Acute Kidney Injury (AKI) Flashcards

1
Q

What is the definition of acute kidney injury (AKI) based on?

A
  1. rises in creatinine

2. decreases in urine output

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2
Q

What is the new definition of AKI?

A

Need to recognise a spectrum of injury to promote earlier detection

Epidemiology and outcomes can be characterised

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3
Q

What 2 categories are used to characterise the stage of AKI?

A
  1. serum creatinine criteria (SCr)

2. Urine output criteria

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4
Q

How is stage 1 AKI characterised?

A

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

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5
Q

How is stage 2 AKI characterised?

A

SCr increase 2 - 2.9 fold from baseline

Urine output < 0.5 ml/kg/hr for 12 hours

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6
Q

How is stage 3 AKI characterised for serum creatinine criteria?

A

SCr increase >/= 3 fold from baseline

OR

SCr increase >/= 354 micromol/L

OR

initiated on RRT (irrespective of stage at time of initiation)

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7
Q

How is stage 3 AKI characterised for urine output criteria?

A

<0.3 mL/kg/hr for 24 hours

OR

annula for 12 hours

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8
Q

What are the 3 types of acute kidney injury?

A
  1. pre-renal AKI
  2. post-renal AKI
  3. intrinsic AKI
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9
Q

What happens in pre-renal AKI?

A

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

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10
Q

What are the most common causes of pre-renal AKI?

A
  1. sepsis
  2. toxins
  3. hypotension
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11
Q

What happens if the pre-renal AKI cannot be treated effectively?

A

It leads to cellular injury and development of intrinsic AKI

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12
Q

What happens in intrinsic AKI?

A

The cells are damaged through necrosis

They release intracellular contents, which damage adjacent cells

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13
Q

What are the most common causes of intrinsic AKI?

A
  1. prolonged pre-renal AKI

2. nephrotoxins

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14
Q

What are the most common causes of post-renal AKI?

A
  1. kidney stones
  2. tumours
  3. retroperitoneal fibrosis
  4. prostatic hypertrophy
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15
Q

What is post-renal AKI?

A

This is AKI caused by a blockage

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16
Q

What is the most common type of AKI?

A

Low blood pressure in the kidneys

This is Ischaemia reperfusion

17
Q

What happens in ischaemia reperfusion?

A

The blood pressure drops for a period which stresses the kidneys

The blood flow to the kidneys is then reduced

18
Q

What % of glomeruli are found in the renal cortex?

Why do the kidneys want to preserve the glomeruli?

A

80%

They do not regenerate after injury

19
Q

What is blood supply usually like to the outer medulla?

A

The blood supply and oxygen tension is relatively low

20
Q

What happens to blood supply in the kidneys when blood pressure drops?

A

Blood is diverted to the cortex to preserve the glomeruli

This leads to injury of the outer medulla

(but this can recover after injury)

21
Q

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?

A
  1. ischaemia/reperfusion leads to loss of polarity and loss of brush border
  2. apoptosis
  3. sloughing of viable and dead cells with luminal obstruction
  4. migration and dedifferentiation of viable cells
  5. proliferation of viable tubular cells
  6. differentiation and reestablishment of polarity
22
Q

What happens if there is sustained loss of capillaries, meaning complete repair of the tubule is not possible?

A

This means the blood supply to the kidneys is not recovered

This leads to hypoxia, fibrosis and chronic kidney disease

23
Q

What happens if an immune response means that complete repair of the tubule is not possible?

A

The macrophages are inappropriately activated and lay down fibrotic tissue

24
Q

What are the 3 main clinical presentations of someone with AKI?

A
  1. acutely ill/post major surgery
  2. poor fluid intake
  3. excessive fluid losses
25
Q

Why may someone present as being acutely ill or post-surgery?

A
  1. hypovolaemia/hypotension

2. sepsis

26
Q

Why may someone have a poor fluid intake?

A
  1. decreased urine output

2. nausea, vomiting

27
Q

Why may someone have excessive fluid losses?

A
  1. fever
  2. diuretics
  3. diarrhoea
  4. high stoma output
  5. haemorrhage
  6. burns
28
Q

What are the 3 main complications of AKI?

A
  1. hyperkalaemia (leads to cardiac arrest)
  2. acidaemia (leads to vascular instability)
  3. pulmonary oedema (leads to respiratory arrest)
29
Q

What usually causes pulmonary oedema in AKI patients?

A

Too much fluid being given to a patient

30
Q

What are 3 further complications of AKI?

A
  1. uraemia
  2. gastrointestinal complications such as nausea/vomiting, gastritis and malnutrition
  3. haematological complications such as anaemia and bleeding
31
Q

What is uraemia and what is it associated with?

A

It is the accumulation of urea

It is associated with pericarditis and encephalopathy

32
Q

What investigations are performed for AKI?

A
  1. full blood count
  2. U and E and bicarbonate
  3. C-reactive protein
  4. liver function tests
  5. calcium and phosphate
  6. immunological screening (for rarer forms)
  7. creatine kinase
  8. urinalysis
33
Q

What is creatinine kinase?

A

it is an enzyme released by muscle in times of muscle breakdown

Increase in creatine kinase occurs in times of trauma

34
Q

What may an increased creatine kinase suggest?

A

Rhabdomyolysis

35
Q

How does the good functional reserve of the kidney affect serum creatinine?

A

The kidneys must lose 50% of their function before serum creatinine rises above the upper limit of normal

36
Q

What is the STOP AKI warning?

A

Sepsis (treat)

Toxins (avoid)

Optimise BP/volume status

Prevent harm

37
Q

What is involved in preventing harm in an AKI patient?

A
  1. identify cause
  2. treat complications
  3. review medication doses
  4. review fluid prescription