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In CKD, uremic toxin accumulation (e.g., indoxyl sulfate, acrolein), impaired antioxidant defense systems, and persistent inflammation collectively promote excessive production of reactive oxygen species (ROS), which disrupt erythrocyte membrane integrity, activate Ca 2+ -permeable cation channels, and trigger downstream eryptotic events (e.g., phosphatidylserine (PS) externalization, cell shrinkage, and cytoskeleton degradation) (Table 2 provides a detailed overview of their mechanisms, effects, and supporting evidence

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