|
|
Research progress and mechanism of sepsis-induced acute kidney injury |
ZHENG Ting YANG Dingping▲ |
Department of Nephrology, Renmin Hospital of Wuhan University, Hubei Province, Wuhan 430060, China |
|
|
Abstract Acute kidney injury is one of the most common and serious complications of severe sepsis. And the incidence and mortality of patients with sepsis-induced acute kidney injury (SAKI) remained high. In recent years, more and more studies have shown that the mechanism of mitochondrial dynamics, autophagy, oxidative stress and inflammatory response plays an extremely important role in the formation of SAKI. Therefore, understanding the development mechanism of SAKI is helpful for better prevention and control, and effectively reduce morbidity and mortality. In this paper, the mechanism of occurrence and development of SAKI is reviewed.
|
|
|
|
|
[1] Singer M,Deutschman CS,Seymour CW,et al. The third international consensus definitions for sepsis and septic shock(Sepsis-3)[J]. The Journal of the American Medical Association,2016,315(8): 801-810.
[2] Ricci Z, Ronco C. Pathogenesis of acute kidney injury during sepsis [J]. Curr Drug Targets,2009,10(5):1179-1183.
[3] Doi K. Role of kidney injury in sepsis [J]. Curr Opin Crit Care,2014,20:588-595.
[4] Nisula S,Kaukonen KM,Vaara ST,et al. Incidence risk factors and 90-day mortality of patients with acute kidney injury in Finnish intensive care units FINNAKE study [J]. Intensive Care Med,2013,39(3):420-428.
[5] Angus DC,Linde-Zwirble WT,Lidicker J,et al. Epidemiology of severe sepsis in the United States:analysis of incidence,outcome,and associated costs of care [J]. Crit Care Med,2001,29(7):1303-1314.
[6] Shinjo H,Sato W,Imai E,et al. Comparis of kidney disease:improving global outcomes and acute kidney injury net work criteria for assessing patients in intensive care units [J]. Clin Exp Nephorl,2014,18(5):737-745.
[7] Fang Y,Ding X,Zhong Y,et al. Actue kidney injury in a Chinese hospitalized population[J].Blood Purif,2010,30(2):120-126.
[8] Wen Y,Jiang L,Xu Y,et al. Prevalence risk factors clinical course and outcome of acute kidney injury in Chinese intensive care units :a prospective cohort study [J].Chin Med J,2013,126(23):4409-4416.
[9] Kellum JA,Lameire N. KDIGO AKI Guide line Work Group Diagnosis,evaluation,and management of acute kidney injury. A KDIGO summary (part 1)[J]. Crit Care,2013,17(1):204.
[10] Goncalves GM,Zamboni DS,Camara NO. The role of innate immunity in septic acute kidney injuries [J]. Shock,2010,34(7):22-26.
[11] Hocherl K,Schmidt C,Kurt B,et al. Inhibition of NF-κB ameliorates sepsis-induced downregulation of aquaporin-2/V2 receptor expression and acute renal failure in vivo [J].Am J Physiol Renal Physiol,2010,298(1):F196-204.
[12] Lopes JA,Fernandes P,Jorge S,et al. Long-term risk of mortality after acute kidney injury in patients with sepsis:a contemporary analysis [J]. BMC Nephrology,2010, 11(1):1-10.
[13] Bagshaw SM,Darmon M,Ostermann M,et al. Current state of the art for renal replacement therapy in critically ill patients with acute kidney injury [J]. Intensive Care Med,2017,43(6):841-854.
[14] Mizushima N,Levine B,Cuervo AM,et al. Autophagy Fights disease through cellular self-digestion [J]. Nature,2008, 451(7182):1069-1075.
[15] Leventhal JS,Ni J,Osmond M,et al. Autophagy limits endotoxemic acute kidney injury and alters renal tubular epithelial cell cytokine expression [J]. PLoS One,2016, 11(3):e0 150 001.
[16] Jiang M, Wei Q,Dong G,et al. Autophagy in proximal tubules protects against acute kidney injury [J]. Kidney Int,2012,82(12):1271-1283.
[17] Mei S,Livingston M,Hao J,et al. Autophagy is activated to protect against endotoxic acute kidney injury [J]. Scientific Reports,2016,6:22 171.
[18] Wu Y,Zhang Y,Wang L,et al. The role of Autophagy in kidney inflammatory injury via the NF-κB route induced by LPS [J]. Int J Med Sci,2015,12(8):655-667.
[19] Zhao H,Zhao M,Wang Y,et al. Glycyrrhizic acid attenuates sepsis induced acute kidney injury by inhibiting NF-κB signaling pathway [J]. Evid Based Complement Alternat Med,2016:8 219 287.
[20] Zhang L,Sun D,Bao Y,et al. Nerolidol protects against LPS-induced acute kidney injury via inhibiting TLR4/NF-κB signaling [J]. Phytolther Res,2017,31(3):459-465.
[21] Hu L,Chen C,Zhang J,et al. IL-35 pretreatment alleviates lipopolysaccharide-induced acute kidney injury in mice by inhibiting NF-κB activation [J]. Inflammation,2017,40(4):1393-1400.
[22] Ye HY,Jin J,Jin LW,et al. Chlorogenic acid attenuates lipopolysaccharide-induced acute kidney injury by inhibiting TLR4/NF-kappaB signal pathway [J]. Inflammation,2017,40(2):523-529.
[23] Zhao H,Zheng Q, Hu X,et al. Betulin attenuates kidney injury in septic rats through inhibiting TLR4/NF-kappaB signaling pathway [J]. Life Sci,2016,144:185-193.
[24] Lerolle N,Nochy D,Guerot E,et al. Histopathyology of septic shock induced renal injury apotosis and leukocytic infiltration [J]. Intensive Care Med,2010,36(3):471-478.
[25] Cantaluppi V,Weber V,Lauritano C,et al. Protective effect of resin on septic plasma-induced tubular injury [J]. Critical Care,2010,14(1):R4.
[26] 宣小燕,张爱华,黄松明.线粒体通透性转换孔与急性肾损伤[J].中华肾脏病杂志,2010,48(16):1243-1246.
[27] Muthuraman A, Sood S,Ramesh M,et al. Therapeutic potential of 7,8-dimethoxvcoumarin on cisplatin and ischemia/reperfusion injury-induced acute renal failure in rats [J]. Naunyn Schmiedebergs Arch Pharmacol,2012, 385(7):739-748.
[28] Fernandes MP,Leite AC,Araujo FF,et al. The cratylia mollis seed leetin induces membrane permeability transition in isolated rat liver mitoehondria and a eyelosporine A-insensitive permeability ransition in trypanosoma cruzi mitochondria [J]. J Eukaryot Microbiol,2014,61(4):381-388.
[29] 张敏,严斌,陶悦,等.内质网应激在脓毒症大鼠肾损伤中的作用[J].中华实验外科杂志,2015,32(4):821-823.
[30] Pathak E,MacMillan-Crow LA,Mayeux PR. Role of mitochondrial oxidants in an in vitro model of sepsis-induced renal injury [J]. J Phar-macol Exp,2012,340(1):192-201.
[31] Levy MM,Fink MP,Marshall JC,et al. 2001 SCCM/ESICM/ACCP/ATS/SIS international sepsis definitions conference [J] Crit Care Med,2003,31(4):1250-1256.
[32] Tran M,Tam D,Bardia A,et al. PGC-1α promotes recovery after acute kidney injury during systemic inflammation in mice [J]. Clin Invest,2011,121:4003-4014.
[33] Rasbach KA,Schnellmann RG. PGC-1alpha over-expression promotes recovery from mitochondrial dysfunction and cell injury [J]. Biochem Biophys Res Commun,2007,355:734-739.
[34] Morigi M,Perico L,Rota C,et al. Sirtun 3-dependent mitochondrial dynamic improvements protect against acute kidney injury [J]. Clin Invest,2015,125(2):715-726.
[35] Parikh SM,Yang Y,He L,et al. Mitochondrial function and disturbances in the septic kidney [J]. Semin Nephrol,2015,35(1):108-119.
[36] Bagshaw SM,Uchino S,Bellomo R,et al. Septic acute kidney injury in critically ill patients:clinical characteristics and outcomes [J]. Clin J Am Soc Nephrol,2007,2(3):431-439.
[37] Langenberg C,Wan L,Egi M,et al. Renal blood flow in experimental septic acute renal failure [J]. Kidney Int,2006,69(11):1996-2002. |
|
|
|