Acute Kidney Injury


Acute Kidney Injury (AKI) is a rapid deterioration in renal function and is itself not a diagnosis. It can be classified by underlying cause into pre-renal, renal and post-renal AKI. Different types of AKI may cause different clinical pictures, and diagnosing the underlying cause is important in giving the best treatment.

Type Pathophysiology Causes
Pre-renal AKI (most common) Reduced perfusion of kidney Hypovolemia, sepsis, drugs causing renal hypo perfusion (e.g. ACEi), renal artery stenosis
Renal AKI (2nd most common) Inflammation/damage to kidney itself nephrotoxic drugs, radiological contrast agents, rhabdomyolysis, glomerulonephritis, vasculitis, ischaemia
Post-renal/obstructive AKI (least common) urinary tract obstruction resulting in back pressure damage stones, benign prostatic hyperplasia, urinary tract malignancy


Presentation depends on the underlying cause. There is often a co-existing illness such as sepsis or renal artery stenosis. Signs and symptoms caused by acute kidney injury itself are non-specific and may include:

- Reduced (oliguria) or no urine output (anuria)
- Constitutional symptoms: anorexia, weight loss, fatigue, lethargy
- Itch
- Nausea and vomiting
- Fluid overload: oedema, shortness of breath, pleural effusion


Specific questions should be directed at identifying the underlying cause. Ask about:


- Current serious infections/sepsis e.g. pneumonia, gastroenteritis
- Injuries/bleeding resulting in hypovolaemia
- Drugs causing renal hypoperfusion (ACEi/ARB, NSAID)
- Severe liver disease which can alter perfusion to the kidneys (hepatorenal syndrome)


- Full drug history looking for nephrotoxic drugs (antibiotics such as gentamicin)
- Recent radiological tests with contrast
- Past medical history of vasculitis, glomerulonephritis, immobility or muscle injury (rhabdomyolysis)


- History of renal calculi/stones
- Does the patient have two functioning kidneys? Previous donation or transplant
- Malignancy

Vital Signs/Observations

Heart rate - increased if dehydration
Blood pressure - low if dehydration (pre-renal) or high if fluid overloaded (renal or post-renal)
Respiratory rate - may be normal or raised
Oxygen saturations - usually normal


The most important aim of examination is to assess hydration status:

- General: skin turgor
- Cardiovascular examination - BP, HR, JVP, capillary refill time
- Respiratory examination - listen to breath sounds for crepitations that could indicate pulmonary oedema
- Abdomen - palpate the kidneys (in case there is a rare cause such as polycystic kidney disease), listen for bruits over the renal arteries (renovascular disease)

Bedside Tests

- Urinalysis (high protein or RBCs could suggest active glomerulonephritis)
- Insert a catheter and attach to a urometer to monitor hourly urine output (see below)

Laboratory Investigations

Urea & Electrolytes allows diagnosis of AKI and monitoring for hyperkalaemia (an emergency)

AKI is diagnosed if any of the following 3 criteria are fulfilled:
- An increase in serum creatinine of >26.4 micromol/l
- An increase in serum creatinine of 50% e.g. baseline creatinine of 80 increased to 120
- Reduction in urine output <0.5 ml/kg/hr for at least 6 consecutive hours

Hyperkalaemia (potassium >5 mmol/l) is a life-threatening complication of AKI, as when the kidneys are not filtering blood and producing urine normally, potassium can build up in the blood leading to cardiac arrhythmias

Other blood tests: FBC and coagulation screen (bleeding, sepsis, anaemia could suggest CKD or myeloma), arterial blood gas (metabolic acidosis)

More specialized blood tests if common cause not found: serology for ANA (SLE), ANCA (vasculitis) or anti-GBM (Goodpasture's disease) antibodies; protein electrophoresis and Bence-Jones protein (multiple myeloma)

Radiological Investigations

Renal ultrasound - if obstruction is likely or abnormal kidney size suspected on examination
Ultrasound-guided renal biopsy - further down the line if the cause of renal AKI has not been found



Pre-renal and post-renal problems are the most easily reversible, so immediate management centres on identifying and treating these:

1) Get IV access, take bloods as above (especially U+E - check potassium), urinalysis

2) If there are signs of fluid depletion (high HR, low BP with no peripheral or pulmonary oedema) give fluid challenge with 250 or 500ml 0.9% saline (crystalloid) bolus.

3) Reassess hydration status and repeat if there is still a deficit. If 1 litre has been given with no improvement or you are concerned the patient is deteriorating get senior/specialist help immediately

4) Stop nephrotoxic drugs (gentamicin, vancomycin, amphotericin, NSAIDs, ACEi/ARB)

5) Treat reversible causes e.g. give IV antibiotics for sepsis

6) Other investigations: urgent renal ultrasound

Further Management

- If a renal cause is suspected then diagnostic renal biopsy may be required
- If there is a poor response to initial treatment and there is persistent or severe pulmonary oedema, hyperkalaemia, metabolic acidosis haemodialysis may be required

Prior to discharge

- Medication review may be required to alter medications that may have precipitated AKI

Follow up

- Some causes such as sepsis may not require further treatment after resolution, but others such as glomerulonephritis may require long-term immunosuppression and clinic follow-up

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