Current Understanding of Inflammatory Responses in Acute Kidney Injury

Abstract

Acute kidney injury has been a tough complex with increased mortality and morbidity. Inflammatory responses, including innate and adaptive immune responses, involve in the initiation and development of acute kidney injury, especially under the ischemic circumstances. Tubular cells and distinct immune cell subgroups play a critical role in the pathogenesis of inflammation. Current gene therapies show their benefits in renal repair. Here, we reviewed the renal inflammatory infiltration, inflammatory mediators, oxidative stress and potential signaling pathways, which give rise to the kidney diseases, in the mechanism of acute kidney injury. Recent studies showed diverse insights in understanding the pathophysiological process of inflammation related renal injury and provided novel clinical targets for ameliorating acute kidney injury by balancing the facilitation of repairing and prevention of impairing. Interestingly, antisense oligonucleotides of target sequence, local electransfering on solid organ and adenovirus-mediated certain gene overexpression have been promising strategies in alleviating acute kidney injury.

Evaluation of renal ischemia‐reperfusion injury by magnetic resonance imaging texture analysis: An experimental study

“…In our study, the BOLD_S(4,‐4)Correlation value was increased at 1 hour after reperfusion and was higher at 48 hours than at 1 hour after reperfusion. Our results indicated that BOLD_S(4,‐4)Correlation had the strongest correlation with interstitial inflammatory cell infiltration, which may be related to the activation of inflammatory response that led to endothelial cell activation, leukocyte adhesion, and embedding, causing changes in the microvessel blood flow 24 …”

“…Our results indicated that BOLD_S(4,-4)Correlation had the strongest correlation with interstitial inflammatory cell infiltration, which may be related to the activation of inflammatory response that led to endothelial cell activation, leukocyte adhesion, and embedding, causing changes in the microvessel blood flow. 24 A previous study found obvious changes in the renal outer medulla on SWI after renal IRI, and the integrity of the hypointense outer medulla on SWI showed significant differences at various time points after IRI. 12 This study further investigated the correlation between renal T A B L E 4 Receiver operating characteristic curve analysis of texture features in the differentiation of the kidney at 1 and 12 hours after reperfusion from that at 24…”

“…24 A previous study found obvious changes in the renal outer medulla on SWI after renal IRI, and the integrity of the hypointense outer medulla on SWI showed significant differences at various time points after IRI. 12 This study further investigated the correlation between renal T A B L E 4 Receiver operating characteristic curve analysis of texture features in the differentiation of the kidney at 1 and 12 hours after reperfusion from that at 24…”

Synergistic renoprotective effects of sesame oil and erythropoietin on ischemic kidney injury after renal transplantation

“…ROS are released during I/R and play a primary role in kidney tissue injury (Salvadori et al 2015). Hu et al (2017) reported that kidney tissue injury induces inflammatory reactions and subsequent release of proinflammatory markers. Such inflammatory reactions affect kidney function and increase proinflammatory markers, as evidenced by increased BUN, ALT, and creatinine levels.…”

Eleutheroside B Protects against Acute Kidney Injury by Activating IGF Pathway

“…An inflammatory cascade reaction is one of the main causes of renal injury caused by cisplatin [24]. Experimental studies of AKI often use models such as ischemia and reperfusion injury-, drug nephrotoxicity, and sepsis endotoxemia [25], all of which involve inflammation [11,26,27]. Apoptosis, or programmed necrosis, of renal tubular epithelial cells is a common pathological feature in AKI models [13,14].…”