glycated Hemoglobin/analysis
• Bone and Bones/metabolism

• K23 DK114477 NIDDK NIH HHS
• NIH HHS

• bone formation indices
• bone mass density
• bone resorption indices
• children
• idiopathic hypercalciuria

• Bone health
• Bone mineral density
• Nephrolithiasis
• Skeletal growth

• Nephrolithiasis/complications
• Nephrolithiasis/physiopathology
• Nephrolithiasis/urine
• Bone Density/physiology
• Hypercalciuria/etiology
• Hypercalciuria/physiopathology
• Hypercalciuria/urine
• Bone Diseases, Metabolic/epidemiology
• Bone Diseases, Metabolic/etiology
• Bone Diseases, Metabolic/physiopathology
• Bone Diseases, Metabolic/urine
• Humans
• Male
• Female
• Skeleton/growth & development
• Skeleton/physiopathology
• Bone Development/physiology
• Bone Resorption/epidemiology
• Bone Resorption/etiology
• Bone Resorption/physiopathology
• Bone Resorption/urine
• Age Factors
• Sex Factors
• Risk Factors
• Vascular Calcification/epidemiology
• Vascular Calcification/physiopathology
• Cardiovascular Diseases/epidemiology
• Cardiovascular Diseases/physiopathology
• Fractures, Bone/epidemiology
• Fractures, Bone/etiology
• Fractures, Bone/physiopathology
• Fractures, Bone/prevention & control

• Humans
• Nephrolithiasis/prevention & control
• Sodium Chloride Symporter Inhibitors/therapeutic use

• Diuretics
• Diuréticos, Cálculos renales
• Hipercaliuria idiopática
• Idiopathic hypercalciuria
• Kidney stones
• Revisión sistemática
• Systematic review

• Child
• Adult
• Humans
• Female
• Hypercalciuria
• Kidney Calculi
• Diuretics/adverse effects
• Osteoporosis/complications

The incidence of urolithiasis (UL) is increasing, and it has become more common in children and adolescents over the past few decades. Hypercalciuria is the leading metabolic risk factor of pediatric UL, and it has high morbidity, with or without lithiasis as hematuria and impairment of bone mass. The reduction in bone mineral density has already been described in pediatric idiopathic hypercalciuria (IH), and the precise mechanisms of bone loss or failure to achieve adequate bone mass gain remain unknown. A current understanding is that hypercalciuria throughout life can be considered a risk of change in bone structure and low bone mass throughout life. However, it is still not entirely known whether hypercalciuria throughout life can compromise the quality of the mass. The peak bone mass is achieved by late adolescence, peaking at the end of the second decade of life. This accumulation should occur without interference in order to achieve the peak of optimal bone mass. The bone mass acquired during childhood and adolescence is a major determinant of adult bone health, and its accumulation should occur without interference. This raises the critical question of whether adult osteoporosis and the risk of fractures are initiated during childhood. Pediatricians should be aware of this pediatric problem and investigate their patients. They should have the knowledge and ability to diagnose and initially manage patients with IH, with or without UL.

• Children
• Adolescents
• Hypercalciuria
• Bone mineral density
• Kidney stone

• Diuretics
• Diuréticos, Cálculos renales
• Hipercaliuria idiopática
• Idiopathic hypercalciuria
• Kidney stones
• Revisión sistemática
• Systematic review

Hypercalciuria is the most common metabolic risk factor for calcium urolithiasis and is associated with bone loss in adult patients. Reduced bone mineral density (BMD) was already described in idiopathic hypercalciuria (IH) children, but the precise mechanisms of bone loss or inadequate bone mass gain remain unknown. Life-long hypercalciuria might be considered a risk to change bone structure and determine low bone mass throughout life. The peak of bone mass should occur without interferences. A beneficial effect of citrate formulations and thiazides on bone mass in adult and pediatric patients with IH have been shown.

To evaluate whether pharmacological therapy has a beneficial effect on bone mass in children and adolescents with IH.

This retrospective cohort study evaluated 40 hypercalciuric children non-responsive to lifestyle and diet changes. After a 2-mo run-in period of citrate formulation (Kcitrate) usage, the first bone densitometry (DXA) was ordered. In patients with sustained hypercalciuria, a thiazide diuretic was prescribed. The second DXA was performed after 12 mo. Bone densitometry was performed by DXA at lumbar spine (L2-L4). A 24-h urine (calcium, citrate, creatinine) and blood samples (urea, creatinine, uric acid, calcium, phosphorus, magnesium, chloride, hemoglobin) were obtained. Clinical data included age, gender, weight, height and body mass index.

Forty IH children; median age 10.5 year and median time follow-up 6.0 year were evaluated. Nine patients were treated with Kcitrate (G1) and 31 with Kcitrate + thiazide (G2). There were no differences in age, gender, body mass index z-score and biochemical parameters between G1 and G2. There were no increases in total cholesterol, kalemia and magnesemia. Calciuria decreased in both groups after treatment. Lumbar spine BMD z-score increased after thiazide treatment in G2. There was no improvement in G1.

Results point to a beneficial effect of thiazide on lumbar spine BMD z-score in children with IH. Further studies are necessary to confirm the results of the present study.

• Children
• Adolescent
• Hypercalciuria
• Bone mineral density
• Thiazides
• Citrate

Vitamin D supplementation in patients with urolithiasis and hypercalciuria is considered to be unsafe. We analyzed the impact of vitamin D supplementation on selected health status parameters in children with idiopathic hypercalciuria. The study included 36 children with urolithiasis resulting from excessive calcium excretion. The level of calcium and 25(OH)D (hydroxylated vitamin D - calcidiol) in serum, urinary calcium excretion and the presence of stones in urinary tract were assessed prospectively. Blood and urine samples were collected at the time when the patient was qualified for the study and every three months up to 24 month of vitamin D intake at a dose of 400 or 800 IU/day. At time zero and at 12, and 24 months of vitamin D supplementation, densitometry was performed. Supplementation with vitamin D caused a statistically significant increase in the concentration of 25(OH)D in serum. There were no significant changes in calcium concentration in serum, excretion of calcium in urine but also in bone density. There was no significant increase in the risk of formation or development of stones in the urinary tract. Supplementation with vitamin D (400–800 IU/day) in children with idiopathic hypercalciuria significantly increases 25(OH)D concentration, does not affect calciuria, but also does not improve bone density.

• bone density
• children
• idiopathic hypercalciuria
• urolithiasis
• vitamin D treatment

• Activin-A
• Bisphosphonates
• Denosumab
• Osteoporosis
• Thalassemia

In the past few decades pediatric urolithiasis has become more frequent. The reason for this increase is not completely clear but has been attributed to changes in climate, nutritional habits and possibly other environmental factors. Although less frequent than adult stone disease, urolithiasis in the pediatric age group is also related to significant morbidity, particularly since stones tend to recur, and, thus, should not be underestimated. Most children with idiopathic stone disease have an underlying metabolic abnormality substantiating the importance of metabolic evaluation already following initial diagnosis of urolithiasis. Identification of the metabolic abnormality allows for more specific prescription of non pharmacological and pharmacological interventions aimed at preventing recurrent stone formation. A better understanding of the causes of kidney stone disease will provide better strategies for stone prevention in children.

• Urolithiasis
• Hypercalciuria
• Cystinuria
• Hyperoxaluria
• Treatment
• Prevention

Idiopathic hypercalciuria (IH) is the leading metabolic risk factor for urolithiasis and affects all age groups without gender or race predominance. IH has a high morbidity with or without lithiasis and reduced bone mineral density (BMD), as described previously in pediatric patients as well as in adults. The pathogenesis of IH is complex and not completely understood, given that urinary excretion of calcium is the end result of an interplay between three organs (gut, bone and kidney), which is further orchestrated by hormones, such as 1,25 dihydroxyvitamin D, parathyroid hormone, calcitonin and fosfatonins (i.e., fibroblast growth-factor-23). Usually, a primary defect in one organ induces compensatory mechanisms in the remaining two organs, such as increased absorption of calcium in the gut secondary to a primary renal loss. Thus, IH is a systemic abnormality of calcium homeostasis with changes in cellular transport of this ion in intestines, kidneys and bones. Reduced BMD has been demonstrated in pediatric patients diagnosed with IH. However, the precise mechanisms of bone loss or failure of adequate bone mass gain are still unknown. The largest accumulation of bone mass occurs during childhood and adolescence, peaking at the end of the second decade of life. This accumulation should occur without interference to achieve the peak of optimal bone mass. Any interference may be a risk factor for the reduction of bone mass with increased risk of fractures in adulthood. This review will address the pathogenesis of IH and its consequence in bone mass.

• Bone mineral disease
• Bone mineral density
• Hypercalciuria
• Children
• Urine