Acute kidney injury: a very basic introduction
Acute kidney injury (AKI), previously termed acute renal failure, describes a reduction in renal function following an insult to the kidneys. In years gone by the kidneys were very much a neglected organ in acute medicine - the recognition of decreasing renal function was often slow and action limited. Around 15% of patients admitted to hospital develop AKI.
Whilst most patients with AKI recover their renal function there are many patients who will have long term impaired kidney function due to AKI. As well as long-term morbidity, AKI may also result in acute complications including death. Whilst exact figures are difficult to calculate NICE estimate that inpatient mortality of AKI in the UK might typically be 25-30% or more.
What causes AKI?
Causes of AKI are traditionally divided into prerenal, intrinsic and postrenal causes
Prerenal
Think of what causes big problems in other major organs. In the heart, a lack of blood flow (ischaemia) to the myocardium causes a myocardial infarction. In a similar fashion, 85% of strokes are caused by ischaemia to the brain. The same goes for the kidneys. One of the major causes of AKI is ischaemia, or lack of blood flowing to the kidneys.
Examples
hypovolaemia secondary to diarrhoea/vomiting
renal artery stenosis
Intrinsic
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.
Examples
glomerulonephritis
acute tubular necrosis (ATN)
acute interstitial nephritis (AIN), respectively
rhabdomyolysis
tumour lysis syndrome
Postrenal
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.
Examples
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
oliguria (urine output less than 0.5 ml/kg/hour)
neurological or cognitive impairment or disability, which may mean limited access to fluids because of reliance on a carer
Preventing AKI
By identifying patients at increased risk of AKI (see above) it may be possible to take steps to reduce the risk. For example, patients who are at risk of AKI and who are undergoing an investigation requiring contrast are usually given IV fluids to reduce the risk. Certain drugs such as ACE inhibitors and ARBs may also be temporarily stopped.
What happens when kidneys stop working?
It’s best to work backwards and think about what kidneys actually do. The kidneys are primarily responsible for fluid balance and maintaining homeostasis. Therefore two of the key ways AKI may be detected are:
a reduced urine output. This is termed oliguria and is defined as a urine output of less than 0.5 ml/kg/hour
fluid overload
a rise in molecules that the kidney normal excretes/maintains a careful balance of. Examples include potassium, urea and creatinine
Symptoms and signs
Many patients with early AKI may experience no symptoms. However, as renal failure progresses the following may be seen:
reduced urine output
pulmonary and peripheral oedema
arrhythmias (secondary to changes in potassium and acid-base balance)
features of uraemia (for example, pericarditis or encephalopathy)
Detection
One of the most common blood tests performed on the wards is ‘urea and electrolytes’ or ‘U&Es’. This returns a number of markers, including
sodium
potassium
urea
creatinine
NICE recommend that we can use a variety of different criteria to make an official diagnosis of AKI. They state:
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
Urinalysis
all patients with suspected AKI should have urinalysis
Imaging
if patients have no identifiable cause for the deterioration or are at risk of urinary tract obstruction they should have a renal ultrasound within 24 hours of assessment.
Management
The management of AKI is largely supportive. This means patients require careful fluid balance to ensure that the kidneys are properly perfused but not excessively to avoid fluid overload. It is also important to review a patient’s medication list to see what treatments may either be exacerbating their renal dysfunction or may be dangerous as a consequence of renal dysfunction. The table below gives some examples of common drugs:
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)
* Paracetamol
* Warfarin
* Statins
* Aspirin (at a cardioprotective dose of 75mg od)
* Clopidogrel
* Beta-blockers * NSAIDs (except if aspirin at cardiac dose e.g. 75mg od)
* Aminoglycosides
* ACE inhibitors
* Angiotensin II receptor antagonists
* Diuretics
* Metformin
* Lithium
* Digoxin
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.
Hyperkalaemia also needs prompt treatment to avoid arrhythmias which may potentially be life-threatening. The table below categorises the different treatments for hyperkalaemia:
Stabilisation of the cardiac membrane * Short-term shift in potassium from extracellular to intracellular fluid compartment * Removal of potassium from the body
* Intravenous calcium gluconate * Combined insulin/dextrose infusion
* Nebulised salbutamol
* Calcium resonium (orally or enema)
* Loop diuretics
* Dialysis
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, pulmonary oedema, acidosis or uraemia (e.g. pericarditis, encephalopathy).
