Current evidence suggests that a sort of uneven interplay exists between decreased protective elements (including vascular density, antioxidant capacity, telomere shortening, PPARγ, and Klotho expression) and stress-inducing factors (such as hypoxia, increased expression of collagen I and III, TGF-β, and oxidative stress) associated with renal inflammation and fibrosis, a hallmark of CKD. This evidence concerns the gene KL and chronic kidney disease.