Inflammaging in Acute Kidney Injury (AKI) and Chronic Kidney Disease (CKD)

Dear Colleagues,

Chronic kidney disease (CKD) is nowadays considered a relevant problem for healthcare systems worldwide. The CKD prevalence is about 30% in the older population, reaching 50% in comorbid patients affected by cardiovascular and metabolic diseases such as diabetes. Of note, patients with advanced CKD stages requiring dialysis and kidney transplantation (end-stage kidney disease, ESKD) show an increased cardiovascular risk with mortality rates higher than those observed for the most common forms of cancer and 10–20 times higher than the non-uremic population matched for age and gender. Moreover, patients in chronic dialysis are also characterized by an increased incidence of other clinical complications such as sepsis, cancer, bone diseases, cognitive alterations, peripheral neuropathy, and reduced immune response. For these reasons, CKD is considered a disease characterized by premature aging in which biological and chronological age are completely different. This accelerated senescence may be ascribed to alterations in the microbiota, dialysis-related biocompatibility, accumulation of uremic toxins, tissue hypoxia, and fluid overload, but in particular, to enhanced inflammation and oxidative stress. In the last years, several new membranes and dialysis devices have been developed with the aim to limit this inflammatory reaction, in particular for uremic patients admitted to the waiting list, to achieve the clinical and social benefits of kidney transplantation.

Acute kidney injury (AKI) is characterized by an increased incidence in hospitalized patients thanks to a better definition and risk stratification of this complex syndrome obtained by recent literature data and to the use of KDIGO 2012 definitions. A relevant epidemiologic aspect is associated with the high mortality rate of AKI patients during hospitalization, particularly in the presence of the most severe forms requiring RRT in a clinical scenario of multiple organ failure. AKI is nowadays considered an inflammatory disease, especially in the presence of tubular injury: indeed, kidney tubular epithelial cells are immunologically active cells able to present antigen and dedicated to the clearance of inflammatory cytokines. Several experimental and clinical studies have undoubtedly demonstrated that this inflammatory response following AKI is responsible for distant organ alterations including heart, lung, brain, liver, and immune system dysfunction. Moreover, epidemiologic studies have shown that AKI is a pivotal and independent risk factor for CKD progression and the consequent increase in the hospitalization rate and healthcare costs. Taken together, these data suggest that AKI may act as an accelerator of kidney and distant organ aging. On this basis, several extracorporeal blood-purification techniques able to remove inflammatory and pro-aging mediators from the bloodstream may exert a protective role.

In this Special Issue, “Inflammaging in CKD and AKI”, we encourage the submission of original papers or reviews on this topic of great interest for the scientific community (nephrologists, intensivists, basic scientists), describing pathogenic mechanisms and possible new therapeutic targets to limit the accelerated tissue senescence typical of patients with both acute and chronic kidney diseases.

Dr. Massimiliano Migliori
Dr. Vincenzo Cantaluppi
Guest Editors

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