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10.1097/CCM.0000000000001472 http://scihub22266oqcxt.onion/10.1097/CCM.0000000000001472 C4896858!4896858!26646460     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Crit+Care+Med 2016 ; 44 (7): e492-501 Nephropedia Template TP {{tp|p=26646460|t=2016. Reversal of acute kidney injury-induced neutrophil dysfunction - A critical role for resistin |pdf=|usr=}}{{26646460}} gab.com Text Reversal of acute kidney injury-induced neutrophil dysfunction - A critical role for resistin JO: Crit Care Med http://www.kidney.de/pget.php?&tw=1&pmid=26646460 #FOAvip Objectives: To assess the reversibility of acute kidney injury (AKI)-induced neutrophil dysfunction and to identify involved mechanisms. Design: Controlled laboratory experiment and prospective observational clinical study. Setting: University laboratory and hospital. Subjects: C57BL/6 wild-type mice. Patients: Patients with septic shock with or without AKI. Interventions: Murine AKI was induced by i.p. injections of folic acid (nephrotoxic AKI) or by i.m. injections of glycerol (rhabdomyolysis-induced AKI). After 24h, we incubated isolated neutrophils for 3h in normal mouse serum or minimum essential medium (MEM) buffer. We further studied the effects of plasma samples from 13 patients with septic shock (with or without severe AKI) on neutrophilic-differentiated NB4 cells (NB4PMN). Measurements and Main Results: Experimental AKI significantly inhibited neutrophil migration and intracellular actin polymerization. Plasma levels of resistin, a pro-inflammatory cytokine and uremic toxin, were significantly elevated during both forms of AKI. Incubation in serum or MEM buffer restored normal neutrophil function. Resistin by itself was able to induce AKI-like neutrophil dysfunction in vitro.Plasma resistin was significantly higher in patients with septic shock with AKI compared to patients with septic shock alone. Compared to plasma from patients with septic shock, plasma from patients with septic shock and AKI inhibited NB4PMN migration. Even after 4d of renal replacement therapy (RRT), plasma from patients with septic shock plus AKI still showed elevated resistin levels and inhibited NB4PMN migration. Resistin inhibited NB4PMN migration and intracellular actin polymerization at concentrations seen during AKI, but not at normal physiological concentrations. Conclusions: AKI-induced neutrophil dysfunction is reversible in vitro. However, standard RRT does not correct this defect in patients with septic shock and AKI. Resistin is greatly elevated during AKI, even with ongoing RRT, and is sufficient to cause AKI-like neutrophil dysfunction by itself. Twit Text FOAVip Reversal of acute kidney injury-induced neutrophil dysfunction - A critical role for resistin ????Crit Care Med http://www.kidney.de/pget.php?&tw=1&pmid=26646460 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26646460 #FOAvip English Wikipedia <ref>{{Cite pmid|26646460}}</ref> Reversal of acute kidney injury-induced neutrophil dysfunction - A critical role for resistin #MMPMID26646460 Singbartl K; Miller L; Ruiz-Velasco V; Kellum JA Crit Care Med 2016[Jul]; 44 (7): e492-501 PMID26646460show ga Objectives: To assess the reversibility of acute kidney injury (AKI)-induced neutrophil dysfunction and to identify involved mechanisms. Design: Controlled laboratory experiment and prospective observational clinical study. Setting: University laboratory and hospital. Subjects: C57BL/6 wild-type mice. Patients: Patients with septic shock with or without AKI. Interventions: Murine AKI was induced by i.p. injections of folic acid (nephrotoxic AKI) or by i.m. injections of glycerol (rhabdomyolysis-induced AKI). After 24h, we incubated isolated neutrophils for 3h in normal mouse serum or minimum essential medium (MEM) buffer. We further studied the effects of plasma samples from 13 patients with septic shock (with or without severe AKI) on neutrophilic-differentiated NB4 cells (NB4PMN). Measurements and Main Results: Experimental AKI significantly inhibited neutrophil migration and intracellular actin polymerization. Plasma levels of resistin, a pro-inflammatory cytokine and uremic toxin, were significantly elevated during both forms of AKI. Incubation in serum or MEM buffer restored normal neutrophil function. Resistin by itself was able to induce AKI-like neutrophil dysfunction in vitro.Plasma resistin was significantly higher in patients with septic shock with AKI compared to patients with septic shock alone. Compared to plasma from patients with septic shock, plasma from patients with septic shock and AKI inhibited NB4PMN migration. Even after 4d of renal replacement therapy (RRT), plasma from patients with septic shock plus AKI still showed elevated resistin levels and inhibited NB4PMN migration. Resistin inhibited NB4PMN migration and intracellular actin polymerization at concentrations seen during AKI, but not at normal physiological concentrations. Conclusions: AKI-induced neutrophil dysfunction is reversible in vitro. However, standard RRT does not correct this defect in patients with septic shock and AKI. Resistin is greatly elevated during AKI, even with ongoing RRT, and is sufficient to cause AKI-like neutrophil dysfunction by itself. äReversal of acute kidney injury-induced neutrophil dysfunction - A cri(epmc).pdf DeepDyve Pubget Overpricing