What this means
This review describes earlier work on kidney aging and small energy-making parts of cells called mitochondria. It suggests DNA changes there may help track kidney health.
Plain-English summary written by an AI model from the abstract. The original is below.
- Who it was tested in
- People
- Kind of research
- A summary of earlier studies
The science
- Original title
- THE KIDNEY AS A WINDOW INTO MAMMALIAN AGING: METABOLIC FRAILTY, MITOCHONDRIAL RESILIENCE, AND THE CONTINUUM FROM INJURY TO AGING.
- Authors
- Parikh SM
- Journal
- Transactions of the American Clinical and Climatological Association
- Published
- Oct 25, 2026
- Study type
- Review · in humans
- PMID
- 42927019 ↗
Abstract
Aging-related decline of kidney function bears major medical and biological implications: chronic kidney disease (CKD) and acute kidney injury (AKI) risk rise sharply with age, and tubular epithelial cells in the kidney are paradoxically long-lived despite engaging in intense oxidative metabolic work. Mitochondrial relation to kidney physiology may unveil new hallmarks of mammalian aging. Our work has identified the central redox cofactor, nicotinamide adenine dinucleotide, as both a measurable and modifiable target to augment energy metabolism within the kidney and confer resistance to acute stressors that otherwise provoke AKI. More recently, we found that aging and transient injuries indefinitely degrade the fidelity of the kidney's mitochondrial DNA (mtDNA). Moreover, mtDNA mutation burden correlates with CKD severity and predicts future AKI events. These findings identify mtDNA mutations as a new, measurable determinant of kidney health and resilience, in turn proposing novel ways to track resilience in related organs.
Parikh SM THE KIDNEY AS A WINDOW INTO MAMMALIAN AGING: METABOLIC FRAILTY, MITOCHONDRIAL RESILIENCE, AND THE CONTINUUM FROM INJURY TO AGING. Transactions of the American Clinical and Climatological Association. 2026. PMID: 42927019. https://pubmed.ncbi.nlm.nih.gov/42927019/