ArticleRenal failure2026
Indoxyl sulfate exacerbates chronic inflammation and susceptibility to severe infection via modulating T-cell CD73/adenosine signaling in chronic kidney disease.
Article in Renal failure, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundChronic kidney disease (CKD) is a major global health issue. Cardiovascular events and infections drive mortality in end-stage renal disease via immune dysregulation. The role of T-cell purinergic signaling and its modulation by indoxyl sulfate (IS) in CKD remains unclear.
methodsMale Sprague-Dawley rats underwent 5/6 nephrectomy. The CKD + IS group received daily IS (100 μg/kg, intraperitoneally) for 24 weeks; control group received saline. Samples were collected 2-6 h post-injection. Sepsis was induced via cecal ligation and puncture. Splenic T-cell mRNA cluster of differentiation (CD) 73, CD39, A2A receptor (A2AR), P2X purinergic receptor (P2RX7), nuclear factor kappa-B (NF-κB) was quantified by quantitative real-time polymerase chain reaction. Plasma cytokines, vascular injury markers (asymmetric dimethylarginine (ADMA), intercellular adhesion molecule 1 (ICAM-1)), and myocardial markers (cardiac troponin T (cTnT), B-type natriuretic peptide (BNP)) were measured by enzyme-linked immunosorbent assay. Peripheral purine metabolites (adenosine triphosphate, adenosine diphosphate, adenosine monophosphate, adenosine (ADO)) were analyzed via ultra-high performance liquid chromatography-tandem mass spectrometry. Survival was monitored for 72 h.
resultsIS exacerbated baseline microinflammation, elevating plasma cytokines (interleukin 2 (IL-2), IL-6, IL-10, IL-17, tumor necrosis factor-alpha (TNF-α)) and T-cell NF-κB. This coincided with disrupted anti-inflammatory purinergic signaling, characterized by downregulated CD73/A2AR and reduced ADO. Post-infection, the CKD + IS group showed profound CD73 suppression and ADO depletion. Despite blunted cytokine surges, this group exhibited aggravated vascular and myocardial injury (elevated ADMA, ICAM-1, cTnT, BNP) and significantly higher 72-hour mortality.
conclusionsIndoxyl sulfate disrupts the T-cell CD73/ADO axis, promoting basal microinflammation while impairing anti-infective immunity and exacerbating organ damage during sepsis. Targeting the IS-CD73-ADO pathway offers a therapeutic strategy for restoring immune homeostasis in uremia.
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