ArticlePediatric research2013
Development of an animal model of nephrocalcinosis via selective dietary sodium and chloride depletion.
Article in Pediatric research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 3 citations in OpenAlex.
- Hypochloremia Secondary to Diuretics in Preterm Infants: Should Clinicians Pay Close Attention?Global pediatric health · 2021Review
- What is nephrocalcinosis?Kidney international · 2015Review
- Detection of nephrocalcinosis using ultrasonography, micro-computed tomography, and histopathology in cats.Journal of veterinary internal medicineArticle
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
backgroundNephrocalcinosis (NC) is an important clinical problem seen in critically ill preterm neonates treated with loop diuretics. No reliable animal models are available to study the pathogenesis of NC in preterm infants. The purpose of this study was to develop a reproducible and clinically relevant animal model of NC for these patients and to explore the impact of extracellular fluid (ECF) volume contraction induced by sodium and chloride depletion in this process.
methodsThree-week-old weanling Sprague-Dawley rats were fed diets deficient in either chloride or sodium or both. A subgroup of rats from each dietary group was injected daily with furosemide (40 mg/kg i.p.).
resultsRats fed a control diet, with or without furosemide, or a chloride-depleted diet alone, did not develop NC. By contrast, 50% of the rats injected with furosemide and fed the chloride-depleted diet developed NC. Moreover, 94% of the rats fed the combined sodium- and chloride-depleted diet developed NC, independently of furosemide use. NC was associated with the development of severe ECF volume contraction; hypochloremic, hypokalemic, metabolic alkalosis; increased phosphaturia; and growth retardation.
conclusionSevere ECF volume contraction induced by chronic sodium and chloride depletion appears to play an important role in the pathogenesis of NC.
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Registered trials
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