Acute kidney injury (AKI) is characterised by a rapid reduction (hours or days) in kidney function. It may be asymptomatic, but oliguria is a frequent early sign. As the kidneys fail to filter blood, creatinine and urea levels in blood rise and urine production slows. AKI is common in hospital patients because it is generally caused by circulatory disturbances (hypoperfusion of the kidney) which are common in severe illness such as sepsis and trauma, as well as after surgery.

Acute kidney injury (AKI)

The main function of the kidneys is to get rid of molecules that the body doesn’t need. In AKI, key molecules like creatinine (produced by muscles) and urea (the main carrier of waste nitrogen) increase in plasma over a short time span (hours to days). When the kidneys fail to function effectively, fluid and electrolyte balance is disturbed, frequently leading to hyperkalaemia and metabolic acidosis. Three basic categories of AKI help distinguish likely causes, although most will be associated with oliguria:

These are usually due to a perfusion problem such as hypotension, hypovolaemia or renal artery stenosis/embolism.

Damage to the kidneys leads to dysfunction. The most common cause is acute tubular necrosis (ATN) due to hypoperfusion, but it can also result from administration of nephrotoxic drugs such as aminoglycoside antibiotics (e.g. streptomycin) and NSAIDs.

Post-renal problems result from any obstruction of the urinary tract. Causes include prostatic hyperplasia or kidney stones. Injury may also be the result of a poorly inserted or blocked urinary cannula.

These can coexist and be inter-related. For example, a patient with pre-renal AKI due to hypotension and lack of kidney perfusion might not be managed effectively and the kidney could become damaged leading to renal AKI. Indeed, this is the most cause of ATN.

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