ArticleUrolithiasis2022
Hydroxycitrate prevents calcium oxalate crystallization and kidney injury in a nephrolithiasis rat model.
Article in Urolithiasis, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Caloric Restriction Mimetic Hydroxycitrate Mitigates Acute Nephrotoxicity via Autophagy Activation and Oxidative Stress Reduction.Biomolecules · 2026Article
- Citrate and calcium kidney stones.Clinical kidney journal · 2025Review
- Thermodynamic and Kinetic Aspects of Calcium Oxalate Crystallization and Renal Lithiasis.Biomolecules · 2025Article
- Metabolomics analysis reveals a protective effect of hydroxycitric acid on calcium oxalate-induced kidney injury.Iranian journal of basic medical sciences · 2024Article
- Recent advances of traditional Chinese medicine against cardiovascular disease: overview and potential mechanisms.Frontiers in endocrinology · 2024Review
- Hydroxycitric acid prevents hyperoxaluric-induced nephrolithiasis and oxidative stress via activation of the Nrf2/Keap1 signaling pathway.Cell cycle (Georgetown, Tex.) · 2023Article
- Osteopontin: An important protein in the formation of kidney stones.Frontiers in pharmacology · 2022Review
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Authors and funding
8 authors.
Funding
Abstract
Hydroxycitrate (HCA) is a derivative of citric acid, and previous studies of HCA have revealed its ability to inhibit the formation of calcium oxalate crystals in vitro. To date, there has been little evidence proving that HCA has the same effectiveness in vivo. The present study was designed to investigate the ameliorating effect of HCA on calcium oxalate deposition and renal impairment in a male rat model. Male Sprague-Dawley rats were randomly divided into four groups: a control group, a model group (glyoxalic acid), a CA group (glyoxalic acid + CA), and an HCA group (glyoxalic acid + HCA). Kidney stone formation was induced by injection of glyoxalic acid (60 mg/kg). The results showed that serum and urinary parameters were significantly improved by HCA treatment. In addition, differences in the formation of calcium oxalate crystals between groups were observed, and HCA was superior to CA in inhibiting crystal accumulation. The ultrastructure of renal tubules and glomeruli occurred in the model group, and the above lesions were significantly reduced in the HCA group. Both OPN and SOD expression levels were promoted by HCA, while CA only promoted OPN. In this article, we provided data on whether HCA affected kidney stones and the expression levels of OPN and SOD in a male rat model.
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Registered trials
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