Acute kidney injury: Difference between revisions
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'''Acute kidney injury''' (AKI) is a clinical syndrome which is characterised by an acute decrease kidney function (<abbr>[[Glomerular filtration rate|GFR]])</abbr> (over hours or days), as evidenced by elevated creatinine. There may also be accumulation of urinary waste products and [[Oliguria and anuria|oliguria/anuria]], but not always. The cause may be prerenal, renal, or postrenal, but the most common causes are prerenal and [[acute tubular necrosis]]. | <section begin="A&IC" /><section begin="clinical biochemistry" /><section begin="radiology" />'''Acute kidney injury''' (AKI) is a clinical syndrome which is characterised by an acute decrease kidney function (<abbr>[[Glomerular filtration rate|GFR]])</abbr> (over hours or days), as evidenced by elevated creatinine. There may also be accumulation of urinary waste products and [[Oliguria and anuria|oliguria/anuria]], but not always. The cause may be prerenal, renal, or postrenal, but the most common causes are prerenal and [[acute tubular necrosis]]. AKI is a common problem in [[Critical illness|critically ill]] patients in the [[intensive care unit]]. <section end="clinical biochemistry" /> | ||
During the evaluation it’s important to determine whether it’s really acute or chronic, and to determine the underlying cause. Management includes treating the cause and correcting severe electrolyte disturbances. In some cases, [[renal replacement therapy]] may be required. | During the evaluation it’s important to determine whether it’s really acute or chronic, and to determine the underlying cause. Management includes treating the cause and correcting severe electrolyte disturbances. In some cases, [[renal replacement therapy]] may be required. | ||
The condition is nowadays called acute kidney injury rather than '''acute renal failure'''. | The condition is nowadays called acute kidney injury rather than '''acute renal failure'''.<section end="radiology" /><section begin="clinical biochemistry" /> | ||
== Etiology == | == Etiology == | ||
AKI is classified according to the underlying cause, whether it’s a prerenal cause, a renal cause, or a postrenal cause. However, there are usually multiple factors involved. | AKI is classified according to the underlying cause, whether it’s a prerenal cause, a renal cause, or a postrenal cause. However, there are usually multiple factors involved. | ||
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** [[Prostate cancer]] | ** [[Prostate cancer]] | ||
** [[Gynaecological cancer]] | ** [[Gynaecological cancer]] | ||
<section end="clinical biochemistry" />Of these, the prerenal causes are the most common, followed by acute tubular necrosis. | |||
Of these, the prerenal causes are the most common, followed by acute tubular necrosis. | |||
Drugs which can cause AKI (by various mechanisms) are most commonly [[Non-steroidal anti-inflammatory drugs|NSAIDs]] and [[Renin angiotensin aldosterone system inhibitors|RAAS inhibitors]]. | Drugs which can cause AKI (by various mechanisms) are most commonly [[Non-steroidal anti-inflammatory drugs|NSAIDs]] and [[Renin angiotensin aldosterone system inhibitors|RAAS inhibitors]]. | ||
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== Clinical features == | == Clinical features == | ||
[[Oliguria and anuria|Oliguria]] is the most common symptom, but in many cases it’s asymptomatic. There may be symptoms of the underlying cause, or symptoms of [[uraemia]]. | [[Oliguria and anuria|Oliguria]] is the most common symptom, but in many cases it’s asymptomatic. There may be symptoms of the underlying cause, or symptoms of [[uraemia]].<section begin="radiology" /><section begin="clinical biochemistry" /> | ||
== Diagnosis and evaluation == | == Diagnosis and evaluation == | ||
'' | <section end="radiology" />In the evaluation of AKI, we use serum [[creatinine]] as a marker of [[Kidney function tests|kidney function]] (''normal range 60 – 100 µmol/L)''; the estimated [[Glomerular filtration rate|GFR]] (eGFR) can ''not'' be used, as it's estimated according to formulas which are made for chronic kidney disease. The definition of AKI requires either (1) an increase in serum creatinine by 27 µmol/L, or (2) an increase to more than 150% of baseline serum creatinine over 48 hours, or (3) a decrease in urine volume to < 3 mL/kg over 6 hours.<section end="clinical biochemistry" /><section end="A&IC" /> | ||
During the evaluation of a person with acute kidney injury, it’s important to answer these 5 questions: | During the evaluation of a person with acute kidney injury, it’s important to answer these 5 questions: | ||
* Is it really AKI, or is it CKD or acute-on-chronic? | * Is it really AKI, or is it CKD, or acute-on-chronic? | ||
** Is this really an acute loss of kidney function or is this a | ** Is this really an acute loss of kidney function or is this a newly discovered CKD? | ||
** Did the patient already have decreased GFR and this is just a worsening? | ** Did the patient already have decreased GFR and this is just a worsening? | ||
* Is there a prerenal cause? | * Is there a prerenal cause? | ||
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* Is there a renoparenchymal disease? | * Is there a renoparenchymal disease? | ||
Patient history, physical examination, previous [[kidney function tests]], and [[ultrasound]] can help answer these questions. An AKI kidney has normal morphology, as opposed to a CKD kidney. A renal cause usually has abnormal [[urine analysis]]. A postrenal cause can have a palpable bladder, or obstruction or | Patient history, physical examination, previous [[kidney function tests]], and [[ultrasound]] can help answer these questions. An AKI kidney has normal macroscopic morphology (as seen with radiologic imaging), as opposed to a CKD kidney, which is usually shorter than normal and has a thinner cortex. A renal cause usually has abnormal [[urine analysis]], with proteinuria, increased urinary sodium, or decreased urinary osmolality, as well as the presence of epithelial casts or brown granular casts in the urine. A postrenal cause can have a palpable bladder, or obstruction or hydronephrosis can be visible on [[ultrasonography]]. Allergic symptoms can suggest nephritis. Low BP can suggest hypovolaemia. | ||
<section begin="radiology" />In case of AKI, the kidney is usually enlarged, which can be visualised on ultrasonography. Ultrasound may also reveal an underlying cause and is therefore usually the first choice imaging modality for AKI. | |||
<section end="radiology" /><section begin="clinical biochemistry" />Previously it was suggested that the urea:creatinine ratio was useful in distinguishing between prerenal and intrinsic AKI, but a study designed to investigate this found that the ratio can not distinguish them<ref>https://pubmed.ncbi.nlm.nih.gov/28545421/</ref>.<section end="clinical biochemistry" /> | |||
If the cause remains unclear despite these investigations, a [[renal biopsy]] may be required. | If the cause remains unclear despite these investigations, a [[renal biopsy]] may be required. | ||
<section begin="A&IC" /> | |||
== Treatment == | == Treatment == | ||
Treating the underlying cause is essential, as well as correcting any severe electrolyte disorders. | Treating the underlying cause is essential, as well as correcting any severe electrolyte disorders. | ||
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If there is hypervolaemia, a [[loop diuretic]] may be used. | If there is hypervolaemia, a [[loop diuretic]] may be used. | ||
If there are indications for it, [[renal replacement therapy]] may be used. | If there are indications for it, [[renal replacement therapy]] may be used. Renal replacement therapy (RRT) is indicated if: | ||
* Oliguria or anuria | |||
* Severe hyperkalaemia | |||
* Severe acidosis | |||
* Uraemic signs | |||
* Drug overdose with dialysable drug | |||
== Prognosis == | == Prognosis == | ||
In many cases patients make a full recovery, but AKI can progress to chronic kidney disease as well. It might take months for kidney functions to recover completely, during which the patient may experience [[polyuria]] because the tubules need a long time to recover. | In many cases patients make a full recovery, but AKI can progress to chronic kidney disease as well. It might take months for kidney functions to recover completely, during which the patient may experience [[polyuria]] because the tubules need a long time to recover. | ||
<section end="A&IC" /> | |||
== References == | |||
[[Category:Nephrology]] | [[Category:Nephrology]] | ||
[[Category:Intensive care]] | |||
Latest revision as of 19:43, 3 November 2024
Acute kidney injury (AKI) is a clinical syndrome which is characterised by an acute decrease kidney function (GFR) (over hours or days), as evidenced by elevated creatinine. There may also be accumulation of urinary waste products and oliguria/anuria, but not always. The cause may be prerenal, renal, or postrenal, but the most common causes are prerenal and acute tubular necrosis. AKI is a common problem in critically ill patients in the intensive care unit.
During the evaluation it’s important to determine whether it’s really acute or chronic, and to determine the underlying cause. Management includes treating the cause and correcting severe electrolyte disturbances. In some cases, renal replacement therapy may be required.
The condition is nowadays called acute kidney injury rather than acute renal failure.
Etiology
AKI is classified according to the underlying cause, whether it’s a prerenal cause, a renal cause, or a postrenal cause. However, there are usually multiple factors involved.
- Prerenal AKI
- Hypovolaemia/hypotension
- Decreased RBF (heart failure, renal artery stenosis)
- Abnormal kidney haemodynamics (sepsis, hepatorenal syndrome)
- Renal AKI
- Tubulointerstitial disorders
- Glomerulonephritis
- Thrombotic microangiopathies (TTP/HUS)
- Obstruction of tubules
- Myeloma proteins
- Crystals
- Postrenal AKI
Of these, the prerenal causes are the most common, followed by acute tubular necrosis.
Drugs which can cause AKI (by various mechanisms) are most commonly NSAIDs and RAAS inhibitors.
Chronic kidney disease is the strongest risk factor for AKI. If a person with CKD develops AKI, the condition is called acute-on-chronic AKI.
Clinical features
Oliguria is the most common symptom, but in many cases it’s asymptomatic. There may be symptoms of the underlying cause, or symptoms of uraemia.
Diagnosis and evaluation
In the evaluation of AKI, we use serum creatinine as a marker of kidney function (normal range 60 – 100 µmol/L); the estimated GFR (eGFR) can not be used, as it's estimated according to formulas which are made for chronic kidney disease. The definition of AKI requires either (1) an increase in serum creatinine by 27 µmol/L, or (2) an increase to more than 150% of baseline serum creatinine over 48 hours, or (3) a decrease in urine volume to < 3 mL/kg over 6 hours.
During the evaluation of a person with acute kidney injury, it’s important to answer these 5 questions:
- Is it really AKI, or is it CKD, or acute-on-chronic?
- Is this really an acute loss of kidney function or is this a newly discovered CKD?
- Did the patient already have decreased GFR and this is just a worsening?
- Is there a prerenal cause?
- Is there a postrenal cause?
- Is there a renal artery occlusion?
- Is there a renoparenchymal disease?
Patient history, physical examination, previous kidney function tests, and ultrasound can help answer these questions. An AKI kidney has normal macroscopic morphology (as seen with radiologic imaging), as opposed to a CKD kidney, which is usually shorter than normal and has a thinner cortex. A renal cause usually has abnormal urine analysis, with proteinuria, increased urinary sodium, or decreased urinary osmolality, as well as the presence of epithelial casts or brown granular casts in the urine. A postrenal cause can have a palpable bladder, or obstruction or hydronephrosis can be visible on ultrasonography. Allergic symptoms can suggest nephritis. Low BP can suggest hypovolaemia.
In case of AKI, the kidney is usually enlarged, which can be visualised on ultrasonography. Ultrasound may also reveal an underlying cause and is therefore usually the first choice imaging modality for AKI.
Previously it was suggested that the urea:creatinine ratio was useful in distinguishing between prerenal and intrinsic AKI, but a study designed to investigate this found that the ratio can not distinguish them[1].
If the cause remains unclear despite these investigations, a renal biopsy may be required.
Treatment
Treating the underlying cause is essential, as well as correcting any severe electrolyte disorders.
If there is hypervolaemia, a loop diuretic may be used.
If there are indications for it, renal replacement therapy may be used. Renal replacement therapy (RRT) is indicated if:
- Oliguria or anuria
- Severe hyperkalaemia
- Severe acidosis
- Uraemic signs
- Drug overdose with dialysable drug
Prognosis
In many cases patients make a full recovery, but AKI can progress to chronic kidney disease as well. It might take months for kidney functions to recover completely, during which the patient may experience polyuria because the tubules need a long time to recover.