Acute tubular necrosis medical therapy: Difference between revisions
Created page with "__NOTOC__ {{Acute tubular necrosis}} Please help WikiDoc by adding content here. It's easy! Click here to learn about editing. ==References==..." |
Aditya Ganti (talk | contribs) No edit summary |
||
(5 intermediate revisions by one other user not shown) | |||
Line 1: | Line 1: | ||
__NOTOC__ | __NOTOC__ | ||
{{Acute tubular necrosis}} | {{Acute tubular necrosis}} | ||
{{CMG}}; {{AE}} {{CK}} | |||
==Overview== | |||
According to the Kidney Disease Improving Global Outcomes (KDIGO) 2012 guidelines, management approach of acute tubular necrosis include examination of all [[Patient|patients]] thoroughly to identify the [[Causes|cause]], precipitating factors, and [[Comorbidity|comorbid conditions]] leading to a rapid reduction in [[Glomerular filtration rate|GFR]], which may be reversible and regular monitor patients for serum creatinine, BUN, and urine output to assess the severity of [[Kidney|renal]] damage. | |||
==Medical Therapy== | |||
* Acute tubular necrosis, which is usually reversible. It may be associated with high [[morbidity]] and [[Mortality rate|mortality]]. Early recognition and management are essential for a better outcome.<ref name="pmid2195259">{{cite journal |vauthors=Finn WF |title=Diagnosis and management of acute tubular necrosis |journal=Med. Clin. North Am. |volume=74 |issue=4 |pages=873–91 |date=July 1990 |pmid=2195259 |doi= |url=}}</ref> | |||
* According to the Kidney Disease Improving Global Outcomes (KDIGO) 2012 guidelines, management approach of acute tubular necrosis include, | |||
** Examine all [[Patient|patients]] thoroughly to identify the [[Causes|cause]], precipitating factors, and [[Comorbidity|comorbid conditions]] leading to a rapid reduction in [[Glomerular filtration rate|GFR]], which may be reversible. | |||
** Regularly monitor patients for serum creatinine, BUN, and urine output to assess the severity of [[Kidney|renal]] damage. | |||
** Assess volume status and manage it accordingly. | |||
*** [[Hypovolemia]]: Proper hydration or isotonic saline administration can be helpful in treating [[Hypovolemia|volume depletion]]. | |||
*** [[Hypervolemia]]: The only indication of using diuretics in [[Acute kidney injury|acute renal failure]] to manage volume overload status. | |||
** Avoiding or minimizing the dosage of nephrotoxic medications, and radiocontrast media. | |||
** According to KDIGO guidelines, following medications have no role in the management and outcome of acute tubular necrosis:<ref name="pmid11505120">{{cite journal |vauthors=Kellum JA, M Decker J |title=Use of dopamine in acute renal failure: a meta-analysis |journal=Crit. Care Med. |volume=29 |issue=8 |pages=1526–31 |date=August 2001 |pmid=11505120 |doi= |url=}}</ref><ref name="pmid17352669">{{cite journal |vauthors=Bagshaw SM, Delaney A, Haase M, Ghali WA, Bellomo R |title=Loop diuretics in the management of acute renal failure: a systematic review and meta-analysis |journal=Crit Care Resusc |volume=9 |issue=1 |pages=60–8 |date=March 2007 |pmid=17352669 |doi= |url=}}</ref> | |||
*** [[Diuretic|Diuretics]], except to treat hypervolemia | |||
*** [[Atrial natriuretic peptide]] | |||
*** [[Dopamine]] | |||
*** [[Fenoldopam]] | |||
** Appropriate management of electrolyte and acid-base imbalance: | |||
*** [[Hyperkalemia]]: [[Hyperkalemia]] is a life-threatening complication associated with acute tubular necrosis. | |||
**** Preferred regimen (1): [[Insulin]] (eg, intravenous injection of 10-15u of short-acting [[insulin]]) along with 50ml of [[dextrose]]. [[Insulin]] along with [[dextrose]] may cause influx of [[potassium]] into the cell due to activation of [[Na+/K+-ATPase|sodium-potassium ATPase]]. | |||
**** Preferred regimen (2): [[Calcium]] (eg, [[calcium gluconate]]), does not lower elevated potassium levels but, it helps to decrease myocardial contractility, thus by preventing arrythmias. | |||
**** Preferred regimen (3): [[Dialysis]] in severe and refractory cases. | |||
*** [[Metabolic acidosis]]: | |||
**** Preferred regimen: [[Sodium bicarbonate]] can be given to treat [[metabolic acidosis]]. | |||
** Renal replacement therapy: | |||
*** Indications for renal replacement therapy include: | |||
**** Severe hyperkalemia | |||
**** Hypervolemia | |||
**** Uremia | |||
**** Severe metabolic alkalosis | |||
==References== | ==References== | ||
{{ | {{Reflist|2}} | ||
{{WH}} | |||
{{WS}} | |||
[[Category: (name of the system)]] | |||
[[Category:Nephrology]] | [[Category:Nephrology]] | ||
Latest revision as of 02:15, 12 August 2018
Acute tubular necrosis Microchapters |
Diagnosis |
---|
Treatment |
Case Studies |
Acute tubular necrosis medical therapy On the Web |
American Roentgen Ray Society Images of Acute tubular necrosis medical therapy |
Risk calculators and risk factors for Acute tubular necrosis medical therapy |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Chandrakala Yannam, MD [2]
Overview
According to the Kidney Disease Improving Global Outcomes (KDIGO) 2012 guidelines, management approach of acute tubular necrosis include examination of all patients thoroughly to identify the cause, precipitating factors, and comorbid conditions leading to a rapid reduction in GFR, which may be reversible and regular monitor patients for serum creatinine, BUN, and urine output to assess the severity of renal damage.
Medical Therapy
- Acute tubular necrosis, which is usually reversible. It may be associated with high morbidity and mortality. Early recognition and management are essential for a better outcome.[1]
- According to the Kidney Disease Improving Global Outcomes (KDIGO) 2012 guidelines, management approach of acute tubular necrosis include,
- Examine all patients thoroughly to identify the cause, precipitating factors, and comorbid conditions leading to a rapid reduction in GFR, which may be reversible.
- Regularly monitor patients for serum creatinine, BUN, and urine output to assess the severity of renal damage.
- Assess volume status and manage it accordingly.
- Hypovolemia: Proper hydration or isotonic saline administration can be helpful in treating volume depletion.
- Hypervolemia: The only indication of using diuretics in acute renal failure to manage volume overload status.
- Avoiding or minimizing the dosage of nephrotoxic medications, and radiocontrast media.
- According to KDIGO guidelines, following medications have no role in the management and outcome of acute tubular necrosis:[2][3]
- Diuretics, except to treat hypervolemia
- Atrial natriuretic peptide
- Dopamine
- Fenoldopam
- Appropriate management of electrolyte and acid-base imbalance:
- Hyperkalemia: Hyperkalemia is a life-threatening complication associated with acute tubular necrosis.
- Preferred regimen (1): Insulin (eg, intravenous injection of 10-15u of short-acting insulin) along with 50ml of dextrose. Insulin along with dextrose may cause influx of potassium into the cell due to activation of sodium-potassium ATPase.
- Preferred regimen (2): Calcium (eg, calcium gluconate), does not lower elevated potassium levels but, it helps to decrease myocardial contractility, thus by preventing arrythmias.
- Preferred regimen (3): Dialysis in severe and refractory cases.
- Metabolic acidosis:
- Preferred regimen: Sodium bicarbonate can be given to treat metabolic acidosis.
- Hyperkalemia: Hyperkalemia is a life-threatening complication associated with acute tubular necrosis.
- Renal replacement therapy:
- Indications for renal replacement therapy include:
- Severe hyperkalemia
- Hypervolemia
- Uremia
- Severe metabolic alkalosis
- Indications for renal replacement therapy include:
References
- ↑ Finn WF (July 1990). "Diagnosis and management of acute tubular necrosis". Med. Clin. North Am. 74 (4): 873–91. PMID 2195259.
- ↑ Kellum JA, M Decker J (August 2001). "Use of dopamine in acute renal failure: a meta-analysis". Crit. Care Med. 29 (8): 1526–31. PMID 11505120.
- ↑ Bagshaw SM, Delaney A, Haase M, Ghali WA, Bellomo R (March 2007). "Loop diuretics in the management of acute renal failure: a systematic review and meta-analysis". Crit Care Resusc. 9 (1): 60–8. PMID 17352669.