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[Dysregulation of plasma 1,25(OH)2D in calcium restriction in hypercalciuric children]
Insights
Calcium restriction increases 1,25(OH)2D in normocalciuric children but not in hypercalciuric children. This suggests impaired dietary vitamin D regulation in hypercalciuric patients.
Area of Science:
- Pediatric Nephrology
- Endocrinology
- Nutritional Science
Context:
- The relationship between calcium intake and vitamin D metabolism in children with varying calcium excretion levels is not well understood.
- Hypercalciuria, a condition of elevated urinary calcium, can be associated with kidney stones and other renal abnormalities.
Purpose:
- To investigate the impact of dietary calcium restriction on plasma 1,25-dihydroxyvitamin D [1,25(OH)2D] levels in normocalciuric and hypercalciuric children.
- To compare phosphate and calcium metabolism between these two groups under different dietary calcium conditions.
Summary:
- Studies included 8 normocalciuric and 8 hypercalciuric children (ages 4-16) under normal calcium intake, calcium restriction, and calcium loading.
- Hypercalciuric children exhibited higher urinary calcium, elevated plasma 1,25(OH)2D, and lower tubular reabsorption of phosphate (TmP) compared to controls.
- While normocalciuric children showed increased 1,25(OH)2D after calcium restriction, hypercalciuric children did not, indicating a potential impairment in vitamin D regulation.
Impact:
- Dietary calcium restriction influences 1,25(OH)2D levels in normocalciuric children through a mechanism independent of parathyroid hormone (PTH) and phosphorus.
- Hypercalciuric children demonstrate an impaired ability to regulate renal vitamin D metabolism in response to dietary calcium changes.
- Findings highlight potential differences in calcium and vitamin D homeostasis between normocalciuric and hypercalciuric pediatric populations.
Background:
The effect of calcium restriction on the plasma concentration of 1,25(OH)2D in normo- and hypercalciuric children remains unknown.
Methods:
We studied phosphate and calcium metabolism of 8 normocalciuric and 8 hypercalciuric children aged 4 to 16 years, under 3 conditions: on a normal dietary calcium intake after a 5-day calcium-restricted diet, and after oral calcium loading. The healthy, normocalciuric children had histories that included no renal failure of abnormalities of phosphate and calcium metabolism. Four of the 8 hypercalciuric children had urolithiasis, 1 had hematuria and the 3 others had idiopathic hypercalciuria. Blood samples were analyzed for calcium, creatinine, immunoreactive parathyroid hormone, cAMP, 25(OH)D and 1,25(OH)2D concentrations. Urine samples were analyzed for calcium, phosphorus, creatinine and cAMP.
Results:
On the normal dietary calcium intake, the hypercalciuric children had higher urinary calcium excretion and plasma 1,25(OH)2D levels and lower TmP that did the controls. The 1,25(OH)2D levels of the normocalciuric children were significantly increased after 5 days of dietary calcium deprivation, but those of the hypercalciuric children were not. The other parameters (essentially PTH, cAMP and TmP) varied similarly in the two groups.
Conclusion:
The results suggest that: a) calcium restriction influences 1,25(OH)2D levels in normocalciuric subjects via a PTH- and phosphor-independent mechanism; b) dietary control of renal vitamin D metabolism is impaired in hypercalciuric patients.