ReviewGut microbes2026
Cardiovascular-kidney-metabolic syndrome through the lens of gut‑derived uremic toxins.
Review in Gut microbes, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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
3 citing papers in PubMed.
- From molecules to medicine: the gut‒heart axis comes of age.Gut microbes · 2026Article
- Oxidative Stress and Mitochondrial Dysfunction in Chronic Kidney Disease: From Molecular Mechanisms to Biomarkers and Targeted Therapies.Antioxidants (Basel, Switzerland) · 2026Review
- Targeting Uremic Toxins in Chronic Kidney Disease: Current Challenges and Emerging Therapeutic Strategies.Toxins · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cardiovascular-Kidney-Metabolic (CKM) syndrome represents a complex, interconnected cluster of cardiovascular disease, chronic kidney disease, and metabolic disorders such as obesity and type 2 diabetes. These conditions share overlapping metabolic, inflammatory, and vascular pathways, with the gut microbiome increasingly recognised as a key contributor and common underlying risk factor. Uremic toxins, traditionally considered waste products of host and microbial metabolism, are now recognised as active mediators of tissue damage across the CKM spectrum, particularly in the context of impaired renal function. Their production and accumulation are amplified by disrupted intestinal barrier integrity, chronic inflammation, and reduced renal clearance, collectively driving systemic toxicity throughout the CKM continuum. This review explores the origins and impact of gut-derived uremic toxins, including trimethylamine-
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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.