Aging is a significant risk factor for the development of chronic kidney disease (CKD), an incurable condition that can progress despite current “standard of care” treatments. Multiple transcriptional and histologic changes are shared by “normal aged” and CKD kidneys. These include increased myofibroblast number, interstitial collagen deposition, chronic immune infiltrates, and increased levels of renal epithelial senescence (senescent cells [SCs], permanently growth-arrested cells with altered behavior, and secretory phenotypes) compared with healthy young kidneys.
Aging is a significant risk factor for the development of chronic kidney disease (CKD), an incurable condition that can progress despite current “standard of care” treatments. Multiple transcriptional and histologic changes are shared by “normal aged” and CKD kidneys. These include increased myofibroblast number, interstitial collagen deposition, chronic immune infiltrates, and increased levels of renal epithelial senescence (senescent cells [SCs], permanently growth-arrested cells with altered behavior, and secretory phenotypes) compared with healthy young kidneys.