ArticleUrolithiasis2016
Renal tubular injury induced by ischemia promotes the formation of calcium oxalate crystals in rats with hyperoxaluria.
Article in Urolithiasis, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- Pre-transplant residual diuresis and oxalic acid concentration influence kidney graft survival.PloS one · 2025Article
- Targeting the NLRP3 inflammasome for calcium oxalate stones: pathophysiology and emerging pharmacological interventions.Frontiers in physiology · 2025Review
- Resveratrol inhibits calcium oxalate crystal growth, reduces adhesion to renal cells and induces crystal internalization into the cells, but promotes crystal aggregation.Current research in food science · 2024Article
- Critically ill, tubular injury, delayed early recovery: characteristics of acute kidney disease with renal oxalosis.Renal failure · 2021Article
- The association of calcium oxalate deposition in kidney allografts with graft and patient survival.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2020Article
- Mitochondrial Dysfunction and Kidney Stone Disease.Frontiers in physiology · 2020Review
- Accelerated Oxalosis Contributing to Delayed Graft Function after Renal Transplantation.Case reports in transplantation · 2019Article
- Toward a new insight of calcium oxalate stones in Drosophila by micro-computerized tomography.Urolithiasis · 2018Article
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Authors and funding
7 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperoxaluria and cell injury are key factors in urolithiasis. Oxalate metabolism may be altered by renal dysfunction and therefore, impact the deposition of calcium oxalate (CaOx) crystals. We investigated the relationship of renal function, oxalate metabolism and CaOx crystal deposition in renal ischemia. One hundred male Sprague-Dawley rats were randomly divided into four groups. Hyperoxaluria model (Group A and B) was established by feeding rats with 0.75 % ethylene glycol (EG). The left renal pedicle was clamped for 30 min to establish renal ischemia Groups (B and C), while Groups A and D underwent sham operation. Then, serum and urine oxalate (Ox), creatinine (Cr) and urea nitrogen (UN) levels were evaluated by liquid chromatography mass spectrometry (LCMS) and ion mass spectrum (IMS) at days 0, 2, 4, 7, and 14. CaOx crystallization was assessed by transmission electron microscope (TEM). A temporal and significant increase of serum Cr and UN levels was observed in Groups B and C compared to values obtained for Groups A and D (P < 0.05). Ox levels in serum and urine were significantly higher in Groups A and B than in the other two groups from day 7 (P < 0.05). In addition, CaOx crystallization was observed in both Groups A and B, but Group B showed earlier and more pronounced crystal deposition in the renal tissue. Our results indicated that renal tubular injury induced by renal ischemia might not affect Ox levels but could promote CaOx crystal retention under hyperoxaluria.
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