**1. Introduction—CKD, Inflammation, and Premature Ageing**

Chronic kidney disease (CKD) is a major global health burden that contributes to increased morbidity and mortality in a ffected patients [1]. Inflammation is a key risk factor for CKD progression [2], and recent data from the CANTOS trial sugges<sup>t</sup> that anti-inflammatory treatment in patients with CKD reduces major adverse cardiovascular events [3]. Compared to the general population, patients with CKD also have a highly accelerated ageing process that is characterized by vascular disease; a persistent, low-grade inflammatory status; sarcopenia; and other maladies [4]. Both inflammation and ageing (i.e., "inflammageing") are established risk factors for mortality in a cluster of "burden of lifestyle diseases", such as CKD [5], which has been recognized as one of the prototype diseases for premature ageing [6]. Persistent inflammation, premature ageing, and CKD share common regulatory patterns of distinct biological pathways. For instance, the transcription factor nuclear factor erythroid 2-related factor 2 (NRF2) is downregulated in all three conditions [7–9]. Thus, both inflammation and premature ageing are major contributing factors to health status and outcome in patients with CKD.

The aim of this review is to summarize the clinical phenotypes of inflammation and premature ageing in CKD. We also summarize the relationship between these two phenotypes. Furthermore, we provide an overview of novel factors contributing to the uremic phenotype, and we describe potential novel targets for the systemic treatment of these interrelated disorders.
