Another plausible mechanism that could contribute to CI in CKD patients is the nonvascular hypothesis involving purine nucleotides, oxidative stress, and fibroblast growth factor 23 (FGF23)‐related pathways, as well as the accumulation of uremic toxins, such as phosphate, indoxyl sulfate (IS), and para‐cresyl sulfate (PCS), which are agonists of the transcription factor, that is, the aryl hydrocarbon receptor (AhR), in endothelial cells (Xie et al., 2022). Here, AHR is linked to chronic kidney disease.