Inflammation and Premature Ageing in Chronic Kidney Disease
Thomas Ebert,
Sven-Christian Pawelzik,
Anna Witasp,
Samsul Arefin,
Sam Hobson,
Karolina Kublickiene,
Paul G. Shiels,
Magnus Bäck,
Peter Stenvinkel
Affiliations
Thomas Ebert
Karolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden
Sven-Christian Pawelzik
Karolinska Institutet, Department of Medicine Solna, Cardiovascular Medicine Unit, SE-171 76 Stockholm, Sweden
Anna Witasp
Karolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden
Samsul Arefin
Karolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden
Sam Hobson
Karolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden
Karolina Kublickiene
Karolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden
Paul G. Shiels
University of Glasgow, Wolfson Wohl Cancer Research Centre, College of Medical, Veterinary & Life Sciences, Institute of Cancer Sciences, Glasgow G61 1QH, UK
Magnus Bäck
Karolinska Institutet, Department of Medicine Solna, Cardiovascular Medicine Unit, SE-171 76 Stockholm, Sweden
Peter Stenvinkel
Karolinska Institutet, Department of Clinical Science, Intervention and Technology, Division of Renal Medicine, SE-141 86 Stockholm, Sweden
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.
