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An acute kidney injury (AKI) is caused by a rapid deterioration in kidney function. This is a common, yet serious occurrence in hospitalised patients, with AKI occurring in up to 20% of hospital admissions.1
AKI can occur when there is a sudden decrease in glomerular filtration rate (GFR).
GFR is maintained by sufficient blood flow into the kidneys, functioning nephrons and a clear pathway for outflow of urine from the kidney. If there are alterations to this system, an AKI can occur.
At the glomerular level, GFR is dependent on a pressure gradient between the incoming blood at the afferent capillaries and the pressure in Bowman’s space.
Separating AKI into pre-renal, intra-renal, and post-renal aetiologies is a helpful tool to aid a systematic approach to the diagnosis.
Pre-renal AKI occurs when there is reduced perfusion to the kidney. This can occur in hypovolaemic, euvolaemic or hypervolaemic states.
Causes of pre-renal AKI include:
- Absolute hypovolaemia: haemorrhage, over-diuresis, vomiting and diarrhoea
- Low effective arterial blood volume (EABV): heart failure, cirrhosis, sepsis, third spacing of fluid
- Anatomical: renal artery stenosis
- Drug-induced: NSAIDs, ACE inhibitors, diuretics
Intra-renal AKI occurs when there is a structural or functional change at the level of the nephron. This can occur independently or as a transformation of a pre-renal AKI.
Causes of intra-renal AKI include:2
- Acute tubular necrosis (ATN): the most common cause of AKI which occurs due to ischaemic or toxic injury to the cells of the proximal convoluted tubules
- Acute interstitial nephritis (AIN): most often eosinophilic nephritis that can be drug-induced (e.g. NSAIDs, penicillin), infection-induced (e.g. tuberculosis, legionella) or immune-mediated (e.g. sarcoidosis, SLE or IgG-related disease (IgG4-RD))
- Glomerular disease: includes nephrotic and nephritic syndromes which may be primary renal disease (e.g. anti-glomerular basement membrane (anti-GBM), or part of systemic disease with immune complex deposition (e.g. IgA vasculitis) or without immune complex deposition (e.g. 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: 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.3
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
- 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
- Use of drugs that can cause or exacerbate kidney injury (Table 1)
- Use of iodine-based contrast media within the past week
- Symptoms or history of urological obstruction, or conditions that may lead to obstruction
- Deteriorating early warning scores
- Age 65 years or over
Table 1. Commonly used medications with potentially nephrotoxic side effects.4
Angiotensin receptor blockers (ARBs)
Affect the vascular tone of the afferent and efferent arterioles, altering interglomerular blood flow
Tubular cell toxicity
Direct toxicity to the epithelial cells of the proximal convoluted tubules
Inflammatory reaction within the interstitium of the kidney
Can result in precipitates of insoluble crystals
Non-steroidal anti-inflammatory drugs (NSAIDs)
NSAIDs can be implicated in multiple causes of renal impairment so their use should be restricted in patients at risk of AKI:
- Pre-renal: NSAIDs block prostaglandin mediated vasodilation of the afferent arteriole, which limits the kidney’s ability to regulate local blood flow
- Intra-renal: NSAIDs can cause acute interstitial nephritis (AIN)
- Post-renal: long term NSAID use can cause renal papillary necrosis where the medullary papilla sloughs off, causing obstruction to urine flow
The timeline of AKI occurs over hours to days. The presenting history will provide clues to the likely cause of the AKI.
AKI can be challenging to recognise as it is often asymptomatic or can present with non-specific symptoms of fatigue, nausea and confusion. These symptoms can often be mistaken as symptoms of the underlying condition that is causing the AKI (e.g. sepsis)
It is important to suspect AKI in any acutely unwell patient.
Important areas of the history to cover include:
- Reason for admission to hospital (e.g. sepsis, burns)
- Underlying medical conditions (e.g. heart failure, cirrhosis, SLE)
- Use of medications known to be nephrotoxic (e.g. NSAIDs, diuretics, penicillin, cisplatin)
- Recent imaging investigations using iodinated contrast, particularly if delivered arterially (e.g. CT with contrast, angiogram)
- Lower urinary tract symptoms (e.g. frequency, urgency, incomplete emptying)
- Known to have a solitary kidney
Typical clinical findings of AKI may include:
- Oliguria or anuria
- Signs of hypovolaemia: dry mucous membranes, reduced skin turgor, tachycardia, hypotension
- Signs of volume overload: hypertension, pulmonary oedema, peripheral oedema, elevated jugular venous pulse
- Signs of uraemia: ecchymosis due to platelet dysfunction, uraemic encephalopathy (e.g. asterixis, confusion, seizures)
- Signs of post-renal obstruction: palpable or tender distended bladder
AKI is detected biochemically by checking urea and electrolytes. Subsequent investigations are guided by history and examination, but an algorithmic approach will yield baseline information that can guide tailored/specialised testing.
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): assess for acidaemia
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 AIN (rare), less commonly used in clinical practice
Relevant imaging investigations include:
- Post-void residual volume (PVR): can be assessed rapidly using a bedside bladder scanner
- Ultrasound of the kidneys, ureters and bladder (KUB): assess kidney size, hydronephrosis, postrenal obstruction, renal lesions
- CT non-contrast: radiopaque and non-radiopaque calculi, ureteric obstruction
- CT urogram: investigate for urinary tract bleeding
- CT triphasic kidneys: dedicated cross-sectional imaging for renal lesions (often used to clarify masses seen on ultrasound)
A renal biopsy can be considered for suspected intra-renal AKI or suspected rapidly progressive glomerulonephritis (RPGN). Where ATN is clinically suspected, a renal biopsy is usually not undertaken, unless specifically trying to exclude a reasonable alternative diagnosis.
Investigation results suggestive of pre-renal aetiology include:5
- 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.6
The KDIGO system confirms an AKI with any of the following present:6
- Urine output less than 0.5ml/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.
General management of AKI includes:
- Withdrawal of nephrotoxic medication
- Adjustment of drug doses which are renally cleared to prevent drug toxicity
- Fluid resuscitation can rapidly improve renal function in hypovolaemia/hypotension
- Urinary catheterisation can be used where there is difficulty in measuring urine output or to relieve urinary obstruction
- Assess for evidence of sepsis and initiate the sepsis six care bundle if required
Many hospitals are using an ABCDE checklist to prompt AKI management:
- A: Address drugs
- B: Boost blood pressure
- C: Calculate fluid balance
- D: Dip urine
- E: Exclude obstruction
Targeted management depending on the underlying cause:
- Diuretics may benefit volume overloaded patients, particularly in pulmonary oedema
- Immunosuppression with glucocorticoids can be considered in AIN or RPGN to slow the progression to irreversible injury7
- Some patients may need an indwelling bladder catheter, nephrostomy tubes or ureteric stent insertion depending on the site and cause of the obstruction
Renal replacement therapy
Renal replacement therapy (RRT) is indicated in more severe cases of AKI:8
- Metabolic acidosis pH < 7.15 or worsening acidaemia
- Refractory electrolyte abnormalities (hyperkalaemia >6.5mmol)
- Presence of dialysable toxins (toxic alcohols, aspirin, lithium)
- Refractory fluid overload (diuretic resistant fluid overload in setting of AKI)
- End-organ uraemic complications (e.g. pericarditis, encephalopathy, uraemic bleeding)
Indications for renal replacement therapy
Indications for RRT can be remembered by the mnemonic AEIOU:
- Electrolyte abnormalities
- Ingested toxins
- Fluid Overload
Additionally, note that oligo/anuria will often accelerate the need for RRT.
AKI can be a significant cause of morbidity and mortality, especially in patients admitted to Intensive Care. Having poorer pre-morbid status prior to developing the AKI is a significant negative predictor for recovery.9
Recognition and prompt management of an AKI are essential in preventing permanent damage or progression to chronic kidney disease (CKD).
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)
- 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 (+65) 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.
- Management of an AKI revolves around ensuring the kidneys are adequately perfused, ensuring the urinary tract is patent, removing nephrotoxins, and monitoring for complications from diminished renal function.
- Dialysis may be indicated in cases of severe AKI, allowing time for renal recovery.
- Recognition and management of AKI are essential to prevent permanent damage or progression to chronic kidney disease (CKD).
Dr John Holland
Renal Specialist Registrar
Dr Ian Logan
Dr Chris Jefferies
- Wang, H. E., Muntner, P., Chertow, G. M., & Warnock, D. G. (2012). Acute kidney injury and mortality in hospitalized patients. American Journal of Nephrology, 35(4), 349–355.
- Santos, W. J. Q., Zanetta, D. M. T., Pires, A. C., Lobo, S. M. A., Lima, E. Q., & Burdmann, E. A. (2006). Patients with ischaemic, mixed and nephrotoxic acute tubular necrosis in the intensive care unit – a homogeneous population? Critical Care, 10(2).
- Zhu, K., Song, H., Zhang, Z., Ma, B., Bao, X., Zhang, Q., & Jin, J. (2020). Acute kidney injury in solitary kidney patients after partial nephrectomy: incidence, risk factors and prediction. Translational Andrology and Urology, 9(3), 1232–1243.
- Patel, J. B., & Sapra, A. (2021). Nephrotoxic Medications. In StatPearls [Internet]. Treasure Island (FL), StatPearls Publishing LLC. Available from: [LINK]
- Mohsenin, V. (2017). Practical approach to detection and management of acute kidney injury in critically ill patient. Journal of Intensive Care, 5(1).
- KDIGO.2012 Kidney Disease: Improving Global Outcomes (KDIGO) Clinical Practice Guideline for Acute Kidney Injury (AKI). (2012). Available from: [LINK]
- González, E., Gutiérrez, E., Galeano, C., Chevia, C., de Sequera, P., Bernis, C., Parra, E. G., Delgado, R., Sanz, M., Ortiz, M., Goicoechea, M., Quereda, C., Olea, T., Bouarich, H., Hernández, Y., Segovia, B., & Praga, M. (2008). Early steroid treatment improves the recovery of renal function in patients with drug-induced acute interstitial nephritis. Kidney International, 73(8), 940–946.
- Negi, S., Koreeda, D., Kobayashi, S., Iwashita, Y., & Shigematu, T. (2016). Renal replacement therapy for acute kidney injury. Renal Replacement Therapy, 2(1).
- Saran, R., Robinson, B., Abbott, K. C., Agodoa, L. Y. C., Bragg-Gresham, J., Balkrishnan, R., Bhave, N., Dietrich, X., Ding, Z., Eggers, P. W., Gaipov, A., Gillen, D., Gipson, D., Gu, H., Guro, P., Haggerty, D., Han, Y., He, K., Herman, W., … Shahinian, V. (2019). US Renal Data System 2018 Annual Data Report: Epidemiology of Kidney Disease in the United States. American Journal of Kidney Diseases, 73(3).