Inflammation and Premature Ageing in Chronic Kidney Disease

Abstract

Persistent low-grade inflammation and premature ageing are hallmarks of the uremic phenotype and contribute to impaired health status, reduced quality of life, and premature mortality in chronic kidney disease (CKD). Because there is a huge global burden of disease due to CKD, treatment strategies targeting inflammation and premature ageing in CKD are of particular interest. Several distinct features of the uremic phenotype may represent potential treatment options to attenuate the risk of progression and poor outcome in CKD. The nuclear factor erythroid 2-related factor 2 (NRF2)–kelch-like erythroid cell-derived protein with CNC homology [ECH]-associated protein 1 (KEAP1) signaling pathway, the endocrine phosphate-fibroblast growth factor-23–klotho axis, increased cellular senescence, and impaired mitochondrial biogenesis are currently the most promising candidates, and different pharmaceutical compounds are already under evaluation. If studies in humans show beneficial effects, carefully phenotyped patients with CKD can benefit from them.

The Role of Eryptosis in the Pathogenesis of Renal Anemia: Insights From Basic Research and Mathematical Modeling

“…The triad of aging, inflammation, and oxidative stress reduces the quality of life of CKD patients. The emblematic term inflammaging has been introduced to highlight the role of these factors in the often rapid deterioration of the patient’s health, longevity, and well-being ( Ebert et al, 2020 ). Interestingly, inflammatory biomarkers such as interleukin 6 and C-reactive protein are not correlated with RBC life span in HD patients ( Ma et al, 2017 ).…”

Editorial on the Special Issue “Comorbidities in Chronic Kidney Disease”

“…Chronic low-grade inflammation is a hallmark of CKD and is closely associated with cellular senescence and accelerated ageing. In this Special Issue, Ebert et al [ 26 ] elaborate on this so-called “inflammageing” in CKD. They address the phenotype of inflammation and premature ageing in CKD patients as well as their mutual activation.…”

Cancer in Dialysis Patients

“…The abnormal immunoactivation is multifactorial, mainly affects monocytes, increased synthesis of proinflammatory cytokines such as interleukin 1 (IL-1), IL-6, tumor necrosis factor (TNF) and chemokines [7][8]. This immunoactivation is additionally stimulated by the increased gut permeability, intestinal dysbiosis [8][9], exogenous factors such as potential dialysis access contamination (catheters and not native fistulas) and dialysis membranes biocompatibility [10].…”

“…The immunosuppression relates to reduced function of T and B lymphocytes, which additional affects the accelerated body aging [7,9,[11][12].…”