ReviewInternational journal of molecular sciences2023
Tissue Sodium Accumulation Induces Organ Inflammation and Injury in Chronic Kidney Disease.
Review in International journal of molecular sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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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.
The trial behind it
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Who cites it
12 citing papers in PubMed, 17 citations in OpenAlex.
- Salt and chronic kidney disease.Nature reviews. Nephrology · 2026Review
- Article
- Unravelling the noncanonical extracellular DNA structures in biofilm and NETosis.Nucleic acids research · 2026Review
- Innovative Insights into Interleukin-Mediated Macrophage Polarization: Metabolic Reprogramming and Inflammatory Pathway Crosstalk in Chronic Kidney Disease and Therapeutic Implications-A Narrative Review.International journal of general medicine · 2026Review
- Nonatherosclerotic Cardiovascular Disease in Chronic Kidney Disease.Cardiology clinics · 2025Review
- Early renal response to long-term salt loading: mitochondrial dysfunction, ER stress, and uromodulin accumulation in the kidney medulla.American journal of physiology. Renal physiology · 2025Article
- The Exposome and the Kidney: A Silent Dialogue Shaping Chronic Kidney Disease.Journal of xenobiotics · 2025Review
- Salt sensitivity and myocardial fibrosis: unraveling the silent cardiovascular remodeling.Frontiers in pharmacology · 2025Review
- Dietary modifications affect renal recovery during the healing phase following ischemic acute ischemic kidney injury.Frontiers in cell and developmental biology · 2025Article
- Pathophysiological Mechanisms of Peritoneal Fibrosis and Peritoneal Membrane Dysfunction in Peritoneal Dialysis.International journal of molecular sciences · 2024Review
- The burden of chronic kidney disease attributable to high sodium intake: a longitudinal study in 1990-2019 in China.Frontiers in nutrition · 2024Article
- The role of intra- and interdialytic sodium balance and restriction in dialysis therapies.Frontiers in medicine · 2023Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
High salt intake is a primary cause of over-hydration in chronic kidney disease (CKD) patients. Inflammatory markers are predictors of CKD mortality; however, the pathogenesis of inflammation remains unclear. Sodium storage in tissues has recently emerged as an issue of concern. The binding of sodium to tissue glycosaminoglycans and its subsequent release regulates local tonicity. Many cell types express tonicity-responsive enhancer-binding protein (TonEBP), which is activated in a tonicity-dependent or tonicity-independent manner. Macrophage infiltration was observed in the heart, peritoneal wall, and para-aortic tissues in salt-loading subtotal nephrectomized mice, whereas macrophages were not prominent in tap water-loaded subtotal nephrectomized mice. TonEBP was increased in the heart and peritoneal wall, leading to the upregulation of inflammatory mediators associated with cardiac fibrosis and peritoneal membrane dysfunction, respectively. Reducing salt loading by a diuretic treatment or changing to tap water attenuated macrophage infiltration, TonEBP expression, and inflammatory marker expression. The role of TonEBP may be crucial during the cardiac fibrosis and peritoneal deterioration processes induced by sodium overload. Anti-interleukin-6 therapy improved cardiac inflammation and fibrosis and peritoneal membrane dysfunction. Further studies are necessary to establish a strategy to regulate organ dysfunction induced by TonEBP activation in CKD patients.
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Registered trials
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