Acute tubular necrosis overview: Difference between revisions
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{{Acute tubular necrosis}} | {{Acute tubular necrosis}} | ||
{{CMG}}; | {{CMG}}; {{AE}} [[user:Sergekorjian|Serge Korjian]], [[user:YazanDaaboul|Yazan Daaboul]] | ||
==Overview== | ==Overview== | ||
Revision as of 16:23, 5 January 2014
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Acute tubular necrosis Microchapters |
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Acute tubular necrosis overview On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Serge Korjian, Yazan Daaboul
Overview
Acute tubular necrosis (ATN) defines a pathologic process rather than a clinical syndrome in which varying degrees of renal tubular injury occur. Clinically, ATN manifests as acute kidney injury although the terms have previously been used interchangeably. ATN is the most common cause of overt AKI. Despite the term, ATN does not necessarily imply cellular necrosis with evidence of non-necrotic injury observed more consistently. Furthermore, clinicopathologic correlation is often irrelevant with severe renal insufficiency sometimes seen with modest pathological findings. ATN can be either ischemic or toxin induced. Classically, ischemic ATN follows hypotension or hypovolemia with patchy involvement usually observed. On the other hand, toxic ATN is usually a dose-dependent injury seen with medications, diagnostic agents, and heavy metals with proximal tubule damage involving almost all nephrons.