Chapter 10

Acute Tubular Necrosis

Amanda DeMauro Renaghan

Amanda DeMauro Renaghan

Division of Nephrology, University of Virginia Health System, Charlottesville, VA, USA

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Mitchell H. Rosner

Mitchell H. Rosner

Division of Nephrology, University of Virginia Health System, Charlottesville, VA, USA

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First published: 18 November 2022

Summary

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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