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Acute kidney injury

Last updated: October 13, 2021

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Acute kidney injury (AKI) is a sudden loss of renal function with a subsequent rise in creatinine and blood urea nitrogen (BUN). It is most frequently caused by decreased renal perfusion (prerenal) but may also be due to direct damage to the kidneys (intrarenal or intrinsic) or inadequate urine drainage (postrenal). In AKI, the acid-base, fluid, and electrolyte balances are disturbed and the urinary excretion of substances such as drugs is impaired. AKI may be asymptomatic or manifest with oliguria or anuria and, when kidney dysfunction is severe, it may manifest with symptoms and signs of uremia; in some cases, polyuria may occur as a result of impaired tubular reabsorption. A diagnosis of AKI can be made based on an increase in serum creatinine concentration and/or decrease in urine output. Initial evaluation includes blood and urine studies, which may help identify the mechanism of kidney injury and any metabolic complications of AKI. Additional specific investigations are guided by the suspected cause. Rapid evaluation, diagnosis, and treatment are necessary to prevent irreversible loss of renal function. Management is based on the mechanism of kidney injury and the underlying causes. Treatment is primarily supportive and aims to ensure adequate kidney perfusion and prevent complications and further kidney damage.

Prerenal acute kidney injury (∼ 60% of cases) [1][2][3]

Prerenal causes include any condition that leads to decreased renal perfusion.

Prolonged prerenal injury leads to intrinsic injury, as decreased renal perfusion causes tubular necrosis.

Intrinsic acute kidney injury (∼ 35% of cases)

Intrinsic causes include any condition that leads to severe direct kidney damage.

Postrenal acute kidney injury (∼ 5% of cases)

Postrenal causes include any condition that results in bilateral obstruction of urinary flow from the renal pelvis to the urethra.

As long as the contralateral kidney remains intact, patients with unilateral ureteral obstruction typically maintain normal serum creatinine levels.



  • Damage to a vascular or tubular component of the nephron necrosis or apoptosis of tubular cells → decreased reabsorption capacity of electrolytes (e.g., Na+), water, and/or urea; (depending on the location of injury along the tubular system) → increased Na+ and H2O in the urine → decreased urine osmolality


Four phases of AKI (some patients may not undergo all phases)


Characteristic features


Initiating event (kidney injury)

  • Symptoms of the underlying illness causing AKI may be present.
  • Hours to days

Oliguric or anuric phase (maintenance phase)

  • 1–3 weeks

Polyuric/diuretic phase

  • ∼ 2 weeks

Recovery phase

  • Months to years


Acute tubular necrosis

Renal cortical necrosis

Contrast-induced nephropathy


A diagnosis of AKI can be made based on an acute increase in serum creatinine and/or decrease in urine output in accordance with the definition of AKI.

Approach [12][13][14]

  • Compare current and previous creatinine levels to determine if the process is acute.
  • Check diagnostic criteria and perform staging of AKI.
  • Determine the most likely mechanism of AKI (i.e., prerenal, intrinsic, or postrenal) based on:
    • A comprehensive chart review, history, and physical examination
    • Supportive diagnostic findings and response to initial interventions
  • Consider further testing for specific underlying causes of AKI.

In the absence of previously documented creatinine levels, stable creatinine levels with findings such as chronic anemia and small hyperechoic kidneys on ultrasound suggest CKD rather than AKI.

Clinical presentation, laboratory tests, imaging, response to initial therapy, and, in some cases, histopathology are required to determine the underlying cause of AKI.

Diagnostic criteria and staging of AKI

  • Acute kidney injury is defined as the presence of any of the following diagnostic criteria of AKI: [12]
    • Increase in serum creatinine by ≥ 0.3 mg/dL (26.5 μmol/L) within 48 hours.
    • Increase in serum creatinine to ≥ 1.5 times baseline level within 7 days.
    • Decrease in urine output to < 0.5 mL/kg/hour for ≥ 6 hours.
  • The KDIGO stages are widely used and correlate with the risk of death, need for renal replacement therapy, and long-term outcomes (e.g., CKD).
  • Other classifications include the RIFLE criteria and the Acute Kidney Injury Network (AKIN) criteria. [12]
Kidney Disease Improving Global outcomes (KDIGO) criteria for staging of AKI [12]
Stage Serum creatinine Urine output
  • Increase of 0.3 mg/dL (26.5 μmol/L)
  • OR 1.5–1.9 times baseline
  • < 0.5 mL/kg/hour for 6–12 hours
  • 2–2.9 times baseline
  • < 0.5 mL/kg/hour for ≥12 hours
  • ≥ 3 times baseline
  • OR increase to ≥ 4 mg/dL (354 μmol/L)
  • OR renal replacement therapy initiated
  • OR in patients < 18 years of age: decrease in eGFR to < 35 mL/min/1.73 m2
  • < 0.3 mL/kg/hour for ≥ 24 hours
  • OR anuria for ≥ 12 hours
If serum creatinine and urine output correlate with different stages, consider staging based on the criterion that corresponds to the highest stage. [14]

Initial investigations

See “Determination of the likely underlying mechanism” below for typical findings and interpretation.

Laboratory studies

Imaging [16]

Imaging of the kidneys and urinary tract is not necessary to establish a diagnosis of AKI but may be needed to determine the etiology.

Obtain an urgent ultrasound to rule out hydronephrosis in patients with risk factors for urinary tract obstruction.

While ultrasound is the initial test of choice to assess for urinary tract obstruction, CT has greater sensitivity for detecting obstructions and stones. [18]

Typical diagnostic findings


Determination of the likely mechanism of acute kidney injury
Prerenal Intrinsic Postrenal
BUN:creatinine ratio
  • > 20:1
  • < 15:1
  • Varies


  • < 1%
  • > 2–3%
  • < 35%
  • > 50%
Urine sodium concentration
  • < 20 mEq/L
  • > 40 mEq/L
Urine osmolality
  • > 500 mOsm/kg
  • < 350 mOsm/kg
  • < 350 mOsm/kg
Urine sediment

Despite the common use of BUN:creatinine ratio and urinary fractional excretions (i.e., FENa, FEUrea) in clinical practice, observational data suggest that they do not reliably distinguish prerenal AKI from intrinsic AKI. [15][19]

The most likely mechanism of AKI is primarily determined based on clinical presentation and response to therapy. Evaluating patients' response to initial interventions is key to confirming the mechanism of AKI and guiding further workup and management steps.

Prerenal AKI [13][14]

Patients with prerenal AKI receiving diuretic therapy may have a falsely elevated FENa. Therefore, FEUrea may be more informative in this setting. [23]

Intrinsic AKI

A falsely low FENa may be seen in some patients with intrinsic AKI, e.g., due to glomerulonephritis, acute interstitial nephritis, rhabdomyolysis, or contrast-induced nephropathy. [23]

Postrenal AKI

Additional investigations

Usually reserved for cases in which intrinsic AKI is initially suspected or interventions aimed at reversing presumed prerenal AKI or postrenal AKI fail to improve renal function. Studies should be guided by clinical suspicion.

Noninvasive testing

Noninvasive testing for specific underlying causes of AKI [1][25]
Examples Concerning features Typical findings
Nephrotoxin-induced AKI
Rapidly progressive glomerulonephritis
  • ANA
  • ↑ dsDNA
  • ↓ Complement
  • ↑ Serum IgA
  • Normal complement
  • Atheroembolic disease
  • Exposure to typical culprit medications
  • Fever, drug rash, flank pain

Renal biopsy [13][25]

  • Not routinely indicated
  • Consider if:
    • The cause of AKI cannot be identified after a thorough initial evaluation
    • Diagnostic confirmation of the cause (e.g., glomerulonephritis, myeloma nephropathy) is needed prior to initiating disease-specific therapy

Approach [12][13][14]

AKI management is primarily supportive. Currently, there are no specific pharmacotherapies for AKI. [14]

Avoid coadministering RAAS inhibitors and NSAIDs in patients with reduced renal perfusion (e.g., in congestive heart failure, renal artery stenosis) because doing so can significantly decrease their GFR.

Early nephrology consult

Treatment of underlying causes [12][13][14]

Treatment for the underlying cause of AKI
AKI subtype Cause Management
  • Discontinuation of offending medications (e.g., ACE-Is, ARBs, NSAIDs)
  • Ensure adequate hydration.
  • Supportive care of AKI (mainstay of treatment) including prevention of further nephrotoxin exposure [30]
  • Management of any complications
  • Vascular causes
  • Ureteral or renal pelvic obstruction

The longer the underlying cause has been present, the greater the chance that AKI will progress to renal failure and/or CKD. Treat potential causes of AKI early.

Renal replacement therapy [12][14]

See also “Indications for acute dialysis.”

The goal of supportive care is to avoid further renal insult and potentially aggravating factors, support adequate kidney perfusion, and ensure early identification and treatment of complications.

Management of medications and nephrotoxic substances [14]

Calculating eGFR using conventional equations does not accurately predict the true GFR in patients with AKI. Reestimate GFR daily based on the patient's urine output and the trajectory of serum creatinine.

Noncontrast imaging studies are preferred if possible. When the use of iodinated contrast is required for a critical diagnostic study or procedure (e.g., for the treatment of STEMI), the lowest clinical diagnostic dose should be used.

Monitoring and management of volume status and blood pressure [13][14]

Hemodynamic support in patients with AKI according to presumed intravascular volume status

Hypovolemia (and/or hypotension)
Euvolemia or indeterminate volume status
  • Consider an IV fluid challenge to assess if the patient responds to fluids (e.g., improvement in creatinine, urine output, and/or blood pressure)
    • Responsive: Carefully continue IV fluid challenges until the patient is no longer responsive.
    • No response: Stop IV fluid challenges but ensure continued fluid needs are met.

Patients with AKI are at high risk of developing fluid overload, which can compromise renal function and may increase mortality. Avoid aggressive fluid resuscitation in patients who are not volume responsive.

Consider loop diuretics ONLY in patients with signs of fluid overload. Diuretics should not be used routinely to improve urine output in patients with AKI because of their lack of benefit and potential for harm. [12]

Choice of parenteral fluid [13][14][35]

The use of balanced IV fluid solutions has been associated with lower mortality and better renal outcomes compared with the use of normal saline in patients with AKI.

Monitoring and management of biochemical alterations

Obtain frequent (at least daily) laboratory studies to monitor for the presence of metabolic complications and response to treatment (e.g., improvement in creatinine levels).

Consider urgent renal replacement therapy for patients with refractory electrolyte or acid-base disturbances.

Additional considerations

The risk of GI bleeding may be increased in AKI due to uremic platelet dysfunction. [42]

Consider a nutrition consult for all patients with AKI. [40]

Follow-up care [43][44]

  • Educate patients on medication management and the prevention of AKI.
  • Monitor serum creatinine, eGFR, blood pressure, and weight following discharge. [43][45]
  • Ensure that patients who require ongoing renal replacement therapy have access to outpatient dialysis services.
  • Consider referral for outpatient nephrology follow-up in patients with significant residual renal dysfunction (i.e., eGFR < 60 mL/min).

Patients who recover from AKI are at high risk of readmission, mortality, cardiovascular events, progressive renal function deterioration, and developing de novo CKD. [43][44]

Adequate discharge planning and follow-up may help improve patient outcomes. [43][44]

Identify patients who are at risk of AKI and implement appropriate preventive strategies. [1][12][27]

Prevention of acute kidney injury
Risk factors Preventive strategies
Acute illness
Nephrotoxic medication exposure
Iodinated radiocontrast agent exposure
Liver failure
Endogenous nephrotoxins

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