The ageing global population faces a rising prevalence of chronic kidney disease (CKD), now recognized as a state of accelerated ageing driven by chronic low-grade inflammation-inflammaging. This review synthesizes current evidence positioning the kidney not merely as a passive target but as an active participant in systemic inflammaging, a process fueled by immunosenescence, metabolic reprogramming, and cellular senescence. We explore how resident renal cells, including tubular epithelial cells, podocytes, and mesangial cells, adopt a senescence-associated secretory phenotype (SASP) that perpetuates inflammation, fibrosis, and functional decline. Key mechanisms (NLRPinflammasome activation, mitochondrial dysfunction, epigenetic alterations, and gut-kidney crosstalk) are discussed in the context of specific renal pathologies, including diabetic nephropathy, acute kidney injury (AKI) to CKD transition, and CKD progression. Emerging diagnostic tools such as senescence and epigenetic clocks, single-cell signatures and extracellular vesicle biomarkers are evaluated for patient stratification, alongside promising therapeutic strategies, including senolytics, SASP neutralization, immunometabolic modulators (e.g., SGLT2 inhibitors), and lifestyle interventions. We conclude with a forward-looking research agenda that prioritizes high-resolution molecular atlases, biomarker-driven trials, and combinatorial therapies to target renal inflammaging and improve health span in an ageing world. 3
