Cell biology and molecular mechanisms of injury in ischemic acute renal failure.
The pathogenesis of acute renal failure has been attributed to persistent vasoconstriction and leukocyte-endothelial interactions, resulting in inflammation and compromise of local blood flow to the outer medulla, the loss of tubular epithelial cell polarity with multiple functional sequelae, necrosis or apoptosis of epithelial cells, and the de-differentiation, migration and proliferation of surviving cells. In this paper, the authors present their views of pathophysiology of ischemic acute renal failure.
Massachusetts General Hospital and Department of Medicine, Harvard Medical School, and the Harvard-Massachusetts Institute of Technology,Charlestown 02129, USA.
A M
AM
Sheridan
J V
JV
Bonventre
D058186:Acute Kidney Injury / Q000473:pathology / Q000503:physiopathology*; D000818:Animals; D017209:Apoptosis; D006439:Hemodynamics; D006801:Humans; D007511:Ischemia / Q000503:physiopathology*; D007668:Kidney / Q000098:blood supply*; D007687:Kidney Tubules, Proximal / Q000473:pathology / Q000503:physiopathology; D007962:Leukocytes / Q000502:physiology; D012079:Renal Circulation