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The progression of chronic kidney disease (CKD) results in the accumulation of uremic toxins in the bloodstream, which leads to endothelial dysfunction. Vascular endothelial cells exposed to uremic toxins have a proinflammatory and a prothrombotic phenotype, and the monolayer structure is damaged, increasing permeability. This impairment of endothelial function can contribute to cardiovascular diseases (CVD) pathogenesis.
