- CKD-aP is highly prevalent and debilitating, with multifactorial pathogenesis that severely impairs quality of life, sleep, mental health and clinical outcomes.
- The kidney-gut-skin axis proposes gut dysbiosis, uraemic toxins, intestinal barrier dysfunction and systemic inflammation drive CKD-aP pathogenesis.
- Gut-targeted and metabolism-targeted therapies show promise but evidence is mainly associative; rigorous CKD-aP-specific mechanistic studies and randomised trials are needed.
Front Cell Infect Microbiol. 2026 May 20;16:1811786. doi: 10.3389/fcimb.2026.1811786. eCollection 2026.
ABSTRACT
Chronic kidney disease-associated pruritus (CKD-aP) is a highly prevalent and debilitating symptom in patients with chronic kidney disease (CKD) and end-stage kidney disease (ESKD), severely impairing quality of life, sleep quality, mental health, and clinical outcomes. Its pathogenesis is multifactorial and remains incompletely understood, involving chronic inflammation, immune imbalance, abnormal neuro-opioid pathways, mineral metabolism disorders and skin barrier damage. The kidney-gut-skin axis has attracted increasing attention as a novel theoretical framework to elucidate the roles of gut microbiota dysbiosis, gut-derived uremic toxins, intestinal barrier impairment and systemic inflammation in the development of CKD-aP. This review summarizes the traditional pathogenic mechanisms of CKD-aP, reviews recent advances linking gut microbial alterations to pruritus-related pathways, and systematically evaluates gut-targeted and metabolism-targeted interventions, including probiotics, prebiotics, synbiotics, AST-120, fecal microbiota transplantation, phytochemicals, Uremia Clearance Granules, and vitamin D-related strategies. Current evidence is mostly associative and is mainly derived from general CKD/ESKD populations, animal models, and in vitro studies; specific clinical validation in CKD-aP cohorts remains limited. Accordingly, gut microbiome-related mechanisms and interventions remain hypothetical and adjunctive, without established causal relationships or validated standard therapies for CKD-aP. Future studies are required to identify CKD-aP-specific pathological alterations, adopt longitudinal design and multi-omics analysis, conduct mechanistic verification, and perform randomized controlled trials with pruritus as a predefined primary endpoint.
PMID:42246001 | PMC:PMC13229877 | DOI:10.3389/fcimb.2026.1811786
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