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1: AKI Flashcards

1
Q

What is the KIGO definition of AKI

A
  1. Increase in serum creatinine of >26 in 48h
  2. Or, increase in serum creatinine 1.5-times baseline in 7-days
  3. Urine output <0.5ml/Kg/h for 6 hours
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2
Q

How is AKI categorised

A

Stage 1, Stage 2, Stage 3

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3
Q

What is creatinine in stage I AKI

A

Increase 1.5 - 2 times baseline

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4
Q

What is urine output in stage 1 one AKI

A

<0.5ml/Kg/h for 6-12h

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5
Q

What is serum creatinine in stage 2 AKI

A

Increase 2-2.9 times baseline

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6
Q

What is urine output in stage 2 AKI

A

<0.5ml/Kg/h for more-than 12h

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7
Q

What is creatinine in stage 3 AKI

A

3-times baseline

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8
Q

What is urine output in stage 3 AKI

A

<0.3ml/Kg/h for >24h

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9
Q

How can aetiology of AKI be divided

A

Pre-renal
Renal
Post-renal

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10
Q

What are 5 causes of pre-renal AKI

A

Hypovolaemia due to: sepsis, haemorrhage, D+V, pancreatitis, burns, NSAIDs, ACEi, Renal-artery stenosis, Hepatorenal syndrome

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11
Q

What are 5 causes of intrinsic renal AKI

A 
ATN
Interstitial nephritis 
Glomerulonephritis 
Infiltration (sarcoid) 
MAHA: TTP, DIC, HUS
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12
Q

What causes post-renal AKI

A

Obstruction due to: stricture, malignancy, BPH

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13
Q

What are risk factors for AKI

A
  • Age
  • Male
  • DM
  • CKD
  • Malignancy
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14
Q

How can AKI be divided clinically

A

Into 4 phases of presentation

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15
Q

What is phase I of AKI

A

(Hours-Days):

- Underlying symptoms of AKI

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16
Q

What is phase 2 AKI

A

(Weeks): Anuric/Oliguric phase

  • Reduce urine output
  • Increase urea and creatinine
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17
Q

How long does AKI last

A

Less than 2-weeks

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18
Q

What happens in phase 2 AKI

A

Decrease urine output

Increase urea and creatinine

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19
Q

What are 4 complications of phase 2 AKI

A
  • Hyperkalaemia
  • Acidosis
  • Uraemia
  • Fluid retention
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20
Q

What is phase 3 AKI

A

Polyuric phase (3-Weeks)

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21
Q

What can phase 3 AKI lead to

A

The kidney can produce more urine meaning urine output increases. However, reabsorption in tubules is still impaired causing electrolyte deficiencies

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22
Q

What is phase 4 AKI

A

Recovery: kidney function and urine production normalise

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23
Q

What can uraemia cause

A

Pericarditis

Encephalitis

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24
Q

Explain reabsorption of urea and creatinine in the kidney

A

Urea is reabsorbed in the kidney. However, very little creatinine is reabsorbed

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25
What is the normal ratio of blood urea nitrogen (BUN) to creatinine
5-20:1
26
What causes pre-renal AKI
Decrease renal perfusion
27
Give 3 broad aetiological categories for AKI
1. Actual decrease blood volume (haemorrhage) 2. Relative decrease blood volume = distributive shock 3. Renal artery disease - renal artery stenosis
28
Explain pathophysiology of pre-renal AKI
- Reduced blood flow through glomerulus decreasing GFR - Reduction in GFR activates the RAAS system - RAAS increases sodium and hence water reabsorption - With water comes urea - causing BUN: Cr >20:1 - Increased sodium reabsorption decreases urinary sodium concentration causing <20 - Increase water reabsorption increases urine concentration - increasing urinary osmolality
29
What is BUN:Creatinine ratio in pre-renal AKI and why
20: 1 | - Due to urea being reabsorbed with water
30
What is urinary sodium in pre-renal AKI and why
<20 - due to increase reabsorption stimulated by RAAS
31
What is urine osmolality in pre-renal AKI and why
>200 - increase water reabsorption stimulated by RAAS
32
What causes intra-renal AKI
Damage to: - Tubules (ATN) - Glomerulus (Glomerulonephritis) - Interstitial (Acute interstitial nephritis)
33
What is the most common cause of tubule damage
Acute Tubular Necrosis
34
What usually causes acute tubular necrosis (ATN)
Most commonly occurs due to ischaemia - often following pre-renal AKI
35
What are other causes of ATN
- Toxins: ethylene glycol, aminoglycosides, contrast - Uric acid (eg. TLS) - Myoglobin (Rhabdomyolysis)
36
Explain what ATN leads to
ATN causes ischaemia and hence death of cells which appear as muddy brown casts in the urine. Death of cells leads to increase pressure in the tubules. This reduces the pressure gradient with the glomerulus - decreasing GFR causing oliguria
37
What is characteristic of ATN
Muddy brown casts
38
Explain urea and creatinine in in ATN
Due to decrease filtration - urea and creatinine are increased
39
What is a cause of glomerular AKI
Glomerular nephritis
40
Explain pathophysiology of glomerular damage causing AKI
- Formation antibody-antigen complexes - Activate complement - Complement damages podocytes - This leads to large molecules (RBC) to filter through - Damage reduces filtration capabilities - hence decreasing GFR - Decrease in GFR leads to oliguria, oedema and HTN
41
What causes interstitial AKI
Acute interstitial nephritis
42
What causes interstitial nephritis
Usually medications cause infiltration of immune cells that result in inflammation
43
What 3 medications cause interstitial nephritis
- NSAID - Diuretics - Penicillin
44
What medication causes acute tubular necrosis
Aminoglycosides
45
In acute interstitial nephritis, if the medication is not stopped what can it lead to
Renal papillary necrosis. | Presents as haematuria and flank pain
46
Explain BUN:Cr in intra-renal AKI and why
BUN: Cr <15:1 Damage to kidney cells impairs reabsorption of urea leading to a low BUN: Cr ration.
47
Explain urinary sodium in intra-renal AKI and why
Urinary sodium is high (>40) as impaired re-absorption at the kidneys
48
Explain urine osmolality in intra-renal AKI and why
Urine osmolality is low - as water is not reabsorbed
49
What may cause post-renal AKI
Obstruction ureter: stone, malignancy
50
Explain when post-renal AKI occurs
If one ureter is obstructed, kidney function is usually preserved. If both are obstructed it leads to AKI
51
Explain pathophysiology of post-renal AKI
Obstruction causes increase in pressure in the kidney. This reduces pressure gradient and hence GFR, leading to oliguria. Reduced filtration of urea and creatinine results in higher circulating concentration. Increase urea to creatinine causes BUN 15:1. Urine sodium <20 and urine osmolality >500
52
What happens over-time in post-renal AKI
Pressure causes destruction renal epithelial cells - reduces reabsorption BUN and urine sodium
53
What is first-step in investigation for AKI
Determine if any life-threatening complications (eg. pulmonary oedema) and treat accordingly
54
What investigations are usually first performed in AKI
ABG (VBG) and ECG to assess for hyperkalaemia
55
When is hyperkalaemia managed
>6.5 or any ECG changes
56
How is hyperkalaemia managed
- Calcium glutinate | - Insulin and 5% Dextrose
57
How is hypovolaemia in AKI managed
500ml Saline Fluid Challenge
58
What is monitored in AKI
- Observations - VBG (for K+) - Fluid balance - Creatinine
59
What is the problem with creatinine
Lags by 24h
60
How is cause of AKI identified
- Urinalysis | - USS
61
When should USS be performed
If suspect pyelonephritis - perform in 6 hours. If suspect obstruction or cannot find cause of AKI - perform in 24h
62
Why may FBC and coagulation studies be ordered in AKI
Look for MAHAs (HUS, TTP, DUS)
63
Why may ANA, anti-GBM be ordered in AKI
Look for intrinsic renal causes
64
Describe management of AKI
- Treat cause - Ensure fluid - Stop nephrotoxic medications
65
What is a mnemonic of medications to stop in AKI as they worsen renal function
NADA NSAIDS ACEi Diuretics ARB
66
What 3 medications are stopped in AKI - as it can lead to toxicity of the medication
Metformin Lithium Digoxin
67
What are 5 criteria to refer AKI to nephrologist
- Stage 3 - Fluid Overload - Difficult fluid balance (low albumin, pregnant) - Caused by intrinsic renal disease - HTN
68
Give 4 complications of AKI
- High Uric Acid - Metabolic acidosis - Hyperkalaemia - Pulmonary oedema
69
How may uraemia present
Pericarditis | Encephalitis

Renal (15 decks)

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