*Review* **Inflammation and Premature Ageing in Chronic Kidney Disease**

**Thomas Ebert 1,\*,**†**, Sven-Christian Pawelzik 2,3,**†**, Anna Witasp 1, Samsul Arefin 1, Sam Hobson 1, Karolina Kublickiene 1, Paul G. Shiels 4, Magnus Bäck 2,3,**‡ **and Peter Stenvinkel 1,\*,**‡


Received: 1 February 2020; Accepted: 29 March 2020; Published: 4 April 2020

**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 di fferent pharmaceutical compounds are already under evaluation. If studies in humans show beneficial e ffects, carefully phenotyped patients with CKD can benefit from them.

**Keywords:** ageing; chronic kidney disease; end-stage kidney disease; inflammation; premature ageing; senescence; uremic toxins

**Key Contribution:** We summarize the current literature on uremic inflammation and premature ageing in Chronic Kidney Disease and discuss potential treatment strategies.
