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Pathophysiologic studies in idiopathic hypercalciuria presenting in childhood
Insights
Idiopathic hypercalciuria (IH) in children often persists into adulthood. Findings suggest a hyperabsorptive mechanism, possibly linked to kidney function, indicating a physiological variant rather than a disease.
Area of Science:
- Pediatric Nephrology
- Endocrinology
- Mineral Metabolism
Background:
- Idiopathic hypercalciuria (IH) is a common metabolic abnormality in children.
- Understanding the underlying mechanisms of IH is crucial for long-term management.
- Previous studies have explored various etiologies, including renal phosphate handling and vitamin D metabolism.
Purpose of the Study:
- To investigate the underlying mechanisms of idiopathic hypercalciuria in a cohort of children.
- To assess the persistence of hypercalciuria over time.
- To differentiate between potential pathogenic pathways in pediatric IH.
Main Methods:
- Diagnosis of IH in 11 children (aged 5-10 years).
- Follow-up investigations 1-12 years later.
- Oral calcium loading tests and measurement of urinary calcium, cAMP, serum iPTH, and iTCT.
- Assessment of tubular reabsorption of phosphate (TmP/GFR).
Main Results:
- Hypercalciuria persisted in 8 of 11 children at follow-up.
- Five patients showed excessive urinary calcium excretion post-calcium load, with low urinary cAMP and normal serum iPTH.
- All patients exhibited findings suggestive of a hyperabsorptive mechanism, with low TmP/GFR potentially indicating a primary pathogenic role.
Conclusions:
- Pediatric idiopathic hypercalciuria frequently persists and appears to be driven by a hyperabsorptive mechanism.
- Low tubular reabsorption of phosphate (TmP/GFR) may be the primary issue, leading to increased vitamin D activation and calcium absorption.
- IH in children may represent a physiological variant rather than a distinct disease state.
Abstract:
Idiopathic hypercalciuria (IH) was diagnosed in 11 children aged 5 3/12 to 10 6/12. Eight patients investigated 1-12 years later still had hypercalciuria. When compared to a control group of 10 healthy children, 5 patients demonstrated an excessive rise in urinary Ca excretion following an oral Ca load. These patients also demonstrated low urinary cAMP, normal serum iPTH and high normal iTCT levels. The remaining 3 patients responded normally to Ca loading, but otherwise showed similar metabolic findings as the above group. These findings suggest a hyperabsorptive mechanism for all our patients. The finding of relatively low values for TmP/GFR in most IH patients further suggests that here, as in many adult patients, this may be the primary pathogenic mechanism, causing low serum P, increased synthesis of 1,25 dihydroxyvitamin D and, thus, absorption of Ca. We believe this represents a physiologic variant state and not a disease state.