Acute kidney injury
A sudden kidney function decline within seven days.
Acute kidney injury (AKI), once known as acute renal failure, describes a rapid decline in kidney function that occurs within a week. This drop is identified by a rise in serum creatinine, a fall in urine output, or both. The condition is both common and serious, affecting 10–15% of hospitalized patients and over half of those in intensive care. Potential complications include metabolic acidosis, dangerously high potassium levels, uremia, fluid imbalances, harm to other organs, and death. People who survive AKI face a higher future risk of chronic kidney disease.
The underlying cause of AKI often dictates the symptoms. As urea and other nitrogen waste build up in the blood, patients may experience fatigue, appetite loss, headache, nausea, and vomiting. A sharp rise in potassium can trigger life-threatening heart rhythm problems. Fluid balance is typically disturbed, though blood pressure may be high, low, or normal. Flank pain can occur if the kidney’s fibrous capsule is stretched, such as from a blood clot or inflammation. Dehydration may cause thirst or visible fluid loss. A physical exam might also reveal clues like a rash (suggesting interstitial nephritis or vasculitis) or a palpable bladder (pointing to obstruction).
Causes of AKI fall into three categories: prerenal, intrinsic renal, and postrenal. Prerenal AKI stems from reduced blood flow to the kidneys, lowering the glomerular filtration rate. Both kidneys must be affected, since one alone can maintain normal function. Common prerenal triggers include low blood volume from dehydration or blood loss, low blood pressure, heart failure (leading to cardiorenal syndrome), cirrhosis-related hepatorenal syndrome, and local vascular issues like NSAID-induced vasoconstriction, renal artery stenosis, or renal vein thrombosis.
Intrinsic AKI involves direct damage to the kidney itself, affecting structures such as the glomeruli, tubules, or interstitium. Typical causes include glomerulonephritis, acute tubular necrosis, and acute interstitial nephritis. Other triggers are rhabdomyolysis and tumor lysis syndrome. Certain medications—like some antibiotics (e.g., amoxicillin/clavulanic acid) and calcineurin inhibitors (e.g., tacrolimus)—can also directly harm tubular cells.
Postrenal AKI results from blockages downstream of the kidney, most often due to urinary tract obstruction. Possible causes include benig
- field
- Nephrology
- known_for
- Sudden decrease in kidney function within seven days
- classification
- Prerenal, intrinsic renal, postrenal
- diagnostic_criteria
- Increase in SCr by ≥0.3 mg/dl within 48 hours, or increase to ≥1.5 times baseline within 7 days, or urine volume <0.5 mL/kg/h for 6 hours
- staging_system
- RIFLE criteria (Risk, Injury, Failure, Loss, End-stage kidney disease)
- complications
- Metabolic acidosis, high potassium, uremia, fluid imbalance, death
Lore & Background
Acute kidney injury is diagnosed based on a person's signs and symptoms, along with laboratory tests measuring serum creatinine and urine output. Other tests include urine microscopy and urine electrolytes. Renal ultrasound can be obtained when a postrenal cause is suspected, and a kidney biopsy may be obtained when intrinsic renal AKI is suspected and the cause is unclear. The underlying cause often dominates the clinical presentation, with symptoms such as fatigue, loss of appetite, headache, nausea, vomiting, and abnormal heart rhythms from high potassium levels.
Reader's Guide
Acute kidney injury represents a critical medical condition with significant implications for patient outcomes. Its classification into prerenal, intrinsic renal, and postrenal causes guides clinical management, which includes treatment of the underlying cause and supportive care such as renal replacement therapy. The introduction of standardized diagnostic criteria by KDIGO in 2012 and the RIFLE staging system have improved consistency in diagnosis and severity assessment. AKI is particularly prevalent in hospitalized and intensive care unit patients, and its complications—including metabolic acidosis, hyperkalemia, and uremia—can be life-threatening. The condition's link to future chronic kidney disease underscores the importance of prompt recognition and management. Despite advances, alternative markers such as NGAL, HAVCR1, IL18, and cystatin C had not, as of 2018, replaced creatinine as the primary marker of kidney function.
Did You Know?
- AKI is seen in 10–15% of people admitted to the hospital and in more than 50% of people admitted to the intensive care unit.
- Prerenal causes of AKI include sepsis, dehydration, excessive blood loss, cardiogenic shock, heart failure, cirrhosis, and certain medications such as ACE inhibitors or NSAIDs.
- The RIFLE criteria define a spectrum from Risk (1.5-fold creatinine increase) to End-stage kidney disease (need for renal replacement therapy for more than 3 months).
- People who have experienced AKI are at increased risk of developing chronic kidney disease in the future.
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