Figure 1.

Pathological features of the kidney aging process. Kidney aging mainly occurs through several events in a sequential manner. These include (i) kidney fibrosis along with a reduction in cortical mass, increased glomerulosclerosis, and promptness of RAS; (ii) cellular senescence occurs through a persisting DNA damage response and an increase in interferon-gamma (IFN-γ); (iii) mitochondrial damage induces an increased level of ROS through, which causes dysfunction with mitochondria; (iv) inflammation and oxidative stress are mediated through an increase in lipid peroxidation, NF-κB activation, and glutathione depletion; (v) ER stress; (vi) autophagy dysfunction; and (vii) telomere shortening occurs by limiting transcription by DNA polymerase, leading to GFR diminution, decreased urinary concentration, reduced urinary acidification, impaired potassium clearance, increased vascular resistance, a contracted kidney mass, and blood flow.