Acute Kidney Injury (AKI)

Acute Kidney Injury (AKI)

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An acute Kidney Injury (AKI) is a sudden decrease in kidney function. This is a serious and common condition amongst hospitalized patients, affecting up to 20% of hospital admissions.


AKI is caused by a rapid decrease in Glomerular Filtration Rate (GFR). This is maintained by adequate blood flow to the kidneys, functioning nephrons and a clear pathway for urine outflow. Any changes to this system can lead to AKI.

GFR is dependent on a pressure difference between the incoming blood at the afferent capillaries and the pressure in Bowman's space.

AKI can be divided into pre-renal, intra-renal, and post-renal causes for diagnosis purposes.


Pre-renal AKI occurs when there is reduced perfusion to the kidney. This can happen in hypovolaemic, euvolaemic, or hypervolaemic states. Some causes of pre-renal AKI include absolute hypovolaemia due to haemorrhage, over-diuresis, vomiting and diarrhoea, low effective arterial blood volume due to heart failure, cirrhosis, sepsis, or third spacing of fluid, anatomical renal artery stenosis, and drug-induced NSAIDs, ACE inhibitors, or diuretics.


Intra-renal AKI is caused by structural or functional changes at the level of the nephron, either independently or as the result of a pre-renal AKI. Major types of this are Acute Tubular Necrosis (ATN), Acute Interstitial Nephritis (AIN), and glomerular disease, which includes nephrotic and nephritic syndromes.

Acute Kidney Injury

Acute kidney injury (AKI) is characterized by an abrupt decline in renal filtration leading to a decrease in urine output and an increase in serum creatinine. AKI is broadly classified into three etiological categories: pre-renal, intra-tubular, and post-renal.


Pre-renal AKI occurs secondary to decreased renal perfusion due to systemic hypoperfusion. Common causes include hypotension, dehydration, and sepsis.


Intra-tubular obstruction AKI is caused by a wide range of pathologies that lead to obstruction in the tubules. Causes include:

  • Glomerular: immune complex-mediated glomerulonephritis, e.g. 75% of those with
  • Tubulointerstitial: interstitial nephritis, e.g. drug-induced, granulomatosis with polyangiitis (GPA))
  • Intra-tubular obstruction: multiple myeloma with paraprotein, pigment (e.g. rhabdomyolysis)
  • Other: scleroderma renal crisis, malignant hypertension


Post-renal AKI is associated with an obstructive pathology leading to congestion of the kidneys. Causes of post-renal AKI can be divided anatomically: ureters, bladder, prostate, urethra, and extrenal.

  • Ureters: nephrolithiasis, retroperitoneal fibrosis
  • Bladder: bladder cancer
  • Prostate: benign prostatic hyperplasia (BPH), prostate cancer
  • Urethra: urethral stricture
  • External: retroperitoneal mass, ovarian tumours

Obstruction at or distal to the level of the bladder can cause a post-renal AKI in both kidneys. Unless there is a solitary kidney, a unilateral obstruction may not cause post-renal AKI as the unaffected kidney may be able to compensate for the reduced function of the affected kidney. This puts patients with a solitary kidney at increased risk of AKI.

Risk factors

Risk factors for acute kidney injury include:

  • Chronic kidney disease (adults with an eGFR < 60 ml/min/1.73 m2 are at high risk)
  • Heart failure
  • Liver disease
  • Diabetes
  • History of acute kidney injury
  • Oliguria (< 0.5 ml/kg/hour)
  • Neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer
  • Hypovolaemia
  • Use of drugs that can cause or exacerbate kidney injury
  • Use of iodine-based contrast media within the past week
  • Symptoms or history of urological obstruction, or conditions that may lead to obstruction
  • Sepsis
  • Deteriorating early warning scores
  • Age 65 years or over

Common medications with potentially nephrotoxic side effects are listed in Table 1.


Various medications can affect the functioning of the kidneys, including ACE inhibitors, angiotensin receptor blockers (ARBs), cyclosporin, NSAIDs, and tacrolimus. These medications can cause a change in the glomerular filtration rate (GFR) by negatively affecting the vascular tone of the afferent and efferent arterioles, changing the interglomerular blood flow. Other medications, such as aminoglycosides, amphotericin B, and cisplatin, can cause direct tubular cell toxicity in the proximal convoluted tubules.

NSAIDs, rifampin, acyclovir, and ampicillin can result in interstitial nephritis, inflammation in the interstitium of the kidney, and crystal nephropathy, which causes the formation of insoluble crystals.

Clinical features

Acute kidney injury (AKI) can present over hours to days. It may be asymptomatic or have non-specific symptoms like fatigue, nausea, and confusion. Important areas of history to uncover include: reason for hospital admission, underlying medical conditions, use of nephrotoxic medications, recent imaging investigations with iodinated contrast, lower urinary tract symptoms, and having a solitary kidney.

Clinical findings of AKI may include oliguria or anuria, signs of hypovolaemia, volume overload, uraemia, and post-renal obstruction.


Checking urea and electrolytes can detect AKI biochemically.


Subsequent investigations of Acute Kidney Injury (AKI) are guided by history and physical examination, but an algorithmic approach will give baseline information to direct specialised testing.

Laboratory Investigations

Relevant laboratory investigations include:

  • Urea and electrolytes: creatinine, blood urea nitrogen (BUN), calcium, phosphate, potassium, sodium
  • Full blood count (FBC): anaemia, leukocytopenia, thrombocytopenia
  • Liver function tests (LFTs): serum albumin
  • Venous blood gas (VBG): assessing for acidaemia

Urine Studies

Relevant urine studies may include:

  • Urine analysis: proteinuria, albuminuria, haemoglobinuria, haematuria, WBC, glucose
  • Urine volume measurement: oliguria, anuria
  • Urinary microscopy and sediment: casts, crystals
  • Urine osmolarity and specific gravity: dehydration, less commonly used in clinical practice
  • Urinary eosinophil count: useful in the evaluation of Acute Interstitial Nephritis (AIN) (rare), less commonly used in clinical practice.


Relevant imaging investigations include:

  • Post-void residual volume (PVR): measured using a bedside bladder scanner
  • Ultrasound of the kidneys, ureters and bladder (KUB): assessing kidney size, hydronephrosis, postrenal obstruction, renal lesions
  • CT non-contrast:radiopaque and non-radiopaque calculi, ureteric obstruction
  • CT urogram: investigating for urinary tract bleeding
  • CT triphasic kidneys: dedicated cross-sectional imaging for renal lesions (often used to clarify masses seen on ultrasound)

Renal Biopsy

A renal biopsy can be considered for suspected intra-renal AKI or suspected rapidly progressive glomerulonephritis (RPGN). Where Acute Tubular Necrosis (ATN) is clinically suspected, a renal biopsy is usually not undertaken, unless specifically trying to exclude a reasonable alternative diagnosis.

Pre-renal AKI

Investigation results suggestive of pre-renal aetiology include:

  • BUN: Creatinine ratio >20:1
  • Fraction of excreted sodium (FENa) <1 %
  • Fractional excretion of urea <35%

Rapid response to isotonic fluid (0.9% NaCl) resuscitation strongly favours a pre-renal AKI.


The kidney disease improving global outcomes (KDIGO) classification tool is the most up to date and commonly used.

The KDIGO system confirms an AKI with any of the following present:

  • Urine output less than 0.5 ml/kg/hr for 6 hours
  • Serum creatinine increase 1.5x the baseline over 7 days
  • Serum creatinine increase by 0.3mg/dL in 48 hours

There are additional criteria to evaluate the severity of the AKI and prognostic factors.


The mainstay of AKI management is prompt identification and removal of the causative agent(s) while providing supportive treatment for the AKI itself.

Acute Kidney Injury

Acute Kidney Injury (AKI) is a rapid deterioration in kidney function marked by elevated serum creatinine and urea or reduced urine output. Causes of AKI can be divided into pre-renal, intra-renal and post-renal.

Those at an increased risk of AKI are older individuals (over 65) who are hospitalized, admitted to an intensive care unit, or have underlying systemic or renal disease. These individuals must be monitored and quickly identified in order to prevent permanent damage or progression to chronic kidney disease (CKD) and end-stage renal disease (ESRD).

The Kidney Disease: Improving Global Outcomes (KDIGO) criteria are the most commonly used criteria for diagnosing AKI, with an increased serum creatinine and reduced urine production being the key diagnostic features.

General Management

General management of AKI includes:

  • Withdrawal of nephrotoxic medication
  • Adjustment of drug doses that are renally cleared in order to prevent drug toxicity
  • Fluid resuscitation to rapidly improve renal function in cases of hypovolaemia/hypotension
  • Urinary catheterisation when unable to measure urine output or to relieve urinary obstruction
  • Assessment for sepsis and initiation of the sepsis six care bundle if necessary

ABCDE Checklist

Many hospitals use an ABCDE checklist to aid in AKI management:

  • A: Address drugs
  • B: Boost blood pressure
  • C: Calculate fluid balance
  • D: Dip urine
  • E: Exclude obstruction

Targeted Management

Targeted management is dependent on the underlying cause and may include:

  • Diuretics for volume overloaded patients, particularly in cases of pulmonary oedema
  • Glucocorticoid immunosuppression for Acute Interstitial Nephritis or Rapidly Progressive Glomerulonephritis to limit damage
  • Indwelling bladder catheter, nephrostomy tubes or ureteric stent insertion when obstructions are present

Renal Replacement Therapy

Renal Replacement Therapy (RRT) is indicated in more severe cases of AKI and can be remembered using the mnemonic AEIOU:

  • A: Acidosis (pH < 7.15 or worsening acidaemia)
  • E: Electrolyte abnormalities (hyperkalaemia >6.5 mmol/l)
  • I: Ingested toxins (toxic alcohols, aspirin, lithium)
  • O: Overload (diuretic-resistant fluid overload in setting of AKI)
  • U: Uraemic complications (e.g. pericarditis, encephalopathy, uraemic bleeding)

Additionally, note that oligo/anuria will often accelerate the need for RRT.


AKI can cause significant morbidity and mortality, particularly in patients admitted to Intensive Care. Those with poorer pre-morbid status tend to have a worse prognosis. Complications of AKI include:

  • Fluid overload (leg oedema, pulmonary oedema, pleural effusions)
  • Electrolyte derangement (hyperphosphatemia, hyperkalaemia)
  • Acid-base disorder (metabolic acidosis)
  • End-organ complications of uraemia
  • Chronic kidney disease (CKD)
  • End-stage renal disease (ESRD)
  • Death

Key Points

  • AKI is a rapid deterioration in kidney function marked by elevated serum creatinine and urea or reduced urine output.
  • The causes of AKI can be grouped as pre-renal, intra-renal or post-renal AKI.
  • Older hospitalised patients, those admitted to the ICU or those who have underlying systemic or renal disease are at increased risk of AKI.
  • The KDIGO criteria are the most commonly used criteria for diagnosing AKI, with an increase in serum creatinine and reduced urine production being the key diagnostic features.

Acute Kidney Injury Management

Management of an acute kidney injury (AKI) involves ensuring adequate kidney perfusion, maintaining a clear urinary tract, removing toxins, and monitoring for decreased renal function complications. Dialysis may be necessary in severe cases of AKI in order to give the kidneys time to recover. Proper recognition and management of AKI is essential to prevent long-term damage or progression to chronic kidney disease (CKD).

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