ReviewToxins2020
Indoxyl Sulfate, a Tubular Toxin, Contributes to the Development of Chronic Kidney Disease.
Review in Toxins, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
80 citing papers in PubMed, 1 synthesis or guideline pooled it, 104 citations in OpenAlex.
- Association of estimated glomerular filtration rate with proliferative diabetic retinopathy: a systematic review and meta-analysis.International urology and nephrology · 2025Pooled it
- Effects of probiotic supplementation on disease progression in patients with moderate to severe chronic kidney disease: a randomized controlled trial.Scientific reports · 2026Trial
- Trial
- Trial
- Review
- Article
- The role of gut microbiota-mitochondrial crosstalk in kidney disease: a bibliometric analysis.International urology and nephrology · 2026Article
- Gut Microbiota and Chronic Kidney Disease: A Complex Interplay with Implications for Diagnosis and Treatment.Probiotics and antimicrobial proteins · 2026Review
- Associations Between Elevated Anticardiolipin IgG, Thrombocytopenia, and Combined Diabetes-Hypertension Etiology in Hemodialysis Patients.Journal of clinical medicine · 2026Article
- Article
- miR-4516-Loaded Engineered Milk Extracellular Vesicles Attenuate Indoxyl Sulfate-Induced Mitochondrial Dysfunction and Improve Renal Function in a CKD Mouse Model.International journal of molecular sciences · 2026Article
- Bridging gut microbiota and renal health: Klotho as a promising therapeutic agent in DKD.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- Targeting gut-liver-kidney axis: microbiota-derived metabolites and therapeutic implications.Cell communication and signaling : CCS · 2026Review
- Gut-Kidney Axis: Unraveling the Role of the Microbiome in Chronic Kidney Disease.Biomedicines · 2026Review
- Plasma Short-Chain Fatty Acids and Cytokine Profiles in Chronic Kidney Disease: A Potential Pathophysiological Link.International journal of molecular sciences · 2026Article
- Gut microbiota-liver-kidney axis in diabetic kidney disease: mechanistic insights into amino acid metabolism and nutritional intervention strategies targeting natural bioactive compounds.Frontiers in nutrition · 2026Review
- The role of gut microbiota dysbiosis in the pathogenesis of hyperuricemic nephropathy.Frontiers in molecular biosciences · 2026Review
- Indoxyl sulfate in the gut-kidney axis: from diet-microbiome interactions to renal injury and targeted therapies.Frontiers in nutrition · 2026Review
- Gut Microbiota in the Hepato-Cardiorenal Axis: Microbial Metabolites, Inflammation, and Emerging Therapeutic Targets.Current pharmaceutical design · 2026Review
- Altered tryptophan metabolism as a contributor to cognitive impairment in chronic kidney disease: a narrative review.Frontiers in neuroscience · 2026Review
20 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Indoxyl sulfate (IS), a uremic toxin, causes chronic kidney disease (CKD) progression via its tubulotoxicity. After cellular uptake, IS directly induces apoptotic and necrotic cell death of tubular cells. Additionally, IS increases oxidative stress and decreases antioxidant capacity, which are associated with tubulointerstitial injury. Injured tubular cells are a major source of transforming growth factor-β1 (TGF-β1), which induces myofibroblast transition from residual renal cells in damaged kidney, recruits inflammatory cells and thereby promotes extracellular matrix deposition in renal fibrosis. Moreover, IS upregulates signal transducers and activators of transcription 3 phosphorylation, followed by increases in TGF-β1, monocyte chemotactic protein-1 and α-smooth muscle actin production, which participate in interstitial inflammation, renal fibrosis and, consequently, CKD progression. Clinically, higher serum IS levels are independently associated with renal function decline and predict all-cause mortality in CKD. The poor removal of serum IS in conventional hemodialysis is also significantly associated with all-cause mortality and heart failure incidence in end-stage renal disease patients. Scavenging the IS precursor by AST-120 can markedly reduce tubular IS staining that attenuates renal tubular injury, ameliorates IS-induced oxidative stress and rescues antioxidant glutathione activity in tubular epithelial cells, thereby providing a protective role against tubular injury and ultimately retarding renal function decline.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.