ArticleBMC nephrology2019
Metabolic consequences of cystinuria.
Article in BMC nephrology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers, 1 of them a synthesis that pooled it.
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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.
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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.
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Who cites it
11 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.
- Metabolic changes in kidney stone disease.Frontiers in immunology · 2023Pooled it
- Partial correction of cystinuria type A in mice via kidney-targeted transposon delivery.Molecular therapy. Nucleic acids · 2025Article
- Mitochondrial SLC3A1 regulates sexual dimorphism in cystinuria.Genes & diseases · 2025Article
- Molecular Variability in Levodopa Absorption and Clinical Implications for the Management of Parkinson's Disease.Journal of Parkinson's disease · 2024Review
- Article
- The antioxidant l-Ergothioneine prevents cystine lithiasis in the Slc7a9Redox biology · 2023Article
- Kidney Stone Prevention.Advances in nutrition (Bethesda, Md.) · 2023Review
- Accurate 24-h urine cystine quantification for patients on cystine-binding thiol drugs.Urolithiasis · 2022Article
- [Nephrolithiasis and nephrocalcinosis in children and adolescents].Urologie (Heidelberg, Germany) · 2022Review
- S-Methyl-L-Ergothioneine to L-Ergothioneine Ratio in Urine Is a Marker of Cystine Lithiasis in a Cystinuria Mouse Model.Antioxidants (Basel, Switzerland) · 2021Article
- CRISPR/Cas9 engineering of albino cystinuria Type A mice.Genesis (New York, N.Y. : 2000) · 2020Article
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10 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundCystinuria is an inherited disorder of renal amino acid transport that causes recurrent nephrolithiasis and significant morbidity in humans. It has an incidence of 1 in 7000 worldwide making it one of the most common genetic disorders in man. We phenotypically characterized a mouse model of cystinuria type A resultant from knockout of Slc3a1.
methodsKnockout of Slc3a1 at RNA and protein levels was evaluated using real-time quantitative PCR and immunofluorescence. Slc3a1 knockout mice were placed on normal or breeder chow diets and evaluated for cystine stone formation over time suing x-ray analysis, and the development of kidney injury by measuring injury biomarkers. Kidney injury was also evaluated via histologic analysis. Amino acid levels were measured in the blood of mice using high performance liquid chromatography. Liver glutathione levels were measured using a luminescent-based assay.
resultsWe confirmed knockout of Slc3a1 at the RNA level, while Slc7a9 RNA representing the co-transporter was preserved. As expected, we observed bladder stone formation in Slc3a1
conclusionsOur results suggest that that diet can affect the development and progression of chronic kidney disease in an animal model of cystinuria, which may have important implications for patients with this disease. Additionally, reduced glutathione may predispose those with cystinuria to injury caused by oxidative stress. Word count: 327.
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