ArticleScientific reports2018
Identification of ABCG2 as an Exporter of Uremic Toxin Indoxyl Sulfate in Mice and as a Crucial Factor Influencing CKD Progression.
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 47 papers.
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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
47 citing papers in PubMed, 63 citations in OpenAlex.
- Trial
- Association between ABCG2 transporter functionality and CKD progression: a retrospective cohort study in patients with CKD stage G3.Clinical and experimental nephrology · 2026Article
- Real-World Effectiveness and Safety of Dotinurad in Chinese Patients with Gout: A Comparative Analysis.Drugs - real world outcomes · 2026Article
- Molecular Mechanisms and Clinical Evidence Supporting the Four Pillars of Therapy in Diabetic Kidney Disease: Emerging Therapeutic Perspectives.International journal of molecular sciences · 2026Review
- Efficacy and Safety of Dotinurad in Patients with Advanced Chronic Kidney Disease.Internal medicine (Tokyo, Japan) · 2026Observational
- Role of the ABCG2 transporter in the biodistribution of the food-borne uremic toxin p-cresyl sulfate.Scientific reports · 2026Article
- Changes in uric acid levels and estimated glomerular filtration rate slope after treatment with dotinurad in patients with hyperuricemia.BMC nephrology · 2026Observational
- Article
- Indoxyl sulfate in the gut-kidney axis: from diet-microbiome interactions to renal injury and targeted therapies.Frontiers in nutrition · 2026Review
- Kidney clearances of protein-bound uremic toxins predict outcomes in chronic kidney disease: a prospective cohort study.Renal failure · 2025Article
- Transporter-Mediated Interactions Between Uremic Toxins and Drugs: A Hidden Driver of Toxicity in Chronic Kidney Disease.International journal of molecular sciences · 2025Review
- The Long-Term Effects of the Selective Inhibitor of Urate Transporter 1, Dotinurad, on Metabolic Parameters and Renal Function in Japanese Patients With Asymptomatic Hyperuricemia.Journal of clinical medicine research · 2025Article
- Article
- Cardiovascular Events During Treatment With Xanthine Oxidoreductase Inhibitors in Patients With Gout and Hyperuricemia in Japan - A JMDC Claims Database Study.Circulation reports · 2025Article
- First verification of human small intestinal uric acid secretion and effect of ABCG2 polymorphisms.Journal of translational medicine · 2025Article
- Eryptosis in renal anemia: mechanisms, clinical implications, and therapeutic targeting.Frontiers in pharmacology · 2025Review
- Acute kidney disease in mice is associated with early cardiovascular dysfunction.Renal failure · 2024Article
- Article
- Prediction and causal inference of hyperuricemia using gut microbiota.Scientific reports · 2024Article
- Review
Corrections and comments
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Authors and funding
17 authors at 5 institutions in 1 country.
Funding
Abstract
Chronic kidney disease (CKD) patients accumulate uremic toxins in the body, potentially require dialysis, and can eventually develop cardiovascular disease. CKD incidence has increased worldwide, and preventing CKD progression is one of the most important goals in clinical treatment. In this study, we conducted a series of in vitro and in vivo experiments and employed a metabolomics approach to investigate CKD. Our results demonstrated that ATP-binding cassette transporter subfamily G member 2 (ABCG2) is a major transporter of the uremic toxin indoxyl sulfate. ABCG2 regulates the pathophysiological excretion of indoxyl sulfate and strongly affects CKD survival rates. Our study is the first to report ABCG2 as a physiological exporter of indoxyl sulfate and identify ABCG2 as a crucial factor influencing CKD progression, consistent with the observed association between ABCG2 function and age of dialysis onset in humans. The above findings provided valuable knowledge on the complex regulatory mechanisms that regulate the transport of uremic toxins in our body and serve as a basis for preventive and individualized treatment of CKD.
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Registered trials
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