Acute Kidney Injury (AKI) Flashcards
What is the definition of acute kidney injury (AKI) based on?
- rises in creatinine
2. decreases in urine output
What is the new definition of AKI?
Need to recognise a spectrum of injury to promote earlier detection
Epidemiology and outcomes can be characterised
What 2 categories are used to characterise the stage of AKI?
- serum creatinine criteria (SCr)
2. Urine output criteria
How is stage 1 AKI characterised?
SCr increase > 26 micromol/L within 48 hours
or SCr increase 1.5 - 1.9 fold from baseline
And urine output < 0.5 ml/kg/hr for 6 consecutive hours
How is stage 2 AKI characterised?
SCr increase 2 - 2.9 fold from baseline
Urine output < 0.5 ml/kg/hr for 12 hours
How is stage 3 AKI characterised for serum creatinine criteria?
SCr increase >/= 3 fold from baseline
OR
SCr increase >/= 354 micromol/L
OR
initiated on RRT (irrespective of stage at time of initiation)
How is stage 3 AKI characterised for urine output criteria?
<0.3 mL/kg/hr for 24 hours
OR
annula for 12 hours
What are the 3 types of acute kidney injury?
- pre-renal AKI
- post-renal AKI
- intrinsic AKI
What happens in pre-renal AKI?
This is functional
There is a drop in the blood flow to the kidneys
There is no cellular damage, but kidneys cannot remove creatinine leading to accumulation
What are the most common causes of pre-renal AKI?
- sepsis
- toxins
- hypotension
What happens if the pre-renal AKI cannot be treated effectively?
It leads to cellular injury and development of intrinsic AKI
What happens in intrinsic AKI?
The cells are damaged through necrosis
They release intracellular contents, which damage adjacent cells
What are the most common causes of intrinsic AKI?
- prolonged pre-renal AKI
2. nephrotoxins
What are the most common causes of post-renal AKI?
- kidney stones
- tumours
- retroperitoneal fibrosis
- prostatic hypertrophy
What is post-renal AKI?
This is AKI caused by a blockage
What is the most common type of AKI?
Low blood pressure in the kidneys
This is Ischaemia reperfusion
What happens in ischaemia reperfusion?
The blood pressure drops for a period which stresses the kidneys
The blood flow to the kidneys is then reduced
What % of glomeruli are found in the renal cortex?
Why do the kidneys want to preserve the glomeruli?
80%
They do not regenerate after injury
What is blood supply usually like to the outer medulla?
The blood supply and oxygen tension is relatively low
What happens to blood supply in the kidneys when blood pressure drops?
Blood is diverted to the cortex to preserve the glomeruli
This leads to injury of the outer medulla
(but this can recover after injury)
What happens to the cells in the tubules in the outer medulla when pre-renal AKI is not treated?
How do cells repair themselves if the blood supply is returned to the kidney?
- ischaemia/reperfusion leads to loss of polarity and loss of brush border
- apoptosis
- sloughing of viable and dead cells with luminal obstruction
- migration and dedifferentiation of viable cells
- proliferation of viable tubular cells
- differentiation and reestablishment of polarity
What happens if there is sustained loss of capillaries, meaning complete repair of the tubule is not possible?
This means the blood supply to the kidneys is not recovered
This leads to hypoxia, fibrosis and chronic kidney disease
What happens if an immune response means that complete repair of the tubule is not possible?
The macrophages are inappropriately activated and lay down fibrotic tissue
What are the 3 main clinical presentations of someone with AKI?
- acutely ill/post major surgery
- poor fluid intake
- excessive fluid losses
Why may someone present as being acutely ill or post-surgery?
- hypovolaemia/hypotension
2. sepsis
Why may someone have a poor fluid intake?
- decreased urine output
2. nausea, vomiting
Why may someone have excessive fluid losses?
- fever
- diuretics
- diarrhoea
- high stoma output
- haemorrhage
- burns
What are the 3 main complications of AKI?
- hyperkalaemia (leads to cardiac arrest)
- acidaemia (leads to vascular instability)
- pulmonary oedema (leads to respiratory arrest)
What usually causes pulmonary oedema in AKI patients?
Too much fluid being given to a patient
What are 3 further complications of AKI?
- uraemia
- gastrointestinal complications such as nausea/vomiting, gastritis and malnutrition
- haematological complications such as anaemia and bleeding
What is uraemia and what is it associated with?
It is the accumulation of urea
It is associated with pericarditis and encephalopathy
What investigations are performed for AKI?
- full blood count
- U and E and bicarbonate
- C-reactive protein
- liver function tests
- calcium and phosphate
- immunological screening (for rarer forms)
- creatine kinase
- urinalysis
What is creatinine kinase?
it is an enzyme released by muscle in times of muscle breakdown
Increase in creatine kinase occurs in times of trauma
What may an increased creatine kinase suggest?
Rhabdomyolysis
How does the good functional reserve of the kidney affect serum creatinine?
The kidneys must lose 50% of their function before serum creatinine rises above the upper limit of normal
What is the STOP AKI warning?
Sepsis (treat)
Toxins (avoid)
Optimise BP/volume status
Prevent harm
What is involved in preventing harm in an AKI patient?
- identify cause
- treat complications
- review medication doses
- review fluid prescription
