Inflammation and Aging in Acute and Chronic Kidney Injury

Dear Colleagues,

Chronic kidney disease (CKD) is increasingly recognized as a significant concern for healthcare systems around the globe. The prevalence of CKD among the elderly population is approximately 30%, and this becomes 50% in patients with concurrent cardiovascular and metabolic conditions, such as diabetes. Importantly, individuals with advanced stages of CKD who require dialysis or kidney transplantation—classified as end-stage kidney disease (ESKD)—face heightened cardiovascular risks, with mortality rates surpassing those observed for many common cancers and being 10 to 20 times higher than their age- and gender-matched peers without uremia. Additionally, patients undergoing chronic dialysis often experience a range of associated complications, including sepsis, cancer, bone diseases, cognitive impairments, peripheral neuropathy, and diminished immune response. Consequently, CKD is viewed as a condition of premature aging, where biological age diverges significantly from chronological age. This accelerated aging may be attributed to several factors, including alterations in microbiota, biocompatibility issues related to dialysis, the accumulation of uremic toxins, tissue hypoxia, fluid overload, and heightened inflammation and oxidative stress. In recent years, innovative membranes and dialysis devices have been developed aimed at curbing this inflammatory response, particularly for uremic patients on the waiting list for kidney transplantation, to realize both clinical and social benefits.

Acute kidney injury (AKI) has seen a rise in incidence among hospitalized patients, largely due to improved definitions and risk stratification informed by recent literature and the KDIGO 2012 guidelines. A critical epidemiological aspect is the alarmingly high mortality rate among hospitalized AKI patients, especially those with severe forms requiring renal replacement therapy in the context of multiple organ failure. Current understanding frames AKI as an inflammatory disease, particularly when tubular injury is present. Kidney tubular epithelial cells play a crucial role as immunologically active cells involved in antigen presentation and the clearance of inflammatory cytokines. Numerous experimental and clinical studies have confirmed that the inflammatory response triggered by AKI can lead to dysfunction in distant organs, including the heart, lungs, brain, liver, and the immune system. Furthermore, epidemiological data indicate that AKI is a key independent risk factor for the progression of CKD, which in turn drives an increase in hospitalization rates and healthcare expenditures. Collectively, these findings suggest that AKI may accelerate both kidney and systemic organ aging. To counteract this, various extracorporeal blood purification techniques designed to eliminate inflammatory and pro-aging mediators from the bloodstream may provide protective benefits.

In this Special Issue titled “Inflammation and Aging in Acute and Chronic Kidney Injury”, we invite the submission of original research articles and reviews on this highly relevant topic for the scientific community, including nephrologists, intensivists, and basic scientists. We encourage contributions that explore pathogenic mechanisms and identify potential therapeutic targets aimed at mitigating the accelerated tissue senescence characteristic of patients with both acute and chronic kidney diseases.

Dr. Massimiliano Migliori
Dr. Vincenzo Cantaluppi
Dr. Marita Marengo
Guest Editors

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• chronic kidney disease
• acute kidney injury
• inflammation
• aging

• Inflammaging in Acute Kidney Injury (AKI) and Chronic Kidney Disease (CKD) in Cells (1 article)