Acute Kidney Injury

Disease class: Renal insufficiency

Also known as

• AKI
• Acute renal failure

 

Subtypes

• kidney tubular necrosis, Acute 

 

Causes

Causes of AKI are traditionally divided into prerenal, intrinsic and postrenal causes

Pre-renal

One of the major causes of AKI is ischaemia, or lack of blood flowing to the kidneys. 

• Hypotension
• hypovolaemia secondary to diarrhoea/vomiting
• renal artery stenosis

 

Renal

Intrinsic damage to the glomeruli, renal tubules or interstitium of the kidneys themselves. This may be due to toxins (drugs, contrast, metabolic waste, etc.) or immune-mediated glomuleronephritis.

• Glomerulonephritis
• Acute tubular necrosis (ATN)
• Acute interstitial nephritis (AIN)
• Rhabdomyolysis
• Tumour lysis syndrome 

 

Post-renal 

If urine drainage from the kidney is obstructed, urine can accumulate. This can prevent normal passage of fluid through the nephrons and impair renal function. An example could be a unilateral ureteric stone or bilateral hydroneprosis secondary to acute urinary retention caused by benign prostatic hyperplasia.

• Urolithiasis
• Benign prostatic hyperplasia
• Prostate cancer
• 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

Urinanalysis

• all patients with suspected AKI should have urinanalysis

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 • 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, acidosis or uraemia.