Acute tubular necrosis natural history, complications and prognosis: Difference between revisions
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==Overview== | ==Overview== | ||
Acute tubular necrosis may usually develop through 3 phases, initiation, maintenance and recovery. Common complications of acute tubular necrosis include electrolyte imbalance(eg, hyperkalemia, hyperphosphatemia, metabolic acidosis), platelet dysfunction and altered consciousness or coma. Prognosis depends on the underlying etiology. | Acute tubular necrosis may usually develop through 3 phases, initiation, maintenance and recovery. Common complications of acute tubular necrosis include [[Electrolyte disturbance|electrolyte imbalance]](eg, [[hyperkalemia]], [[hyperphosphatemia]], [[hypocalcemia]], and [[metabolic acidosis]]), [[platelet]] dysfunction, [[uremia]], and altered [[consciousness]] or [[coma]]. [[Prognosis]] depends on the underlying [[etiology]] and severity of [[kidney]] damage. When compared to ischemic acute tubular necrosis, nephrotoxic and mixed acute tubular necrosis have the good [[prognosis]]. | ||
==Natural History, Complications, and Prognosis== | ==Natural History, Complications, and Prognosis== | ||
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** Maintenance phase | ** Maintenance phase | ||
** Phase of recovery | ** Phase of recovery | ||
* [[Kidney|Renal]] [[injury]] by [[ischemia]], [[Hypoxemia|hypoxia]], and nephrotoxins can occur in initiation phase | * [[Kidney|Renal]] [[injury]] by [[ischemia]], [[Hypoxemia|hypoxia]], and nephrotoxins can occur in initiation phase. | ||
* After a renal [[injury]], it may progress to [[Renal insufficiency|renal failure]] depending upon the severity. once the [[Acute kidney injury|acute renal failure]] is evident, there is marked decrease in [[glomerular filtration rate]] ([[Glomerular filtration rate|GFR]]) resulting in [[oliguria]]. | * After a renal [[injury]], it may progress to [[Renal insufficiency|renal failure]] depending upon the severity. once the [[Acute kidney injury|acute renal failure]] is evident, there is marked decrease in [[glomerular filtration rate]] ([[Glomerular filtration rate|GFR]]) resulting in [[oliguria]]. | ||
* [[Oliguria]] | * [[Oliguria]] leads to accumulation of metabolic waste products and [[uremia]]. [[Uremia]] may responsible for [[altered mental status]], cognitive impairment, and other complications. | ||
* The duration of maintenance phase may vary from days to weeks. | * The duration of maintenance phase may vary from days to weeks. | ||
* Maintenance phase is followed by a recovery phase which may usually last 3-6 weeks. [[Polyuria]] can occur due to decreased concentration capacity of [[Kidney|kidneys]] in the maintenance phase. | * Maintenance phase is followed by a recovery phase which may usually last upto 3-6 weeks. [[Polyuria]] can occur due to decreased concentration capacity of [[Kidney|kidneys]] in the maintenance phase. | ||
* Eventually [[kidney]] recovery may take place resulting in normal [[glomerular filtration rate]] ([[Glomerular filtration rate|GFR]]). | * Eventually [[kidney]] recovery may take place resulting in normal [[glomerular filtration rate]] ([[Glomerular filtration rate|GFR]]). | ||
===Complications=== | ===Complications=== | ||
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** [[Hyponatraemia]] | ** [[Hyponatraemia]] | ||
** [[Metabolic acidosis]] | ** [[Metabolic acidosis]] | ||
** | ** [[Hypomagnesemia]] | ||
** [[Water retention|Fluid retention]] | |||
** [[Hyperphosphatemia]] | ** [[Hyperphosphatemia]] | ||
** [[Hemorrhagic diathesis|Bleeding diathesis]] due to [[platelet]] dysfunction | ** [[Hemorrhagic diathesis|Bleeding diathesis]] due to [[platelet]] dysfunction | ||
** [[Oliguria]] | ** [[Oliguria]] | ||
** [[Uremia]] | |||
** [[Pericarditis]] and [[pericardial effusion]] | |||
** [[Infection]] | ** [[Infection]] | ||
** [[Shock]] | ** [[Shock]] |
Latest revision as of 15:44, 9 June 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 usually develop through 3 phases, initiation, maintenance and recovery. Common complications of acute tubular necrosis include electrolyte imbalance(eg, hyperkalemia, hyperphosphatemia, hypocalcemia, and metabolic acidosis), platelet dysfunction, uremia, and altered consciousness or coma. Prognosis depends on the underlying etiology and severity of kidney damage. When compared to ischemic acute tubular necrosis, nephrotoxic and mixed acute tubular necrosis have the good prognosis.
Natural History, Complications, and Prognosis
Natural History
- Acute tubular necrosis may usually develop through 3 phases, include[1]
- Phase of initiation
- Maintenance phase
- Phase of recovery
- Renal injury by ischemia, hypoxia, and nephrotoxins can occur in initiation phase.
- After a renal injury, it may progress to renal failure depending upon the severity. once the acute renal failure is evident, there is marked decrease in glomerular filtration rate (GFR) resulting in oliguria.
- Oliguria leads to accumulation of metabolic waste products and uremia. Uremia may responsible for altered mental status, cognitive impairment, and other complications.
- The duration of maintenance phase may vary from days to weeks.
- Maintenance phase is followed by a recovery phase which may usually last upto 3-6 weeks. Polyuria can occur due to decreased concentration capacity of kidneys in the maintenance phase.
- Eventually kidney recovery may take place resulting in normal glomerular filtration rate (GFR).
Complications
- Common complications of acute tubular necrosis include:[2]
Prognosis
- Prognosis of acute tubular necrosis depends on the underlying etiology responsible for the tubular damage.[3][4]
- Prognosis is generally good in nephrotoxic acute tubular necrosis with mortality rate approximately 10%.
- Prognosis of ischemic acute tubular necrosis depends on early diagnosis and treatment of underlying condition causing renal ischemia with mortality rate approximately 30%.
- Poor prognostic factors associated with increased mortality include:[5]
References
- ↑ Ramoutar V, Landa C, James LR (August 2014). "Acute tubular necrosis (ATN) presenting with an unusually prolonged period of marked polyuria heralded by an abrupt oliguric phase". BMJ Case Rep. 2014. doi:10.1136/bcr-2013-201030. PMC 4154042. PMID 25150229.
- ↑ 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.
- ↑ Liaño F, Gallego A, Pascual J, García-Martín F, Teruel JL, Marcén R, Orofino L, Orte L, Rivera M, Gallego N (1993). "Prognosis of acute tubular necrosis: an extended prospectively contrasted study". Nephron. 63 (1): 21–31. doi:10.1159/000187139. PMID 8446248.
- ↑ Weisberg LS, Allgren RL, Genter FC, Kurnik BR (September 1997). "Cause of acute tubular necrosis affects its prognosis. The Auriculin Anaritide Acute Renal Failure Study Group". Arch. Intern. Med. 157 (16): 1833–8. PMID 9290542.
- ↑ Esson ML, Schrier RW (November 2002). "Diagnosis and treatment of acute tubular necrosis". Ann. Intern. Med. 137 (9): 744–52. PMID 12416948.