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10.1093/ndt/gft503 http://scihub22266oqcxt.onion/10.1093/ndt/gft503 C4071050!4071050!24378526     free     free     free       Nephrol+Dial+Transplant 2014 ; 29 (7): 1312-9 Nephropedia Template TP {{tp|p=24378526|t=2014. Epithelial transport during septic acute kidney injury |pdf=|usr=}}{{24378526}} gab.com Text Epithelial transport during septic acute kidney injury JO: Nephrol Dial Transplant http://www.kidney.de/pget.php?&tw=1&pmid=24378526 #FOAvip A goal for scientists studying septic acute kidney injury (AKI) should be to formulate a conceptual model of disease that is able to coherently reconcile the molecular and inflammatory consequences of sepsis with impaired epithelial tubular function, diminished glomerular filtration rate (GFR) and ultimately kidney failure. Recent evidence has shed light on how sepsis modulates the tubular regulation of ion, glucose, urea and water transport and acid?base homeostasis in the kidney. The present review summarizes recent discoveries on changes in epithelial transport under septic and endotoxemic conditions as well as the mechanisms that link inflammation with impaired tubular membrane transport. This paper also proposes that the tubular dysfunction that is mediated by inflammation in sepsis ultimately leads to increased sodium and chloride delivery to the distal tubule and macula densa, contributing to tubuloglomerular feedback and impaired GFR. We feel that this conceptual model resolves many of the physiologic and clinical paradoxes that septic AKI presents to practicing researchers and clinicians. Twit Text FOAVip Epithelial transport during septic acute kidney injury ????Nephrol Dial Transplant http://www.kidney.de/pget.php?&tw=1&pmid=24378526 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24378526 #FOAvip English Wikipedia <ref>{{Cite pmid|24378526}}</ref> Epithelial transport during septic acute kidney injury #MMPMID24378526 Morrell ED; Kellum JA; Hallows KR; Pastor-Soler NM Nephrol Dial Transplant 2014[Jul]; 29 (7): 1312-9 PMID24378526show ga A goal for scientists studying septic acute kidney injury (AKI) should be to formulate a conceptual model of disease that is able to coherently reconcile the molecular and inflammatory consequences of sepsis with impaired epithelial tubular function, diminished glomerular filtration rate (GFR) and ultimately kidney failure. Recent evidence has shed light on how sepsis modulates the tubular regulation of ion, glucose, urea and water transport and acid?base homeostasis in the kidney. The present review summarizes recent discoveries on changes in epithelial transport under septic and endotoxemic conditions as well as the mechanisms that link inflammation with impaired tubular membrane transport. This paper also proposes that the tubular dysfunction that is mediated by inflammation in sepsis ultimately leads to increased sodium and chloride delivery to the distal tubule and macula densa, contributing to tubuloglomerular feedback and impaired GFR. We feel that this conceptual model resolves many of the physiologic and clinical paradoxes that septic AKI presents to practicing researchers and clinicians. äEpithelial transport during septic acute kidney injury (epmc).pdf DeepDyve Pubget Overpricing