Abstract
Systemic low-grade inflammation is common in patients with chronic kidney disease (CKD). The prevalence of signs of inflammation are inversely related to the level of kidney function and positively associated with the magnitude of proteinuria. Cytokines and acute-phase proteins are key mediators as well as markers of inflammation. The etiology of inflammation in CKD is multifactorial. Comorbidities such as older age, minority race, and the presence of diabetes are independent predictors of inflammation in CKD patients. Endotoxin translocation across the gut and damage/danger-associated molecular patterns may contribute to excess inflammation in CKD. Dysregulated immune responses and the resultant inflammation are mediators and/or catalysts in the progression of renal disease, pathogenesis of cardiovascular disease, and the development of insulin resistance, protein energy wasting, anemia, and abnormal bone-mineral metabolism in patients with CKD. Progress in treatment of inflammation in patients with CKD is hampered by the complexity of the molecular pathways related to inflammation and the essential nature of some of these signaling mechanisms for cell/organism survival. However, a number of novel treatment strategies to attenuate inflammation in CKD are currently being explored.
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