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Genetic hypercalciuric stone-forming rats.

David A Bushinsky·Kevin K Frick·Keith Nehrke
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Abstract

PURPOSE OF REVIEW: We will describe the pathophysiology of hypercalciuria and the mechanism of the resultant stone formation in a rat model and draw parallels to human hypercalciuria and stone formation. RECENT FINDINGS: Through inbreeding we have established a strain of rats that excrete 8-10 times more urinary calcium than control rats. These genetic hypercalciuric rats absorb more dietary calcium at lower 1,25-dihydroxyvitamin D3 levels. Elevated urinary calcium excretion on a low-calcium diet indicated a defect in renal calcium reabsorption and/or an increase in bone resorption. Bone from hypercalciuric rats released more calcium when exposed to 1,25-dihydroxyvitamin D3. Bisphosphonate significantly reduced urinary calcium excretion in rats fed a low-calcium diet. Clearance studies showed a primary defect in renal calcium reabsorption. The intestine, bone and kidneys of the hypercalciuric rats had increased numbers of vitamin D receptors. When hydroxyproline is added to their diet they form calcium oxalate stones, the most common stone type in humans. Increased numbers of vitamin D receptors may cause hypercalciuria in these rats and humans. SUMMARY: Understanding the mechanism of hypercalciuria and stone formation in this animal model will help clinicians devise effective treatment strategies for preventing recurrent stone formation in humans.

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AdsorptionAnimalsCalcium OxalateCalcium, DietaryDisease Models, AnimalHumansKidneyKidney CalculiRatsRats, Mutant StrainsReceptors, CalcitriolVitamin DComparative StudyJournal ArticleResearch Support, N.I.H., ExtramuralReview

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David A Bushinsky, Kevin K Frick, Keith Nehrke. 2006. Genetic hypercalciuric stone-forming rats.. https://doi.org/10.1097/01.mnh.0000232881.35469.a9

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