ArticleAmerican journal of physiology. Renal physiology2013
1,25(OH)₂D₃-enhanced hypercalciuria in genetic hypercalciuric stone-forming rats fed a low-calcium diet.
Article in American journal of physiology. Renal physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 23 citations in OpenAlex.
- Article
- Association between Serum Klotho and Kidney Stones in US Middle-Aged and Older Individuals with Diabetes Mellitus: Results from 2007 to 2016 National Health and Nutrition Survey.American journal of nephrology · 2023Article
- The association between single nucleotide polymorphism in vitamin D receptor and calcium oxalate urolithiasis in dogs.Journal of veterinary internal medicine · 2021Article
- Chlorthalidone with potassium citrate decreases calcium oxalate stones and increases bone quality in genetic hypercalciuric stone-forming rats.Kidney international · 2021Article
- Article
- Expression of vitamin D receptor, CYP27B1 and CYP24A1 hydroxylases and 1,25-dihydroxyvitamin DUrolithiasis · 2020Observational
- Chlorthalidone Is Superior to Potassium Citrate in Reducing Calcium Phosphate Stones and Increasing Bone Quality in Hypercalciuric Stone-Forming Rats.Journal of the American Society of Nephrology : JASN · 2019Article
- Integrative microRNA-gene expression network analysis in genetic hypercalciuric stone-forming rat kidney.PeerJ · 2016Article
- Effect of Potassium Citrate on Calcium Phosphate Stones in a Model of Hypercalciuria.Journal of the American Society of Nephrology : JASN · 2015Article
- Modeling hypercalciuria in the genetic hypercalciuric stone-forming rat.Current opinion in nephrology and hypertension · 2015Review
- Association study of DGKH gene polymorphisms with calcium oxalate stone in Chinese population.Urolithiasis · 2014Article
- Expression of fibroblast growth factor 23, vitamin D receptor, and sclerostin in bone tissue from hypercalciuric stone formers.Clinical journal of the American Society of Nephrology : CJASN · 2014Article
- Persistence of 1,25D-induced hypercalciuria in alendronate-treated genetic hypercalciuric stone-forming rats fed a low-calcium diet.American journal of physiology. Renal physiology · 2014Article
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6 authors at 2 institutions in 1 country.
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Abstract
The inbred genetic hypercalciuric stone-forming (GHS) rats exhibit many features of human idiopathic hypercalciuria and have elevated levels of vitamin D receptors (VDR) in calcium (Ca)-transporting organs. On a normal-Ca diet, 1,25(OH)2D3 (1,25D) increases urine (U) Ca to a greater extent in GHS than in controls [Sprague-Dawley (SD)]. The additional UCa may result from an increase in intestinal Ca absorption and/or bone resorption. To determine the source, we asked whether 1,25D would increase UCa in GHS fed a low-Ca (0.02%) diet (LCD). With 1,25D, UCa in SD increased from 1.2 ± 0.1 to 9.3 ± 0.9 mg/day and increased more in GHS from 4.7 ± 0.3 to 21.5 ± 0.9 mg/day (P < 0.001). In GHS rats on LCD with or without 1,25D, UCa far exceeded daily Ca intake (2.6 mg/day). While the greater excess in UCa in GHS rats must be derived from bone mineral, there may also be a 1,25D-mediated decrease in renal tubular Ca reabsorption. RNA expression of the components of renal Ca transport indicated that 1,25D administration results in a suppression of klotho, an activator of the renal Ca reabsorption channel TRPV5, in both SD and GHS rats. This fall in klotho would decrease tubular reabsorption of the 1,25D-induced bone Ca release. Thus, the greater increase in UCa with 1,25D in GHS fed LCD strongly suggests that the additional UCa results from an increase in bone resorption, likely due to the increased number of VDR in the GHS rat bone cells, with a possible component of decreased renal tubular calcium reabsorption.
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