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Renal Research Institute, New York, New York Inflammation in CKD Inflammation is prevalent in the majority of patients with chronic kidney disease (CKD). This is indicated by higher levels of inflammatorymarkers such as C-reactive protein (CRP), serum amyloid A, and cytokines such as interleukin-6 (IL-6) and tumor necrosis factor alpha (TNF-a) (1). Increased levels of inflammatory markers can be observed at any CKD stage for reasons not yet fully understood. A relationship between elevated inflammatory biomarkers and a progressive reduction of residual renal function has been reported (1–3). Evidence also exists suggesting a link between inflammation and protein energy malnutrition. Proinflammatory cytokines may suppress appetite, promote muscle wasting, and hypoalbuminemia, and may be involved in atherogenesis (4). Strong evidence links the symptom complex of malnutrition, inflammation, and atherosclerosis (MIA syndrome) with mortality in CKD 5D patients (5,6). In this context, inflammation is of importance in a chain of interconnected events (Fig. 1). What follows is an outline of the interconnection between the depicted events; we will put forward a hypothesis linking fluid overload (FO) to inflammation and vice versa.