Acute kidney injury !

Acute kidney injury is a sudden drop in kidney function over hours or days, so waste products, fluid and salts build up in the body.

Updated 2026-10-30

Structures involved

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In biochemistry

Microorganisms that cause it

Leptospira interrogans

In histology

In embryology

ACE inhibitors and ARBs: fetal kidney damage

In the clinical exam

In physiology

Why it happens

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What it is

Abrupt fall in kidney function over hours to days, shown by a rise in serum creatinine or a drop in urine output, with build-up of waste products, fluid and electrolytes.

Who gets it

Common in hospital, especially intensive care, and in the community with diarrhoea and dehydration. In tropical Latin America, leptospirosis, malaria, dengue, snakebite and severe dehydration are important causes. In Peru, age-standardised incidence rose from 10.5 to 12.1 per 100,000 and mortality fell from 2.7 to 2.4 per 100,000 (2005–2010 vs 2011–2016).

Causes

Prerenal: low kidney perfusion from dehydration, bleeding, sepsis, heart failure or cirrhosis
Prerenal: drugs that lower glomerular perfusion, such as NSAIDs, ACE inhibitors, angiotensin receptor blockers and diuretics
Intrinsic: acute tubular necrosis from prolonged ischaemia or toxins (iodinated contrast, aminoglycosides, rhabdomyolysis)
Intrinsic: acute interstitial nephritis (drugs, infection), glomerulonephritis and vascular causes
Postrenal: obstruction to urine flow (prostatic enlargement, stone in a single kidney, pelvic tumours, blocked catheter)

Risk factors

Older age
Chronic kidney disease
Diabetes, heart failure and liver disease
Sepsis and major surgery, especially cardiac surgery
Nephrotoxic drugs and iodinated contrast
Volume depletion

Pathophysiology

In prerenal injury the kidney is intact but underperfused, and function recovers quickly when flow returns. Prolonged ischaemia or toxins damage tubular cells (acute tubular necrosis): they slough, block the tubules and let filtrate leak back. In postrenal injury back-pressure from obstruction lowers filtration; both kidneys, or a single working kidney, must be affected.

Classification

KDIGO stage 1: creatinine 1.5–1.9 times baseline or a rise of ≥0.3 mg/dL within 48 h, or urine output <0.5 mL/kg/h for 6–12 h
KDIGO stage 2: creatinine 2.0–2.9 times baseline, or urine output <0.5 mL/kg/h for ≥12 h
KDIGO stage 3: creatinine ≥3 times baseline or ≥4.0 mg/dL, start of dialysis, or urine output <0.3 mL/kg/h for ≥24 h or anuria for ≥12 h
By cause: prerenal, intrinsic (renal) and postrenal

Symptoms and signs

Often none: found on blood tests
Low urine output (oliguria) or none (anuria); output can also be normal
Fluid overload: oedema and breathlessness
Nausea, vomiting, confusion and drowsiness from uraemia
Features of the cause: thirst and low blood pressure, rash and fever, suprapubic pain from a full bladder

Diagnosis

Clinical: Assessment of volume status, the drug list (nephrotoxins, renin–angiotensin blockers, NSAIDs), recent contrast and sepsis, and examination for a full bladder. The aim is to sort the cause into prerenal, intrinsic or postrenal.
Tests: Serial creatinine and urine output define and stage AKI (KDIGO). Electrolytes, bicarbonate, urea; urinalysis and microscopy (muddy brown casts in tubular necrosis, red cell casts in glomerulonephritis). A low fractional excretion of sodium points to a prerenal cause. ECG if potassium is high.
Imaging: Kidney and bladder ultrasound early when obstruction is possible: it shows hydronephrosis, bladder volume and kidney size (small kidneys suggest underlying chronic disease).

Differential diagnosis

Chronic kidney disease (previous creatinine values, small kidneys)
Acute-on-chronic kidney disease
Hepatorenal syndrome in cirrhosis
Rhabdomyolysis
Rapidly progressive glomerulonephritis
A rise in creatinine without true loss of function (some drugs)

Goal of treatment

Treat the cause, restore perfusion or relieve obstruction, avoid further kidney harm, control fluid, potassium and acid, and start dialysis when complications cannot be controlled otherwise.

Treatment

Acute: Prerenal causes: fluid resuscitation with crystalloids when the patient is volume depleted, treatment of sepsis and shock, and blood pressure support.
Medical: Stopping or holding nephrotoxic drugs and those that lower glomerular perfusion (NSAIDs, ACE inhibitors, angiotensin receptor blockers, diuretics); doses of renally cleared drugs are adjusted.
Procedure: Postrenal causes: relief of the obstruction with a bladder catheter, ureteral stent or nephrostomy.
Acute: Hyperkalaemia emergency: cardiac membrane stabilisation with intravenous calcium, shifting potassium into cells with insulin and glucose or beta-agonists, then removing it (binders, diuretics or dialysis).
Medical: Loop diuretics for fluid overload in patients who respond; they do not speed kidney recovery.
Procedure: Kidney replacement therapy (intermittent haemodialysis or continuous therapy in intensive care) for refractory acidosis, hyperkalaemia or fluid overload, some poisonings and uraemic complications.
Follow-up: Daily weight, fluid balance, creatinine and electrolytes; follow-up after discharge, because AKI raises the risk of later chronic kidney disease.

Complications

Hyperkalaemia and arrhythmias
Fluid overload and pulmonary oedema
Metabolic acidosis
Uraemia: pericarditis, encephalopathy, bleeding
Drug toxicity from reduced clearance
Progression to chronic kidney disease
Higher mortality, especially in critical illness

Prognosis

Prerenal and postrenal injury usually recover when the cause is treated quickly. Severe AKI in critically ill patients carries high mortality, and survivors have a higher risk of chronic kidney disease.

Prevention

Keeping at-risk patients well hydrated and avoiding unnecessary nephrotoxins and contrast
Monitoring creatinine when starting drugs that affect the kidney
Early treatment of diarrhoea, sepsis and urinary obstruction

Test yourself

Think of the answer, then tap the question to see it.

What are the three broad categories of causes of acute kidney injury?

Prerenal (low perfusion), intrinsic (damage within the kidney) and postrenal (obstruction to urine flow).

Which two criteria does KDIGO use to define and stage acute kidney injury?

The rise in serum creatinine from baseline and the fall in urine output over time.

Which urine sediment finding is classic for acute tubular necrosis?

Muddy brown granular casts.

Which imaging test is done early in unexplained acute kidney injury?

Kidney and bladder ultrasound, to look for obstruction (hydronephrosis).

What are the classic indications for urgent dialysis in acute kidney injury?

Refractory acidosis, hyperkalaemia or fluid overload, some intoxications and uraemic complications such as pericarditis or encephalopathy (AEIOU).

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Educational information, not medical advice. For any symptom, see a health professional.

Sources: Acute Kidney Injury (StatPearls (NCBI Bookshelf), 2026); National trends in age-standardized incidence and mortality rates of acute kidney injury in Peru (Jornal brasileiro de nefrologia, 2020) · adapted, CC BY 4.0.

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Representative model, for educational purposes only.

Kidneys highlighted on the Durgical 3D model