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Review
. 2025 Jul 24:16:1615681.
doi: 10.3389/fphar.2025.1615681. eCollection 2025.

Renal aging and its consequences: navigating the challenges of an aging population

Affiliations
Review

Renal aging and its consequences: navigating the challenges of an aging population

Meiqi Zhang et al. Front Pharmacol. .

Abstract

With the aggravation of population aging, kidney aging and its impact on health have been widely concerned. Renal aging not only involves structural and functional changes but also is significantly linked to the occurrence and progression of some kidney diseases. Mechanisms of renal aging include oxidative stress, reduced Klotho levels, cellular senescence, and chronic inflammation. These changes lead to a sustained reduction in renal filtration, reabsorption, secretion, as well as endocrine function, which in turn affects overall health. Renal structural changes mainly include glomerulosclerosis, tubular degeneration and interstitial fibrosis. These structural changes are closely related to the decline of kidney function and may lead to the occurrence of chronic kidney disease (CKD). In addition, elderly individuals experience a higher rate of acute kidney injury (AKI) and face poorer prospects for recovery. The prevalence of age-related kidney disease, especially diabetic nephropathy (DN), increases with age. End-stage renal disease (ESRD) refers to the most advanced stage of CKD, in which the kidneys of patients show signs of premature aging compared with those of healthy people. Measures to prevent and delay renal aging in daily life, including healthy lifestyle, proper diet, and adequate exercise, are also discussed in this manuscript.

Keywords: AKI; CKD; DN; ESRD; renal aging.

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Conflict of interest statement

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

Figures

FIGURE 1
FIGURE 1
Mechanisms associated with renal aging. Aging is associated with many mechanisms, such as DDR, cellular senescence, oxidative stress, mitochondrial dysfunction, and signaling pathway activation, which all lead to cell division cycle arrest and promote the formation of senescence. ATM, ataxia telangiectasia mutation; DDR, DNA-damage response; ROS, reactive oxygen species; SASP, senescence-associated secretory phenotype.
FIGURE 2
FIGURE 2
Structural changes in aging kidneys. Macroscopically, a pathological reduction in kidney size and morphological changes in kidney tissue was observed, including glomerular sclerosis, interstitial fibrosis, and tubular atrophy. Microscoisally, compensatory renal cell hypertrophy, glomerular basement membrane (GBM) thickening, podocyte loss, and tubular epithelial cell (TEC) atrophy are seen. ECM, extracellular matrix.
FIGURE 3
FIGURE 3
Association between aging and various renal diseases. AGE, advanced glycation end product; AKI, acute kidney injury; CKD, chronic kidney disease; DN, diabetic nephropathy; ESRD, end stage renal disease; ICAM, intercellular cell adhesion molecule; JNK, c-JunN-terminal kinase; MAPK, mitogen-activated protein kinase; NADPH, nicotinamide adenine dinucleotide phosphate; TNF, tumor necrosis factor; VCAM, vascular cell adhesion molecule; VEGF, vascular cell adhesion molecule.

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