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 (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:
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.
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 for acute kidney injury include:
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.
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.
Relevant laboratory investigations include:
Relevant urine studies may include:
Relevant imaging investigations include:
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.
Investigation results suggestive of pre-renal aetiology include:
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:
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 (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 of AKI includes:
Many hospitals use an ABCDE checklist to aid in AKI management:
Targeted management is dependent on the underlying cause and may include:
Renal Replacement Therapy (RRT) is indicated in more severe cases of AKI and can be remembered using the mnemonic AEIOU:
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:
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).
