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[Idiopathic hypercalciuria in childhood]
1I. Gyermekklinika, Semmelweis Orvostudományi Egyetem, Budapest.
Insights
Idiopathic hypercalciuria (IHU) in children can cause kidney stones and other urinary issues. Treatment focuses on sodium restriction and hydration, avoiding dietary calcium, with hydrochlorothiazide for severe cases.
Area of Science:
- Pediatric Nephrology
- Metabolic Bone Disease
- Urolithiasis
Context:
- Idiopathic hypercalciuria (IHU) is a primary cause of nephrolithiasis and hematuria in children.
- IHU is linked to osteoporosis development in adults.
- Diagnostic criteria for elevated calcium excretion are age-dependent.
Purpose:
- To review the mechanisms, diagnosis, and treatment of idiopathic hypercalciuria in childhood.
- To discuss current and evolving therapeutic strategies for IHU.
- To explore the molecular basis of hypercalciuric syndromes.
Summary:
- Diagnosis relies on age-specific values and urinary calcium/creatinine ratios (>0.6 mmol/mmol).
- Dietary calcium restriction is contraindicated; sodium restriction and high fluid intake are recommended.
- Hydrochlorothiazide, potassium citrate, and magnesium citrate are treatment options for recurrent cases.
Impact:
- Revised treatment guidelines emphasize hydration and sodium restriction over calcium restriction.
- Understanding molecular mechanisms may lead to genome-based classification of hypercalciuric syndromes.
- Early diagnosis and management of IHU can prevent long-term complications like osteoporosis.
Abstract:
This review describes the supposed mechanisms leading to idiopathic hypercalciuria (IHU) in childhood, further the diagnostic criteria and the proposed treatment modalities are discussed. IHU is not only one of the main causes of renal stone disease in children but it's also at the origin of the postglomerular haematuria and the frequency-dysuria syndrome. Its role in the development of osteoporosis in adults is also documented. The diagnosis of raised calcium excretion is based on age specific values during early infancy. In older children and adults a urinary calcium/creatinine ratio exceeding 0.6 mmol/mmol is regarded as elevated. Dietary calcium restriction can no longer be recommended for the treatment of IHU because it results in secondary hyperoxaluria and on the long-term causes decreased bone mineral density. Patients should be kept on dietary sodium restriction and high fluid intake. In cases IHU associated with recurrent episodes of macroscopic haematuria or recurrent stone disease a therapeutic trial with hydrochlorothiazide in the dose of 0.5-1 mg/kg/day with potassium-citrate supplementation and possibly magnesium citrate should be started. In some special forms of hypercalciuria such as the X-linked recessive nephrolithiasis syndrome or Bartter syndrome the localization and in some cases even the molecular mechanism of the events leading to increased calcium excretion are elucidated. In IHU enhanced Ca(++)-ATPase, and Na-Li countertransport activity and decreased Na+/K+ ATPase activity were described in the erythrocyte membrane model. It is expected that with the molecular genetic development the clinical classification of the hypercalciuric syndromes will become a rational genome-based one.