Acute tubular necrosis history and symptoms: Difference between revisions
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===History=== | ===History=== | ||
Obtaining history is the most important aspect of making a [[diagnosis]] of acute tubular necrosis. It provides insight into the [[Etiology|cause]], precipitating factors, and associated comorbid conditions leading to decreased [[Kidney|renal]] blood flow and acute tubular damage. A complete [[History and Physical examination|history]] will help determine the correct [[therapy]] and the [[prognosis]]. Specific areas of focus when obtaining the history are outlined below:<ref name="pmid25795495">{{cite journal |vauthors=Alobaidi R, Basu RK, Goldstein SL, Bagshaw SM |title=Sepsis-associated acute kidney injury |journal=Semin. Nephrol. |volume=35 |issue=1 |pages=2–11 |date=January 2015 |pmid=25795495 |pmc=4507081 |doi=10.1016/j.semnephrol.2015.01.002 |url=}}</ref><ref name="pmid16949378">{{cite journal |vauthors=McCullough PA, Adam A, Becker CR, Davidson C, Lameire N, Stacul F, Tumlin J |title=Risk prediction of contrast-induced nephropathy |journal=Am. J. Cardiol. |volume=98 |issue=6A |pages=27K–36K |date=September 2006 |pmid=16949378 |doi=10.1016/j.amjcard.2006.01.022 |url=}}</ref><ref name="pmid16011448">{{cite journal |vauthors=Perazella MA |title=Drug-induced nephropathy: an update |journal=Expert Opin Drug Saf |volume=4 |issue=4 |pages=689–706 |date=July 2005 |pmid=16011448 |doi=10.1517/14740338.4.4.689 |url=}}</ref><ref name="pmid28580076">{{cite journal |vauthors=Park JT |title=Postoperative acute kidney injury |journal=Korean J Anesthesiol |volume=70 |issue=3 |pages=258–266 |date=June 2017 |pmid=28580076 |pmc=5453887 |doi=10.4097/kjae.2017.70.3.258 |url=}}</ref><ref name="pmid28486690">{{cite journal |vauthors=Ngajilo D, Ehrlich R |title=Rhabdomyolysis with acute tubular necrosis following occupational inhalation of thinners |journal=Occup Med (Lond) |volume=67 |issue=5 |pages=401–403 |date=July 2017 |pmid=28486690 |doi=10.1093/occmed/kqx048 |url=}}</ref> | Obtaining history is the most important aspect of making a [[diagnosis]] of acute tubular necrosis. It provides insight into the [[Etiology|cause]], precipitating factors, and associated [[Comorbidity|comorbid]] conditions leading to decreased [[Kidney|renal]] blood flow and acute tubular damage. A complete [[History and Physical examination|history]] will help determine the correct [[therapy]] and the [[prognosis]]. Specific areas of focus when obtaining the history are outlined below:<ref name="pmid25795495">{{cite journal |vauthors=Alobaidi R, Basu RK, Goldstein SL, Bagshaw SM |title=Sepsis-associated acute kidney injury |journal=Semin. Nephrol. |volume=35 |issue=1 |pages=2–11 |date=January 2015 |pmid=25795495 |pmc=4507081 |doi=10.1016/j.semnephrol.2015.01.002 |url=}}</ref><ref name="pmid16949378">{{cite journal |vauthors=McCullough PA, Adam A, Becker CR, Davidson C, Lameire N, Stacul F, Tumlin J |title=Risk prediction of contrast-induced nephropathy |journal=Am. J. Cardiol. |volume=98 |issue=6A |pages=27K–36K |date=September 2006 |pmid=16949378 |doi=10.1016/j.amjcard.2006.01.022 |url=}}</ref><ref name="pmid16011448">{{cite journal |vauthors=Perazella MA |title=Drug-induced nephropathy: an update |journal=Expert Opin Drug Saf |volume=4 |issue=4 |pages=689–706 |date=July 2005 |pmid=16011448 |doi=10.1517/14740338.4.4.689 |url=}}</ref><ref name="pmid28580076">{{cite journal |vauthors=Park JT |title=Postoperative acute kidney injury |journal=Korean J Anesthesiol |volume=70 |issue=3 |pages=258–266 |date=June 2017 |pmid=28580076 |pmc=5453887 |doi=10.4097/kjae.2017.70.3.258 |url=}}</ref><ref name="pmid28486690">{{cite journal |vauthors=Ngajilo D, Ehrlich R |title=Rhabdomyolysis with acute tubular necrosis following occupational inhalation of thinners |journal=Occup Med (Lond) |volume=67 |issue=5 |pages=401–403 |date=July 2017 |pmid=28486690 |doi=10.1093/occmed/kqx048 |url=}}</ref> | ||
* History of recent [[surgery]] | * History of recent [[surgery]] | ||
* [[Sepsis]] / septic shock | * [[Sepsis]] / septic shock | ||
| Line 12: | Line 12: | ||
* Severe [[Hypovolemia|volume loss]] (eg, [[diarrhea]], [[Nausea and vomiting|vomiting]], [[bleeding]] and third-spacing) | * Severe [[Hypovolemia|volume loss]] (eg, [[diarrhea]], [[Nausea and vomiting|vomiting]], [[bleeding]] and third-spacing) | ||
* [[Medication]] history (eg, exposure to [[Nephrotoxicity|nephrotoxic]] drugs and [[radiocontrast]] substances) | * [[Medication]] history (eg, exposure to [[Nephrotoxicity|nephrotoxic]] drugs and [[radiocontrast]] substances) | ||
* Tissue [[injury]] involving [[Muscle|muscles]] ([[crush injury]], [[Burn|burns]], [[rhabdomyolysis]]) | * Tissue [[injury]] involving [[Muscle|muscles]] (eg, [[crush injury]], [[Burn|burns]], [[rhabdomyolysis]]) | ||
* [[Blood transfusion]] reaction | * [[Blood transfusion]] reaction | ||
* Associated conditions: History of pre-existing medical conditions such as [[multiple myeloma]] and [[diabetes mellitus]] may cause a decreased renal function | * Associated conditions: History of pre-existing medical conditions such as [[multiple myeloma]] and [[diabetes mellitus]] may cause a decreased renal function | ||
Latest revision as of 19:15, 15 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
History taking is an important aspect in making a diagnosis of acute tubular necrosis. It provides clues to precipitating factors, causes and associated comorbid conditions leading to decreased renal perfusion and kidney injury. Most common symptoms of acute tubular necrosis include decreased or absent urinary output, postural dizziness, edema, excess thirst, tachycardia, altered mental status and easy fatiguability.
History
Obtaining history is the most important aspect of making a diagnosis of acute tubular necrosis. It provides insight into the cause, precipitating factors, and associated comorbid conditions leading to decreased renal blood flow and acute tubular damage. A complete history will help determine the correct therapy and the prognosis. Specific areas of focus when obtaining the history are outlined below:[1][2][3][4][5]
- History of recent surgery
- Sepsis / septic shock
- Profound hypotension
- Severe volume loss (eg, diarrhea, vomiting, bleeding and third-spacing)
- Medication history (eg, exposure to nephrotoxic drugs and radiocontrast substances)
- Tissue injury involving muscles (eg, crush injury, burns, rhabdomyolysis)
- Blood transfusion reaction
- Associated conditions: History of pre-existing medical conditions such as multiple myeloma and diabetes mellitus may cause a decreased renal function
Symptoms
Common symptoms of acute tubular necrosis include: Symptoms are mostly related to decreased renal perfusion and acute kidney damage.
- Decreased or absent urine output
- Dark colored urine
- Lassitude
- Excessive thirst
- Generalised edema
- Postural dizziness
- Rapid pulses
- Muscle cramps
- Confusion
- Altered mental status
- Stupor or coma
References
- ↑ Alobaidi R, Basu RK, Goldstein SL, Bagshaw SM (January 2015). "Sepsis-associated acute kidney injury". Semin. Nephrol. 35 (1): 2–11. doi:10.1016/j.semnephrol.2015.01.002. PMC 4507081. PMID 25795495.
- ↑ McCullough PA, Adam A, Becker CR, Davidson C, Lameire N, Stacul F, Tumlin J (September 2006). "Risk prediction of contrast-induced nephropathy". Am. J. Cardiol. 98 (6A): 27K–36K. doi:10.1016/j.amjcard.2006.01.022. PMID 16949378.
- ↑ Perazella MA (July 2005). "Drug-induced nephropathy: an update". Expert Opin Drug Saf. 4 (4): 689–706. doi:10.1517/14740338.4.4.689. PMID 16011448.
- ↑ Park JT (June 2017). "Postoperative acute kidney injury". Korean J Anesthesiol. 70 (3): 258–266. doi:10.4097/kjae.2017.70.3.258. PMC 5453887. PMID 28580076.
- ↑ Ngajilo D, Ehrlich R (July 2017). "Rhabdomyolysis with acute tubular necrosis following occupational inhalation of thinners". Occup Med (Lond). 67 (5): 401–403. doi:10.1093/occmed/kqx048. PMID 28486690.