ReviewCurrent opinion in nephrology and hypertension2015
Modeling hypercalciuria in the genetic hypercalciuric stone-forming rat.
Review in Current opinion in nephrology and hypertension, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.
What it found
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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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
8 citing papers in PubMed, 1 synthesis or guideline pooled it, 16 citations in OpenAlex.
- Association between Circulating Vitamin D Level and Urolithiasis: A Systematic Review and Meta-Analysis.Nutrients · 2017Pooled it
- Case report: disease mechanisms and medical management of calcium nephrolithiasis in rheumatologic diseases.BMC urology · 2023Article
- Molecular mechanisms altering tubular calcium reabsorption.Pediatric nephrology (Berlin, Germany) · 2022Review
- Article
- Low Sodium Diet Decreases Stone Formation in Genetic Hypercalciuric Stone-Forming Rats.Nephron · 2019Article
- Vitamin D, Hypercalciuria and Kidney Stones.Nutrients · 2018Review
- Progress in Understanding the Genetics of Calcium-Containing Nephrolithiasis.Journal of the American Society of Nephrology : JASN · 2017Review
- Integrative microRNA-gene expression network analysis in genetic hypercalciuric stone-forming rat kidney.PeerJ · 2016Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purpose of reviewIn this review, we discuss how the genetic hypercalciuric stone-forming (GHS) rats, which closely model idiopathic hypercalciuria and stone formation in humans, provide insights into the pathophysiology and consequences of clinical hypercalciuria. RECENT
findingsHypercalciuria in the GHS rats is due to a systemic dysregulation of calcium transport, as manifest by increased intestinal calcium absorption, increased bone resorption and decreased renal tubule calcium reabsorption. Increased levels of vitamin D receptor in intestine, bone and kidney appear to mediate these changes. The excess receptors are biologically active and increase tissue sensitivity to exogenous vitamin D. Bones of GHS rats have decreased bone mineral density (BMD) as compared with Sprague-Dawley rats, and exogenous 1,25(OH)2D3 exacerbates the loss of BMD. Thiazide diuretics improve the BMD in GHS rats. SUMMARY: Studying GHS rats allows direct investigation of the effects of alterations in diet and utilization of pharmacologic therapy on hypercalciuria, urine supersaturation, stone formation and bone quality in ways that are not possible in humans.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.