Acute tubular necrosis classification: Difference between revisions
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==Overview== | ==Overview== | ||
Acute tubular necrosis may be classified based on the etiopathogenesis into three categories ischemic, toxin-induced, and mixed. | |||
==Classification== | ==Classification== | ||
* Acute tubular necrosis may be classified into three categories based on the underlying | * Acute tubular necrosis may be classified into three categories based on the underlying etiopathologic mechanisms involved.<ref name="pmid16646986">{{cite journal |vauthors=Santos WJ, Zanetta DM, Pires AC, Lobo SM, Lima EQ, Burdmann EA |title=Patients with ischaemic, mixed and nephrotoxic acute tubular necrosis in the intensive care unit--a homogeneous population? |journal=Crit Care |volume=10 |issue=2 |pages=R68 |date=2006 |pmid=16646986 |pmc=1550879 |doi=10.1186/cc4904 |url=}}</ref> | ||
** Ischemic acute tubular necrosis | ** Ischemic acute tubular necrosis | ||
** Nephrotoxic acute tubular necrosis | ** Nephrotoxic acute tubular necrosis | ||
** Mixed acute tubular necrosis | ** Mixed acute tubular necrosis | ||
* Ischemic ATN resulting from conditions leading to inadequate blood flow to the kidneys during 48 hrs (eg, shock, sepsis, hemorrhage, volume loss, and hypotension) without nephrotoxin exposure that results in acute renal failure and rise in serum creatinine levels. | * Ischemic [[Acute tubular necrosis|ATN]] resulting from conditions leading to inadequate blood flow to the [[Kidney|kidneys]] during 48 hrs (eg, [[shock]], [[sepsis]], [[Bleeding|hemorrhage]], [[Hypovolemia|volume loss]], and [[hypotension]]) without nephrotoxin exposure that results in [[Acute kidney injury|acute renal failure]] and rise in serum [[creatinine]] levels. | ||
* Nephrotoxic ATN occurs as a result of exposure of kidneys to various nephrotoxic medications and chemicals (eg, aminoglycosides, radiocontrast media, ACE inhibitors, NSAIDs, cyclosporine, and sulfa drugs) during 72 hrs preceding the increase in serum creatinine. | * Nephrotoxic [[Acute tubular necrosis|ATN]] occurs as a result of exposure of [[Kidney|kidneys]] to various nephrotoxic [[Medication|medications]] and chemicals (eg, [[Aminoglycoside|aminoglycosides]], [[Radiocontrast|radiocontrast media]], [[ACE inhibitor|ACE inhibitors]], [[Non-steroidal anti-inflammatory drug|NSAIDs]], [[cyclosporine]], and [[Sulfonamide (medicine)|sulfa drugs]]) during 72 hrs preceding the increase in serum [[creatinine]]. | ||
Revision as of 20:10, 10 May 2018
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]
Overview
Acute tubular necrosis may be classified based on the etiopathogenesis into three categories ischemic, toxin-induced, and mixed.
Classification
- Acute tubular necrosis may be classified into three categories based on the underlying etiopathologic mechanisms involved.[1]
- Ischemic acute tubular necrosis
- Nephrotoxic acute tubular necrosis
- Mixed acute tubular necrosis
- Ischemic ATN resulting from conditions leading to inadequate blood flow to the kidneys during 48 hrs (eg, shock, sepsis, hemorrhage, volume loss, and hypotension) without nephrotoxin exposure that results in acute renal failure and rise in serum creatinine levels.
- Nephrotoxic ATN occurs as a result of exposure of kidneys to various nephrotoxic medications and chemicals (eg, aminoglycosides, radiocontrast media, ACE inhibitors, NSAIDs, cyclosporine, and sulfa drugs) during 72 hrs preceding the increase in serum creatinine.
References
- ↑ Santos WJ, Zanetta DM, Pires AC, Lobo SM, Lima EQ, Burdmann EA (2006). "Patients with ischaemic, mixed and nephrotoxic acute tubular necrosis in the intensive care unit--a homogeneous population?". Crit Care. 10 (2): R68. doi:10.1186/cc4904. PMC 1550879. PMID 16646986.