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{{Acute renal failure}} | {{Acute renal failure}} | ||
{{CMG}} {{AE}} [[User:Ayesha A. Khan|Ayesha A. Khan, MD]][mailto:Ayesha.khan@stvincentcharity.com] | |||
==Overview== | ==Overview== | ||
Acute renal failure (ARF), also known as acute kidney failure, is a rapid loss of [[renal function]] due to damage to the [[kidney]]s, resulting in retention of nitrogenous ([[urea]] and [[creatinine]]) and non-nitrogenous waste products that are normally excreted by the kidney. Depending on the severity and duration of the renal dysfunction, this accumulation is accompanied by metabolic disturbances, such as [[metabolic acidosis]] (acidification of the blood) and [[hyperkalaemia]] (elevated potassium levels), changes in body [[fluid balance]], and effects on many other organ systems. It can be characterized by [[oliguria]] or [[anuria]] (decrease or cessation of urine production), although ''nonoliguric ARF'' may occur. It is a serious disease and treated as a [[medical emergency]]. | |||
==Historical Perspective== | |||
Before the advancement of modern medicine, acute renal failure might be referred to as uremic poisoning. [[Uremia]] was the term used to describe the contamination of the [[blood]] with [[urine]]. Starting around 1847 this term was used to describe reduced urine output, now known as [[oliguria]], which was thought to be caused by the urine's mixing with the blood instead of being voided through the [[urethra]]. Acute renal failure due to [[acute tubular necrosis]] (ATN) was recognised in the 1940s in the United Kingdom, where crush victims during the Battle of Britain developed patchy necrosis of renal tubules, leading to a sudden decrease in renal function.<ref>{{cite journal |author=Bywaters EG, Beall D |title=Crush injuries with impairment of renal function. |journal=[[British Medical Journal|Br Med J]] |volume= |issue=1 |pages=427-32 |year=1941 |pmid=9527411 |doi= |url=http://jasn.asnjournals.org/cgi/pmidlookup?view=long&pmid=9527411}}</ref> During the Korean and Vietnam wars, the incidence of ARF decreased due to better acute management and intravenous infusion of fluids.<ref>{{cite journal |author=Schrier RW, Wang W, Poole B, Mitra A |title=Acute renal failure: definitions, diagnosis, pathogenesis, and therapy |journal=J. Clin. Invest. |volume=114 |issue=1 |pages=5–14 |year=2004 |pmid=15232604 |pmc=437979 |doi=10.1172/JCI22353 |url=}}</ref> | |||
==Classification== | |||
Acute renal failure can complicate a wide spectrum of disorders, and for the purpose of diagnosis and management is divided according to the mechanism that lead to renal compromise. The three categories are pre-renal [[azotemia]] (diseases that cause renal [[hypoperfusion]]), renal azotemia (diseases directly affecting the renal parenchyma), and post-renal azotemia (diseases affecting the [[urinary tract]] causing [[urinary tract obstruction|obstruction]]). However, the first consensus definition described and the most used definition is known as the RIFLE criteria. The acronym combines a classification of 3 levels of renal dysfunction (Risk, Injury, Failure) with 2 clinical outcomes (Loss, ESRD) to give the RIFLE stages of AKI. | |||
==Pathophysiology== | |||
[[Acute kidney injury]] (AKI) is the leading cause of [[nephrology]] consultation and is associated with high [[mortality rates. The primary causes of [[AKI]] include ischemia, [[hypoxia]] or [[nephrotoxicity]]. An underlying feature is a rapid decline in [[GFR]] usually associated with decreases in [[renal blood flow]]. Inflammation represents an important additional component of AKI leading to the extension phase of injury, which may be associated with insensitivity to vasodilator therapy. It is suggested that targeting the extension phase represents an area potential of treatment with the greatest possible impact. The underlying basis of [[renal]] injury appears to be impaired energetics of the highly metabolically active [[nephron]] segments (i.e., proximal tubules and thick ascending limb) in the [[renal]] outer [[medulla]], which can trigger conversion from transient [[hypoxia]] to intrinsic [[renal failure]]. [[Injury]] to [[kidney]] cells can be lethal or sublethal. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow. The nature of the recovery response is mediated by the degree to which sublethal cells can restore normal function and promote regeneration. The successful recovery from AKI depends on the degree to which these repair processes ensue and these may be compromised in elderly or CKD patients. Recent data suggest that AKI represents a potential link to CKD in surviving patients. Finally, earlier diagnosis of AKI represents an important area in treating patients with AKI that has spawned increased awareness of the potential that biomarkers of AKI may play in the future. | |||
==Causes== | |||
[[Glomerular filtration rate]] depends on multiple factors, particularly the [[renal blood flow]]. The pressure difference across the renal vasculature i.e the difference in pressure between the renal arterioles and venules is directly proportional to the [[GFR]]. Any decrease in [[renal blood flow]], injury to the renal tubules or obstruction to the urinary tract outflow can cause decreased urinary output. | |||
==Differentiating Acute renal failure from other Diseases== | |||
Various parameters like [[fractional sodium excretion]], urinary sodium concentration, urine osmolality and U/P [[creatinine]] ratio have been used to diagnose acute renal failure. The [[fractional sodium excretion]] is identifies as the most effective non-invasive test in formulating the differential diagnosis of acute renal failure <ref name="pmid7363517">{{cite journal |author=Espinel CH, Gregory AW |title=Differential diagnosis of acute renal failure |journal=[[Clinical Nephrology]] |volume=13 |issue=2 |pages=73–7 |year=1980 |month=February |pmid=7363517 |doi= |url=}}</ref>. | |||
==Epidemiology and Demographics== | |||
Acute kidney injury is common among hospitalized patients. It affects some 3-7% of patients admitted to the hospital and approximately 25-30% of patients in the [[intensive care unit]] <ref name="isbn1-4160-3110-3">{{cite book |author= |title=Brenner and Rector's The Kidney |publisher=Saunders |location=Philadelphia |year=2007 |pages= |isbn=1-4160-3110-3 |oclc= |doi= |accessdate=}}</ref>. | |||
==Risk Factors== | |||
Acute renal failure always occurs in connection with some other medical condition or event. Being hospitalized with a serious condition requiring intensive care is the biggest risk factor. The risk factors for acute renal failure is divided into three major categories, namely pre-renal factors, renal factors and post-renal factors. | |||
==Diagnosis== | |||
===History and Symptoms=== | |||
When a patient presents with [[uremia|uremic]] symptoms, first step is to differentiate an acute from a chronic process. A recent rise in serum [[creatinine]] levels indicate an acute pathology of renal failure, whereas chronically elevated [[creatinine]] levels are seen in [[chronic renal failure]]. However, [[chronic renal insufficiency]] is also associated with [[osteopathy]], [[neuropathy]] and small, scarred [[kidney]]s. | |||
===Laboratory Findings=== | |||
Renal failure is generally diagnosed either when [[creatinine]] or [[blood urea nitrogen]] tests are markedly elevated in an ill patient, especially when oliguria is present. Previous measurements of renal function may offer comparison, which is especially important if a patient is known to have [[chronic renal failure]] as well. If the cause is not apparent, a large amount of [[blood test]]s and examination of a [[urine]] specimen is typically performed to elucidate the cause of acute renal failure. | |||
===Ultrasound=== | |||
[[Medical ultrasonography]] of the renal tract is essential to rule out obstruction of the urinary tract. | |||
===Other Diagnostic Studies=== | |||
Kidney [[biopsy]] may be performed in the setting of acute renal failure, to provide a definitive diagnosis and sometimes an idea of the [[prognosis]], unless the cause is clear and appropriate screening investigations are reassuringly negative. | |||
==Treatment== | |||
===Surgery=== | |||
If the cause of the acute renal failure is obstruction of the urinary tract, relief of the obstruction (with a [[nephrostomy]] or [[urinary catheter]]) may be necessary. Lack of improvement with fluid resuscitation, therapy-resistant hyperkalemia, metabolic acidosis, or fluid overload may necessitate artificial support in the form of [[dialysis]] or [[hemofiltration]]. Depending on the cause, a proportion of patients will never regain full renal function, thus having [[end stage renal failure]] requiring lifelong [[dialysis]] or a [[kidney transplant]]. | |||
==References== | ==References== | ||
{{Reflist|2}} | {{Reflist|2}} | ||
{{WH}} | |||
[[Category:Needs | {{WS}} | ||
[[Category:Needs overview]] | |||
[[Category:Medical emergencies]] | |||
[[Category:Kidney diseases]] | |||
[[Category:Organ failure]] | |||
[[Category:Causes of death]] | |||
[[Category:Nephrology]] | |||
[[Category:Emergency medicine]] | |||
[[Category:Intensive care medicine]] | |||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ayesha A. Khan, MD[2]
Overview
Acute renal failure (ARF), also known as acute kidney failure, is a rapid loss of renal function due to damage to the kidneys, resulting in retention of nitrogenous (urea and creatinine) and non-nitrogenous waste products that are normally excreted by the kidney. Depending on the severity and duration of the renal dysfunction, this accumulation is accompanied by metabolic disturbances, such as metabolic acidosis (acidification of the blood) and hyperkalaemia (elevated potassium levels), changes in body fluid balance, and effects on many other organ systems. It can be characterized by oliguria or anuria (decrease or cessation of urine production), although nonoliguric ARF may occur. It is a serious disease and treated as a medical emergency.
Historical Perspective
Before the advancement of modern medicine, acute renal failure might be referred to as uremic poisoning. Uremia was the term used to describe the contamination of the blood with urine. Starting around 1847 this term was used to describe reduced urine output, now known as oliguria, which was thought to be caused by the urine's mixing with the blood instead of being voided through the urethra. Acute renal failure due to acute tubular necrosis (ATN) was recognised in the 1940s in the United Kingdom, where crush victims during the Battle of Britain developed patchy necrosis of renal tubules, leading to a sudden decrease in renal function.[1] During the Korean and Vietnam wars, the incidence of ARF decreased due to better acute management and intravenous infusion of fluids.[2]
Classification
Acute renal failure can complicate a wide spectrum of disorders, and for the purpose of diagnosis and management is divided according to the mechanism that lead to renal compromise. The three categories are pre-renal azotemia (diseases that cause renal hypoperfusion), renal azotemia (diseases directly affecting the renal parenchyma), and post-renal azotemia (diseases affecting the urinary tract causing obstruction). However, the first consensus definition described and the most used definition is known as the RIFLE criteria. The acronym combines a classification of 3 levels of renal dysfunction (Risk, Injury, Failure) with 2 clinical outcomes (Loss, ESRD) to give the RIFLE stages of AKI.
Pathophysiology
Acute kidney injury (AKI) is the leading cause of nephrology consultation and is associated with high [[mortality rates. The primary causes of AKI include ischemia, hypoxia or nephrotoxicity. An underlying feature is a rapid decline in GFR usually associated with decreases in renal blood flow. Inflammation represents an important additional component of AKI leading to the extension phase of injury, which may be associated with insensitivity to vasodilator therapy. It is suggested that targeting the extension phase represents an area potential of treatment with the greatest possible impact. The underlying basis of renal injury appears to be impaired energetics of the highly metabolically active nephron segments (i.e., proximal tubules and thick ascending limb) in the renal outer medulla, which can trigger conversion from transient hypoxia to intrinsic renal failure. Injury to kidney cells can be lethal or sublethal. Sublethal injury represents an important component in AKI, as it may profoundly influence GFR and renal blood flow. The nature of the recovery response is mediated by the degree to which sublethal cells can restore normal function and promote regeneration. The successful recovery from AKI depends on the degree to which these repair processes ensue and these may be compromised in elderly or CKD patients. Recent data suggest that AKI represents a potential link to CKD in surviving patients. Finally, earlier diagnosis of AKI represents an important area in treating patients with AKI that has spawned increased awareness of the potential that biomarkers of AKI may play in the future.
Causes
Glomerular filtration rate depends on multiple factors, particularly the renal blood flow. The pressure difference across the renal vasculature i.e the difference in pressure between the renal arterioles and venules is directly proportional to the GFR. Any decrease in renal blood flow, injury to the renal tubules or obstruction to the urinary tract outflow can cause decreased urinary output.
Differentiating Acute renal failure from other Diseases
Various parameters like fractional sodium excretion, urinary sodium concentration, urine osmolality and U/P creatinine ratio have been used to diagnose acute renal failure. The fractional sodium excretion is identifies as the most effective non-invasive test in formulating the differential diagnosis of acute renal failure [3].
Epidemiology and Demographics
Acute kidney injury is common among hospitalized patients. It affects some 3-7% of patients admitted to the hospital and approximately 25-30% of patients in the intensive care unit [4].
Risk Factors
Acute renal failure always occurs in connection with some other medical condition or event. Being hospitalized with a serious condition requiring intensive care is the biggest risk factor. The risk factors for acute renal failure is divided into three major categories, namely pre-renal factors, renal factors and post-renal factors.
Diagnosis
History and Symptoms
When a patient presents with uremic symptoms, first step is to differentiate an acute from a chronic process. A recent rise in serum creatinine levels indicate an acute pathology of renal failure, whereas chronically elevated creatinine levels are seen in chronic renal failure. However, chronic renal insufficiency is also associated with osteopathy, neuropathy and small, scarred kidneys.
Laboratory Findings
Renal failure is generally diagnosed either when creatinine or blood urea nitrogen tests are markedly elevated in an ill patient, especially when oliguria is present. Previous measurements of renal function may offer comparison, which is especially important if a patient is known to have chronic renal failure as well. If the cause is not apparent, a large amount of blood tests and examination of a urine specimen is typically performed to elucidate the cause of acute renal failure.
Ultrasound
Medical ultrasonography of the renal tract is essential to rule out obstruction of the urinary tract.
Other Diagnostic Studies
Kidney biopsy may be performed in the setting of acute renal failure, to provide a definitive diagnosis and sometimes an idea of the prognosis, unless the cause is clear and appropriate screening investigations are reassuringly negative.
Treatment
Surgery
If the cause of the acute renal failure is obstruction of the urinary tract, relief of the obstruction (with a nephrostomy or urinary catheter) may be necessary. Lack of improvement with fluid resuscitation, therapy-resistant hyperkalemia, metabolic acidosis, or fluid overload may necessitate artificial support in the form of dialysis or hemofiltration. Depending on the cause, a proportion of patients will never regain full renal function, thus having end stage renal failure requiring lifelong dialysis or a kidney transplant.
References
- ↑ Bywaters EG, Beall D (1941). "Crush injuries with impairment of renal function". Br Med J (1): 427–32. PMID 9527411.
- ↑ Schrier RW, Wang W, Poole B, Mitra A (2004). "Acute renal failure: definitions, diagnosis, pathogenesis, and therapy". J. Clin. Invest. 114 (1): 5–14. doi:10.1172/JCI22353. PMC 437979. PMID 15232604.
- ↑ Espinel CH, Gregory AW (1980). "Differential diagnosis of acute renal failure". Clinical Nephrology. 13 (2): 73–7. PMID 7363517. Unknown parameter
|month=ignored (help) - ↑ Brenner and Rector's The Kidney. Philadelphia: Saunders. 2007. ISBN 1-4160-3110-3.