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10.1097/MCC.0000000000000153 http://scihub22266oqcxt.onion/10.1097/MCC.0000000000000153 C4495653!4495653!25320909     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       Curr+Opin+Crit+Care 2014 ; 20 (6): 588-95 Nephropedia Template TP {{tp|p=25320909|t=2014. Sepsis-induced AKI revisited: pathophysiology, prevention and future therapies |pdf=|usr=}}{{25320909}} gab.com Text Sepsis-induced AKI revisited: pathophysiology, prevention and future therapies JO: Curr Opin Crit Care http://www.kidney.de/pget.php?&tw=1&pmid=25320909 #FOAvip Purpose of review: Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with increased morbidity and mortality. Sepsis is the most common cause of AKI. Considerable evidence now suggests that the pathogenic mechanisms of sepsis-induced AKI are different from those seen in other etiologies of AKI. This review focuses on the recent advances in this area and discusses possible therapeutic interventions that might derive from these new insights into the pathogenesis of sepsis-induced AKI. Recent findings: The traditional paradigm that sepsis-induced AKI arises from ischemia has been challenged by recent evidence that total renal blood flow (RBF) in is not universally impaired during sepsis, and AKI can develop in the presence of normal or even increased RBF. Animal and human studies suggest that adaptive responses of tubular epithelial cells to injurious signals are responsible for renal dysfunction. Simultaneously occurring renal inflammation and microcirculatory dysfunction further amplify these mechanisms. Summary: An understanding of the pathologic mechanisms of sepsis-induced AKI emphasizes the important role of maladaptive responses to the septic insult. Preventive and therapeutic measures should be based on counteracting these maladaptive responses of tubular epithelial cells, inflammation, and microvascular dysfunction. Twit Text FOAVip Sepsis-induced AKI revisited: pathophysiology, prevention and future therapies ????Curr Opin Crit Care http://www.kidney.de/pget.php?&tw=1&pmid=25320909 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25320909 #FOAvip English Wikipedia <ref>{{Cite pmid|25320909}}</ref> Sepsis-induced AKI revisited: pathophysiology, prevention and future therapies #MMPMID25320909 Zarbock A; Gomez H; Kellum JA Curr Opin Crit Care 2014[Dec]; 20 (6): 588-95 PMID25320909show ga Purpose of review: Acute kidney injury (AKI) is a common complication in critically ill patients and is associated with increased morbidity and mortality. Sepsis is the most common cause of AKI. Considerable evidence now suggests that the pathogenic mechanisms of sepsis-induced AKI are different from those seen in other etiologies of AKI. This review focuses on the recent advances in this area and discusses possible therapeutic interventions that might derive from these new insights into the pathogenesis of sepsis-induced AKI. Recent findings: The traditional paradigm that sepsis-induced AKI arises from ischemia has been challenged by recent evidence that total renal blood flow (RBF) in is not universally impaired during sepsis, and AKI can develop in the presence of normal or even increased RBF. Animal and human studies suggest that adaptive responses of tubular epithelial cells to injurious signals are responsible for renal dysfunction. Simultaneously occurring renal inflammation and microcirculatory dysfunction further amplify these mechanisms. Summary: An understanding of the pathologic mechanisms of sepsis-induced AKI emphasizes the important role of maladaptive responses to the septic insult. Preventive and therapeutic measures should be based on counteracting these maladaptive responses of tubular epithelial cells, inflammation, and microvascular dysfunction. äSepsis-induced AKI revisited: pathophysiology, prevention and future t(epmc).pdf DeepDyve Pubget Overpricing