ArticleBMC nephrology2019
Gut derived-endotoxin contributes to inflammation in severe ischemic acute kidney injury.
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 18 papers, 1 of them a synthesis that pooled it.
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Who cites it
18 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- The Links between Microbiome and Uremic Toxins in Acute Kidney Injury: Beyond Gut Feeling-A Systematic Review.Toxins · 2020Pooled it
- Gut microbiota and sepsis-associated acute kidney injury: a narrative review.Frontiers in immunology · 2026Review
- Interplay between gut microbiota and acute kidney injury: a review of their mutual influence and causation.Renal failure · 2025Review
- The plasma lipopolysaccharide level is associated with contrast-induced acute kidney injury in patients with ST-segment elevation myocardial infarction.BMC cardiovascular disorders · 2025Observational
- Gut Microbiota Metabolites Targeting the Immune Response in Sepsis: Mechanisms and Therapies.International journal of general medicine · 2025Review
- The AKI-to-CKD Transition: The Role of Uremic Toxins.International journal of molecular sciences · 2023Review
- Gut microbiota and neonatal acute kidney injury biomarkers.Pediatric nephrology (Berlin, Germany) · 2023Review
- Vitamins as regulators of calcium-containing kidney stones - new perspectives on the role of the gut microbiome.Nature reviews. Urology · 2023Review
- Prediction models combining zonulin, LPS, and LBP predict acute kidney injury and hepatorenal syndrome-acute kidney injury in cirrhotic patients.Scientific reports · 2023Article
- Impact of enteric bacterial infections at and beyond the epithelial barrier.Nature reviews. Microbiology · 2023Review
- Genetic Deletion of LRP5 and LRP6 in Macrophages Exacerbates Colitis-Associated Systemic Inflammation and Kidney Injury in Response to Intestinal Commensal Microbiota.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- The Role of Gut-Derived, Protein-Bound Uremic Toxins in the Cardiovascular Complications of Acute Kidney Injury.Toxins · 2022Review
- The role and mechanism of butyrate in the prevention and treatment of diabetic kidney disease.Frontiers in microbiology · 2022Review
- Contribution of gut microbiota toward renal function in sepsis.Frontiers in microbiology · 2022Review
- Mechanism Involved in Acute Liver Injury Induced by Intestinal Ischemia-Reperfusion.Frontiers in pharmacology · 2022Review
- Astaxanthin Alleviates Ochratoxin A-Induced Cecum Injury and Inflammation in Mice by Regulating the Diversity of Cecal Microbiota and TLR4/MyD88/NF-Oxidative medicine and cellular longevity · 2021Article
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Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRecent researches indicate that the intestinal consequences of renal ischemia reperfusion (IR) would predispose to the translocation of gut-derived endotoxin. Here, we designed experiments to test the hypothesis that the gut-derived endotoxin has a potential role in mediating local inflammatory processes in the acutely injured kidney.
methodsRats were performed sham or renal IR surgery (60 min of bilateral renal ischemia, then 24 h of reperfusion) (n = 5). The intestinal structural and mucosa permeability were evaluated. Serum endotoxin and bacterial load in liver and mesenteric lymph nodes (MLN) were measured. Separate groups were pretreated with oral norfloxacin 20 mg/kg/day or saline for 4 weeks and divided into sham plus saline, sham plus norfloxacin, renal IR plus saline and renal IR plus norfloxacin group. Serum biochemistry and endotoxin were determined. Kidney pathological changes were scored. Protein or mRNA expression of toll-like receptor 4 (TLR4) and proinflammatory mediators were measured in kidney homogenate.
resultsRenal IR led to marked intestinal integrity disruption and increase in intestinal permeability. These are accompanied by low grade of endotoxemia as well as increased bacterial load in liver and MLN. The group pretreated with norfloxacin showed significant attenuation of the increase in serum urea, ALAT, ASAT and endotoxin. The increased renal protein or mRNA of TLR4 and proinflammatory mediators (IL-6 and MCP-1) in the unpretreated animals was significantly attenuated in the norfloxacin-pretreated animals. However, norfloxacin pretreatment did not produce any protective effects on renal tubular integrity.
conclusionsOur results show for the first time that gut-derived endotoxin, resulting from an increased intestinal permeability after severe renal IR, subsequently amplifies intrarenal inflammatory response by activation renal TLR4 signaling. Our study results do not establish that antibiotic administration was effective in improving the overall renal outcome. However, our findings may be the first step to understanding how to tailor therapies to mitigate intrarenal inflammation in select groups of patients.
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