Obesity, diabetes mellitus, hypertension and cardiovascular disease are risk factors for chronic kidney disease (CKD) and kidney failure. Chronic, low-grade inflammation is recognized as a major pathogenic mechanism that underlies the association between CKD and obesity, impaired glucose tolerance, insulin resistance and diabetes, through interaction between resident and/or circulating immune cells with parenchymal cells. Thus, considerable interest exists in approaches that target inflammation as a strategy to manage CKD. The initial phase of the inflammatory response to injury or metabolic dysfunction reflects the release of pro-inflammatory mediators including peptides, lipids and cytokines, and the recruitment of leukocytes. In self-limiting inflammation, the evolving inflammatory response is coupled to distinct processes that promote the resolution of inflammation and restore homeostasis. The discovery of endogenously generated lipid mediators — specialized pro-resolving lipid mediators and branched fatty acid esters of hydroxy fatty acids — which promote the resolution of inflammation and attenuate the microvascular and macrovascular complications of obesity and diabetes mellitus highlights novel opportunities for potential therapeutic intervention through the targeting of pro-resolution, rather than anti-inflammatory pathways.

肥胖、糖尿病、高血压和心血管疾病是慢性肾脏病 (CKD) 和肾衰竭的危险因素。慢性低度炎症被认为是 CKD 与肥胖、葡萄糖耐量降低、胰岛素抵抗和糖尿病之间关联的主要致病机制，通过驻留和/或循环免疫细胞与实质细胞之间的相互作用。因此，人们对将炎症作为治疗 CKD 策略的方法产生了相当大的兴趣。对损伤或代谢功能障碍的炎症反应的初始阶段反映了促炎介质的释放，包括肽、脂质和细胞因子，以及白细胞的募集。在自限性炎症中，不断发展的炎症反应与促进炎症消退和恢复体内平衡的不同过程相结合。内源性脂质介质的发现 - 专门的促分解脂质介质和羟基脂肪酸的支链脂肪酸酯 - 促进炎症的消退并减轻肥胖和糖尿病的微血管和大血管并发症，突出了潜在治疗干预的新机会靶向促消退，而不是抗炎途径。