Acute Kidney Injury, commonly abbreviated AKI, is a sudden deterioration in kidney function occurring over hours or days, sometimes developing over a longer period of acute illness. The term replaced the older expression acute renal failure because many patients experience a substantial but incomplete decline in kidney function rather than complete cessation of renal activity. AKI causes accumulation of creatinine and other waste products and can disturb fluid, electrolyte and acid-base balance. It is usually a complication or consequence of another illness rather than an isolated disease. AKI can be mild and reversible or severe and life-threatening, depending on its cause, duration, baseline kidney health and associated organ dysfunction.
Causes are often divided physiologically into reduced renal perfusion, intrinsic kidney injury and urinary outflow obstruction. Reduced perfusion, sometimes called prerenal AKI, can result from dehydration, vomiting, diarrhoea, bleeding, sepsis, low blood pressure or reduced cardiac output. Intrinsic renal injury can involve direct damage to kidney tubules, glomeruli, interstitium or blood vessels, including inflammatory diseases and toxic drug effects. Postrenal AKI occurs when urine flow is obstructed by problems such as kidney stones, prostate enlargement or tumours. More than one mechanism may coexist, especially in seriously ill patients. Correctly identifying the mechanism is crucial because treatment for dehydration differs fundamentally from treatment for an obstructed urinary tract or inflammatory renal disease.
Risk is higher in older adults and people with pre-existing kidney disease, diabetes, heart failure, liver disease or other severe systemic illnesses. Hospitalisation, major surgery, sepsis, significant blood loss and exposure to potentially nephrotoxic medicines can further increase risk. Medicines associated with AKI include some non-steroidal anti-inflammatory drugs, certain antibiotics and combinations of medicines that alter renal blood flow or fluid balance. Contrast exposure can also contribute in susceptible patients.
The presence of risk factors does not mean AKI will inevitably occur; rather, it reduces renal reserve or increases vulnerability to acute physiological stress. Prevention therefore involves recognising high-risk situations, maintaining appropriate hydration and reviewing medicines during acute illness rather than simply avoiding one particular drug.
AKI can be clinically silent, particularly in its early stages, and may first be detected through routine blood testing. When symptoms occur, reduced urine output, thirst, nausea, vomiting, swelling, fatigue, dizziness, confusion and breathlessness can develop. Oliguria, meaning unusually low urine production, is an important clinical sign but is not required for AKI because some patients maintain normal urine volume despite substantial loss of filtration.
Creatinine rises when kidney filtration falls, but serum creatinine changes relatively slowly and can underestimate the very early phase of injury. Clinicians therefore consider the change from a known baseline, urine output, clinical context and other laboratory findings rather than interpreting a single creatinine concentration in isolation.
Diagnosis generally begins with serial blood measurements of creatinine, urine assessment and review of fluid balance, blood pressure and the likely cause. Urinalysis can reveal blood, protein or other abnormalities suggesting intrinsic renal disease. Ultrasound is particularly useful when urinary obstruction is possible. Further imaging, immune tests or kidney biopsy may be required when the mechanism remains unclear. Electrolytes are important because AKI can cause dangerous hyperkalaemia and acid-base disturbances.
Clinicians also assess for complications such as pulmonary oedema, severe acidosis, uraemic symptoms and cardiac effects of electrolyte abnormalities. Comparing current results with previous renal function is essential because a creatinine level that appears only moderately abnormal can represent a major acute change in a person whose baseline kidney function was previously normal.
Treatment is directed at the underlying cause and at preventing secondary complications. Dehydration may require carefully administered intravenous fluids, while infection may require antibiotics and treatment of sepsis. Medicines that contribute to renal injury may need to be stopped or adjusted under medical supervision. Obstruction requires restoration of urinary drainage, potentially through catheterisation, stenting or another procedure. Excess fluid may require restriction and diuretic treatment in selected circumstances, while severe metabolic disturbances may require dialysis. Dialysis in AKI is often temporary and may be used until renal function recovers, although some patients sustain permanent damage. Rapid treatment can therefore make a substantial difference to recovery, but management must avoid both under-treatment and excessive fluid administration.
Recovery from AKI varies widely. Many people regain much or all of their previous kidney function after the precipitating problem is corrected, particularly when the episode is recognised early. More severe injury can require weeks or months for recovery, and some people are left with permanent reduction in kidney function or develop CKD. AKI can also increase future susceptibility to additional renal injury. Follow-up testing after discharge is therefore important even when symptoms have resolved.
The prognosis depends not only on the kidney injury itself but also on the illness that caused it, such as sepsis, major surgery or severe cardiovascular disease. A person who appears to have recovered clinically may still require laboratory confirmation that renal function has returned to baseline.
AKI is frequently confused with kidney failure, but the terms describe different concepts. AKI refers to a sudden change in kidney function and can range from mild impairment to complete temporary failure. Kidney failure generally refers to very advanced loss of renal function, conventionally when kidney function is below about 15 percent of normal in chronic disease. AKI is also not the same as CKD, which requires persistent abnormality over time. A person with CKD can experience AKI, producing acute-on-chronic deterioration, and a severe AKI episode can subsequently contribute to CKD. The term injury does not imply a physical blow to the kidneys; most AKI results from physiological, toxic, inflammatory or obstructive processes occurring internally.
