Inflammation and Premature Ageing in Chronic Kidney Disease

• Published in: Toxins Vol. 12; no. 4; p. 227
• Main Authors: Ebert, Thomas, Pawelzik, Sven-Christian, Witasp, Anna, Arefin, Samsul, Hobson, Sam, Kublickiene, Karolina, Shiels, Paul G, Bäck, Magnus, Stenvinkel, Peter
• Format: Journal Article
• Language: English
• Published: Switzerland MDPI AG 04.04.2020; MDPI
• Subjects: Age; ageing; Aging; Aging, Premature - metabolism; Aging, Premature - mortality; Aging, Premature - physiopathology; Animals; Biomarkers - metabolism; Calcification; chronic kidney disease; Cytokines; end-stage kidney disease; Fibroblast growth factors; Genotype & phenotype; Growth factors; Health Status; Homology; Humans; Immune system; Inflammation; Inflammation - metabolism; Inflammation - mortality; Inflammation - physiopathology; Inflammation - therapy; Inflammation Mediators - metabolism; Kidney - metabolism; Kidney - pathology; Kidney - physiopathology; Kidney diseases; Kidneys; Kinases; Klotho protein; Medicin och hälsovetenskap; Metabolism; Mitochondria; Mortality; Oxidative stress; Phenotype; Phenotypes; premature ageing; Prognosis; Proteins; Quality of Life; Renal Insufficiency, Chronic - metabolism; Renal Insufficiency, Chronic - mortality; Renal Insufficiency, Chronic - physiopathology; Renal Insufficiency, Chronic - therapy; Review; Risk Factors; Sarcopenia; Senescence; Signal Transduction; Smooth muscle; Telomerase; Therapeutic applications; Toxins, Biological - metabolism; Transcription factors; Tumor necrosis factor-TNF; Uremia - metabolism; Uremia - mortality; Uremia - physiopathology; Uremia - therapy; senescence; ageing; chronic kidney disease; premature ageing; end-stage kidney disease; uremic toxins; inflammation
• ISSN: 2072-6651; 2072-6651
• DOI: 10.3390/toxins12040227

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.