Acute Tubular Necrosis
Amanda DeMauro Renaghan
Division of Nephrology, University of Virginia Health System, Charlottesville, VA, USA
Search for more papers by this authorMitchell H. Rosner
Division of Nephrology, University of Virginia Health System, Charlottesville, VA, USA
Search for more papers by this authorAmanda DeMauro Renaghan
Division of Nephrology, University of Virginia Health System, Charlottesville, VA, USA
Search for more papers by this authorMitchell H. Rosner
Division of Nephrology, University of Virginia Health System, Charlottesville, VA, USA
Search for more papers by this authorJonathan C. Craig MBChB, DipCH, MMed(Clin Epi), PhD, FAHMS
Matthew Flinders Distinguished Professor Vice President and Executive Dean
College of Medicine and Public Health, Flinders University, Adelaide, Australia
Search for more papers by this authorDonald A. Molony MD
Professor of Medicine Distinguished Teaching Professor of the University of Texas System
Division of Renal Diseases and Hypertension AND Center for Clinical Research and Evidence-based Medicine, McGovern Medical School University of Texas, Houston, TX, USA
Search for more papers by this authorGiovanni F.M. Strippoli MD, PhD, MPH, MM (Epi)
Professor of Nephrology Adjunct Professor of Epidemiology
Department of Emergency and Organ Transplantation – University of Bari, Bari, Italy
School of Public Health, University of Sydney, Sydney, NSW, Australia
Search for more papers by this authorSummary
The two most common etiologies of Acute kidney injury are prerenal azotemia, caused by reversible renal hypoperfusion, and acute tubular necrosis (ATN). ATN results from intrinsic parenchymal damage mediated by endothelial and epithelial cell injury, intratubular obstruction, and immunologic and inflammatory processes. ATN is a histopathologic and pathophysiologic entity that is the end result of numerous ischemic, nephrotoxic, and inflammatory insults. Certain patients and populations are at greater risk for the development of ATN based on age, comorbidities, severity of illness, and exposures to procedures and medications. The histologic lesions of ATN predominantly affect the proximal tubules and vary with the severity of kidney injury and the stage of evolution of the lesion. In ATN, renal blood supply (RBF) can decrease by as much as 30–50%, with a disproportionate decrease in medullary blood flow relative to total RBF contributing to pronounced medullary ischemia.
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