Acute tubular necrosis classification: Difference between revisions
Jump to navigation
Jump to search
No edit summary |
No edit summary |
||
| Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{Acute tubular necrosis}} | {{Acute tubular necrosis}} | ||
| Line 10: | Line 7: | ||
==Classification== | ==Classification== | ||
* Acute tubular necrosis may be classified into | * Acute tubular necrosis may be classified into three categories based on the underlying pathologic 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 | ** Ischemic acute tubular necrosis | ||
** Nephrotoxic | ** 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. | |||
Revision as of 20:02, 10 May 2018
|
Acute tubular necrosis Microchapters |
|
Diagnosis |
|---|
|
Treatment |
|
Case Studies |
|
Acute tubular necrosis classification On the Web |
|
American Roentgen Ray Society Images of Acute tubular necrosis classification |
|
Risk calculators and risk factors for Acute tubular necrosis classification |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]
Overview
ATN can be broadly classified into ischemic or toxin-induced.
Classification
- Acute tubular necrosis may be classified into three categories based on the underlying pathologic 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.