Acute tubular necrosis overview: Difference between revisions
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==Overview== | ==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. | 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.<ref name="pmid18235086">{{cite journal| author=Rosen S, Stillman IE| title=Acute tubular necrosis is a syndrome of physiologic and pathologic dissociation. | journal=J Am Soc Nephrol | year= 2008 | volume= 19 | issue= 5 | pages= 871-5 | pmid=18235086 | doi=10.1681/ASN.2007080913 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=18235086 }} </ref> 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.<ref name="Fogo">Fogo A, Cohen AH, Colvin RB et al. Fundamentals of Renal Pathology 2013. Acute Tubular Necrosis.[[http://dx.doi.org/10.1007/978-3-642-39080-7_15]]</ref> | ||
==References== | ==References== | ||
Revision as of 18:19, 19 January 2014
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [2]; 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.[1] 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.[2]
References
- ↑ Rosen S, Stillman IE (2008). "Acute tubular necrosis is a syndrome of physiologic and pathologic dissociation". J Am Soc Nephrol. 19 (5): 871–5. doi:10.1681/ASN.2007080913. PMID 18235086.
- ↑ Fogo A, Cohen AH, Colvin RB et al. Fundamentals of Renal Pathology 2013. Acute Tubular Necrosis.[[1]]