Acute kidney injury: a very basic introduction Flashcards
Acute kidney injury?
- Acute kidney injury (AKI), previously termed acute renal failure, describes a reduction in renal function following an insult to the kidneys.
- 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
Specimen from a patient who had an acute kidney injury. Note the marked pallor of the cortex in certain areas, contrasting to the darker areas of surviving medullary tissue.
What causes AKI? Prerenal
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 (ischaemia) to the myocardium causes a myocardial infarction.
- In a similar fashion 85% of strokes are causes be 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
This patient had an invasive papillary tumour of the distal left ureter, indicated by the arrow. This resulted in the ureter becoming blocked, resulting in a left hydroureter and hydronephrosis. Note the thinning of the renal cortex of the left kidney compared to the right.
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?
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
What happens when kidneys stop working?
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
Other Investigations?
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?
- 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.
Drugs usually safe to continue in AKI?
- Paracetamol
- Warfarin
- Statins
- Aspirin (at a cardioprotective dose of 75mg od)
- Clopidogrel
- Beta-blockers
