ArticleScientific reports2018
Urothelium proliferation is a trigger for renal crystal deposits in a murine lithogenesis model.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed, 11 citations in OpenAlex.
- Unveiling potential natural promoters of calcium oxalate kidney stones in the urine via anion-exchange chromatography, crystal assays, and proteomics.Molecular and cellular biochemistry · 2026Article
- Integrative multi-layer genetic analysis identifies novel susceptibility genes for urolithiasis.Urolithiasis · 2026Article
- Whole exome sequencing reveals heparan sulfate proteoglycan 2 (HSPG2) as a potential causative gene for kidney stone disease in a Thai family.Urolithiasis · 2024Article
- Loss of Ecrg4 improves calcium oxalate nephropathy.PloS one · 2022Article
- Initial Evaluation of Uroplakins UPIIIa and UPII in Selected Benign Urological Diseases.Biomolecules · 2021Article
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Authors and funding
11 authors at 6 institutions in 1 country.
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Abstract
Most mouse kidney stone models induce nephrocalcinosis rather than urolithiasis. The aim of our study was to find an accelerated experimental model in order to study the early events of stone formation, that is, at the time of crystal binding to intrarenal urothelium. C57B6 mice exposed to vitamin D supplements and water containing hydroxyl-L-proline, ammonium chloride and calcium chloride were studied for 42 days. A group receiving urothelial cell mitogen Fibroblast Growth Factor 7 (FGF7) was compared to control group receiving saline. Calcium oxalate monohydrate (COM) crystals were detected in urines by day 2 and within urinary spaces in specialized fornix areas in both groups as soon as day 14 with enhanced deposits in FGF7 group compared to controls at day 21. Urothelial cells proliferation, uroplakin III downregulation and de novo expression of osteopontin receptor CD44 detected in FGF7 group, were delayed in the control group (day 42). Crystal aggregates within specialized fornix areas by day 42 were located in urinary spaces but also within and under a multilayered metaplastic urothelium, simultaneous to macrophages influx. Point of note, administration of a normal diet by day 21 was responsible for a spontaneous crystal clearance. Our data show that under supersaturation conditions, urothelial cell proliferation and calcium oxalate crystal retention occur within specialized fornix areas. Enhanced crystal deposits following FGF7 administration suggest that urothelium proliferation would be a relevant trigger for renal stone formation.
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