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“Uremic toxin pathways” collectively refer to the metabolic and transport routes responsible for the generation, biotransformation, and excretion of uremic toxins—endogenous compounds that accumulate in the plasma of patients with impaired kidney function[1][2][3][6]. These toxins originate from protein and amino acid metabolism (principally involving gut microbiota and hepatic processing) and can be classified into small water-soluble compounds, middle molecules (peptides), and protein-bound solutes[1][2][3][6]. While the pathways themselves include enzymatic, microbial, hepatic, and renal transporter activities, "uremic toxin pathways" do not represent a single molecular target but rather an aggregate of mechanisms involved in uremic retention, systemic toxicity, and related comorbidities in CKD and AKI. As such, they are not targets for drugs in the classical sense but are the subject of interventions designed to reduce toxin production or enhance clearance[1][2][3][6][7].
Not applicable as a drug target; however, interventions aim to reduce uremic toxin burden through mechanisms such as adsorption (sequestering toxins in the gut), microbiome modulation (e.g., probiotics, antibiotics), or enhanced dialysis clearance (e.g., improved membrane technology).
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