One of the major causes of AKI is ischaemia, or lack of blood flowing to the kidneys.
- Hypovolaemia secondary to diarrhoea/vomiting
- Renal artery stenosis
The second group of causes relate to intrinsic damage to the glomeruli, renal tubules or interstitium of the kidneys themselves. This may be due to toxins (drugs, contrast etc) or immune-mediated glomuleronephritis.
- Acute tubular necrosis (ATN)
- Acute interstitial nephritis (AIN), respectively
- Tumour lysis syndrome
The third group relates to problems after the kidneys. This is where there is an obstruction to the urine coming from the kidneys resulting in things 'backing-up' and affecting the normal renal function. An example could be a unilateral ureteric stone or bilateral hydroneprosis secondary to acute urinary retention caused by benign prostatic hyperplasia.
- Kidney stone in ureter or bladder
- Benign prostatic hyperplasia
- External compression of the ureter
Who is at an increased risk of AKI?
One of the keys to reducing the incidence of AKI is identifying patient who are at increased risk. NICE support this approach and have published guidelines suggesting which patients are at greater risk.
Risk factors for AKI include:
- Chronic kidney disease
- Other organ failure/chronic disease e.g. heart failure, liver disease, diabetes mellitus
- History of acute kidney injury
- Use of drugs with nephrotoxic potential (e.g. NSAIDs, aminoglycosides, ACE inhibitors, angiotensin II receptor antagonists [ARBs] and diuretics) within the past week
- Use of iodinated contrast agents within the past week
- Age 65 years or over
- Neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer
- Final pathway is tubular cell death.
- Renal medulla is a relatively hypoxic environment making it susceptible to renal tubular hypoxia.
- Renovascular autoregulation maintains renal blood flow across a range of arterial pressures.
- Estimates of GFR are the best indices of renal function. Useful clinical estimates can be obtained by considering serum creatinine, age, race, gender and body size. eGFR calculations such as the Cockcroft and Gault equation are less reliable in populations with high GFRs.
- Nephrotoxic stimuli such as aminoglycosides and radiological contrast media induce apoptosis. Myoglobinuria and haemolysis result in necrosis. Overlap exists and proinflammatory cytokines play and important role in potentiating ongoing damage.
- Post-operative renal failure is more likely to occur in patients who are elderly, have peripheral vascular disease, high BMI, have COPD, receive vasopressors, are on nephrotoxic medication or undergo emergency surgery.
- Avoiding hypotension will reduce the risk of renal tubular damage.
- There is no evidence that administration of ACE inhibitors or dopamine reduces the incidence of post-operative renal failure.
- Reduced urine output (100%)
- Impaired renal function (100%)
- Hyperkalaemia (100%)
- urine dipstick
- urinary tract infection: leucocytes +/- nitrites
- glomerulonephritis: haematuria + leucocytes
- acute interstitial nephritis: leucocytes by themselves
- microscopy, culture and sensitivity
- if any evidence of UTI on the urine dipstick
- protein:creatinine ratio if glomerulonephritis is suspected
- urea and electrolytes
- important to detect hyperkalaemia as this may require urgent treatment
- as a minimum a FBC, CRP and bone profile should also be performed
- if the cause is not known further blood tests should be considered including:
- creatinine kinase
- complement levels
- immunoglobulin levels
- antistreptolysin O titre
- an ultrasound scan should be performed in new cases of AKI
- if obstructive uropathy or pyelonephritis is suspected this should be performed urgently
- UK guidelines suggest this should be performed within 24 hours if obstruction is suspected or there is no identifiable cause.
Prerenal uraemia - kidneys hold on to sodium to preserve volume
|Pre-renal uraemia||Acute tubular necrosis|
|Urine sodium||< 20 mmol/L||> 30 mmol/L|
|Fractional sodium excretion*||< 1%||> 1%|
|Fractional urea excretion**||< 35%||>35%|
|Urine:plasma osmolality||> 1.5||< 1.1|
|Urine:plasma urea||> 10:1||< 8:1|
|Specific gravity||> 1020||< 1010|
|Urine||'bland' sediment||brown granular casts|
|Response to fluid challenge||Yes||No|
*fractional sodium excretion = (urine sodium/plasma sodium) / (urine creatinine/plasma creatinine) x 100
**fractional urea excretion = (urine urea /blood urea ) / (urine creatinine/plasma creatinine) x 100
Detect acute kidney injury, in line with the (p)RIFLE, AKIN or KDIGO definitions, by using any of the following criteria:
- A rise in serum creatinine of 26 micromol/litre or greater within 48 hours
- A 50% or greater rise in serum creatinine known or presumed to have occurred within the past 7 days
- A fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours in adults and more than
Once diagnosed, AKI can be staged using the KDIGO classification:
|Stage||Serum creatinine||Urine output|
|1||1.5-1.9 * baseline creatine or|
> 26 umol/L within 24 hours
|< 0.5 mL/kg/hour for 6 hours|
|2||2.0-2.9 * baseline creatine||< 0.5 mL/kg/hour for 12 hours|
|3||> 3.0 * baseline creatine or|
> 353.6 umol/L or
initiation of renal replacement therapy or
decrease of eGFR to < 35 mL/min
|< 0.3 mL/kg/hour for 24 hours or|
anuria for 12 hours
|Usually safe to continue in AKI||Should be stopped in AKI as may worsen renal function||May have to be stopped in AKI as increased risk of toxicity (but doesn't usually worsen AKI itself)|
• Aspirin (at a cardioprotective dose of 75mg od)
• ACE inhibitors
• Angiotensin II receptor antagonists
Treatments which are not recommend include the routine use of loop diuretics (to artificially boost urine output) and low-dose dopamine (in an attempt to increase renal perfusion). There is however a role for loop diuretics in patients who experience significant fluid overload.
Specialist input from a nephrologist is required for cases where the cause is not known or where the AKI is severe.
All patients with suspected AKI secondary to urinary obstruction require prompt review by a urologist.
Renal replacement therapy (e.g. haemodialysis) is used when a patient is not responding to medical treatment of complications, for example hyperkalaemia, acidosis or uraemia.