Chronic kidney disease in the elderly: Unraveling the complexities of aging and renal decline

Background. The prevalence of chronic kidney disease (CKD) increases with age, primarily characterized by a decline in glomerular filtration rate (GFR) and elevated albuminuria. CKD in the elderly is influenced by both age-related changes in kidney function and the presence of common comorbidities. Objective. This literature review aims to explore the etiology and pathogenesis of CKD in the elderly population, focusing on the underlying mechanisms that contribute to kidney decline and disease progression. Results. Aging kidneys exhibit structural and functional alterations, such as reduced GFR and nephron loss, making the elderly more vulnerable to CKD. Common comorbidities, including hypertension, diabetes mellitus, and the use of medications such as nonsteroidal anti-inflammatory drugs (NSAIDs) and antibiotics, exacerbate kidney function deterioration in older adults. Pathophysiological mechanisms underlying CKD in the elderly include premature aging driven by senescence-associated secretory phenotype (SASP) secretion, reduced autophagy in podocytes, mitochondrial dysfunction, and epigenetic modifications such as DNA methylation, histone modification, chromatin remodeling, and noncoding RNA (ncRNA) regulation. Additionally, inflammation and immunosenescence increase pro-inflammatory cytokine production, contributing to renal damage and muscle wasting, further accelerating kidney aging and the development of CKD. Conclusion. The pathogenesis of CKD in the elderly is multifactorial, involving aging-related cellular and molecular changes alongside the impact of comorbidities and medications. Targeting cellular senescence and other molecular pathways may offer novel therapeutic strategies to mitigate CKD progression in older populations.