1: AKI Flashcards
What is the KIGO definition of AKI
- Increase in serum creatinine of >26 in 48h
- Or, increase in serum creatinine 1.5-times baseline in 7-days
- Urine output <0.5ml/Kg/h for 6 hours
How is AKI categorised
Stage 1, Stage 2, Stage 3
What is creatinine in stage I AKI
Increase 1.5 - 2 times baseline
What is urine output in stage 1 one AKI
<0.5ml/Kg/h for 6-12h
What is serum creatinine in stage 2 AKI
Increase 2-2.9 times baseline
What is urine output in stage 2 AKI
<0.5ml/Kg/h for more-than 12h
What is creatinine in stage 3 AKI
3-times baseline
What is urine output in stage 3 AKI
<0.3ml/Kg/h for >24h
How can aetiology of AKI be divided
Pre-renal
Renal
Post-renal
What are 5 causes of pre-renal AKI
Hypovolaemia due to: sepsis, haemorrhage, D+V, pancreatitis, burns, NSAIDs, ACEi, Renal-artery stenosis, Hepatorenal syndrome
What are 5 causes of intrinsic renal AKI
ATN Interstitial nephritis Glomerulonephritis Infiltration (sarcoid) MAHA: TTP, DIC, HUS
What causes post-renal AKI
Obstruction due to: stricture, malignancy, BPH
What are risk factors for AKI
- Age
- Male
- DM
- CKD
- Malignancy
How can AKI be divided clinically
Into 4 phases of presentation
What is phase I of AKI
(Hours-Days):
- Underlying symptoms of AKI
What is phase 2 AKI
(Weeks): Anuric/Oliguric phase
- Reduce urine output
- Increase urea and creatinine
How long does AKI last
Less than 2-weeks
What happens in phase 2 AKI
Decrease urine output
Increase urea and creatinine
What are 4 complications of phase 2 AKI
- Hyperkalaemia
- Acidosis
- Uraemia
- Fluid retention
What is phase 3 AKI
Polyuric phase (3-Weeks)
What can phase 3 AKI lead to
The kidney can produce more urine meaning urine output increases. However, reabsorption in tubules is still impaired causing electrolyte deficiencies
What is phase 4 AKI
Recovery: kidney function and urine production normalise
What can uraemia cause
Pericarditis
Encephalitis
Explain reabsorption of urea and creatinine in the kidney
Urea is reabsorbed in the kidney. However, very little creatinine is reabsorbed
What is the normal ratio of blood urea nitrogen (BUN) to creatinine
5-20:1
What causes pre-renal AKI
Decrease renal perfusion
Give 3 broad aetiological categories for AKI
- Actual decrease blood volume (haemorrhage)
- Relative decrease blood volume = distributive shock
- Renal artery disease - renal artery stenosis
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
What is BUN:Creatinine ratio in pre-renal AKI and why
20: 1
- Due to urea being reabsorbed with water
What is urinary sodium in pre-renal AKI and why
<20 - due to increase reabsorption stimulated by RAAS
What is urine osmolality in pre-renal AKI and why
> 200 - increase water reabsorption stimulated by RAAS
What causes intra-renal AKI
Damage to:
- Tubules (ATN)
- Glomerulus (Glomerulonephritis)
- Interstitial (Acute interstitial nephritis)
What is the most common cause of tubule damage
Acute Tubular Necrosis
What usually causes acute tubular necrosis (ATN)
Most commonly occurs due to ischaemia - often following pre-renal AKI
What are other causes of ATN
- Toxins: ethylene glycol, aminoglycosides, contrast
- Uric acid (eg. TLS)
- Myoglobin (Rhabdomyolysis)
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
What is characteristic of ATN
Muddy brown casts
Explain urea and creatinine in in ATN
Due to decrease filtration - urea and creatinine are increased
What is a cause of glomerular AKI
Glomerular nephritis
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
What causes interstitial AKI
Acute interstitial nephritis
What causes interstitial nephritis
Usually medications cause infiltration of immune cells that result in inflammation
What 3 medications cause interstitial nephritis
- NSAID
- Diuretics
- Penicillin
What medication causes acute tubular necrosis
Aminoglycosides
In acute interstitial nephritis, if the medication is not stopped what can it lead to
Renal papillary necrosis.
Presents as haematuria and flank pain
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.
Explain urinary sodium in intra-renal AKI and why
Urinary sodium is high (>40) as impaired re-absorption at the kidneys
Explain urine osmolality in intra-renal AKI and why
Urine osmolality is low - as water is not reabsorbed
What may cause post-renal AKI
Obstruction ureter: stone, malignancy
Explain when post-renal AKI occurs
If one ureter is obstructed, kidney function is usually preserved. If both are obstructed it leads to AKI
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
What happens over-time in post-renal AKI
Pressure causes destruction renal epithelial cells - reduces reabsorption BUN and urine sodium
What is first-step in investigation for AKI
Determine if any life-threatening complications (eg. pulmonary oedema) and treat accordingly
What investigations are usually first performed in AKI
ABG (VBG) and ECG to assess for hyperkalaemia
When is hyperkalaemia managed
> 6.5 or any ECG changes
How is hyperkalaemia managed
- Calcium glutinate
- Insulin and 5% Dextrose
How is hypovolaemia in AKI managed
500ml Saline Fluid Challenge
What is monitored in AKI
- Observations
- VBG (for K+)
- Fluid balance
- Creatinine
What is the problem with creatinine
Lags by 24h
How is cause of AKI identified
- Urinalysis
- USS
When should USS be performed
If suspect pyelonephritis - perform in 6 hours.
If suspect obstruction or cannot find cause of AKI - perform in 24h
Why may FBC and coagulation studies be ordered in AKI
Look for MAHAs (HUS, TTP, DUS)
Why may ANA, anti-GBM be ordered in AKI
Look for intrinsic renal causes
Describe management of AKI
- Treat cause
- Ensure fluid
- Stop nephrotoxic medications
What is a mnemonic of medications to stop in AKI as they worsen renal function
NADA
NSAIDS
ACEi
Diuretics
ARB
What 3 medications are stopped in AKI - as it can lead to toxicity of the medication
Metformin
Lithium
Digoxin
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
Give 4 complications of AKI
- High Uric Acid
- Metabolic acidosis
- Hyperkalaemia
- Pulmonary oedema
How may uraemia present
Pericarditis
Encephalitis
