Age-related disease: Kidneys

Age-associated loss of kidney function has been recognized for decades. Aging kidneys result in gradual functional deterioration as well as macroscopic and microscopic histological abnormalities. Likewise, the higher prevalence of systemic comorbidities, including hypertension and diabetes mellitus, significantly impacts the kidney's function resulting in a decline in glomerular filtration rate (GFR) and renal blood flow (RBF). This decline in GFR may be due to decreased glomerular capillary ultrafiltration coefficient and glomerular capillary plasma flow rate. Additionally, glomerular capillary hydraulic pressure rises in response to an initial decrease in afferent arteriolar resistance. Along with these anatomical changes, renal mass loss, the hyalinization of afferent arterioles, tubulointerstitial fibrosis, and hemodynamic alterations are commonly observed. Besides, age-related physiological changes are believed to reduce the kidney's capacity to repair itself, making the older population more susceptible to acute kidney illness, chronic kidney disease (CKD), and other renal disorders. Intracellularly, the phenomenon of cellular senescence, which involves various cellular signaling processes, is a crucial factor in kidney aging. This chapter highlights the most recent developments in understanding the cellular and molecular mechanisms involved in renal aging, focusing on the role of the renin–angiotensin system (RAS), chronic inflammation, oxidative stress, telomere shortening, and other signaling involved. Emphasis on risk factors and age-dependent changes in important signaling events is discussed, thereby highlighting probable novel targets to slow down the progression of renal diseases or even the natural process of kidney aging per se. Recent developments in the care and management process are also discussed, with the scope that early detection and treatment could safeguard the kidneys of the most vulnerable older population from further deteriorating functions.