Acute kidney injury Flashcards

1
Q

Define acute kidney injury (used to be called acute renal failure)

A

Acute decline in renal function (decreased GFR), leading to a rise in serum creatinine (≥26.5 micromol/L) and/or a fall in urine output

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2
Q

Acute kidney injury can be staged into 3 stages (AKI 1/2/3)

How much has the serum creatinine rised by compared to baseline in each stage

A

AKI 1 - 1.5-2.99 times (rise of 50–99% from baseline within 7 days)

AKI 2 - 2-2.99 times (100–199% creatinine rise from baseline within 7 days)

AKI 3 - >3 times (200% or more creatinine rise from baseline within 7 days) - NEED RRT

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3
Q

Immediate dangerous consequences of AKI (hint: AEIOU)

A
Acidosis
Electrolyte imbalance
Intoxication - from toxins
Overload - from fluid
Uraemia complications
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4
Q

3 types of AKI

A

Pre-renal
Intra-renal
Post-renal

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5
Q

Pre-renal AKI refers to damage due to

A

Kidney hypoperfusion –> decreased GFR –> accumulation of toxins in blood

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6
Q

Blood urea nitrogen to creatinine ratio

A

5-20 : 1 (much more urea than creatinine in blood because a lot of urea reabsorbed whereas most creatinine excreted)

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7
Q

Causes of pre-renal AKI (4)

A

Absolute fluid loss

  • dehydration
  • haemorrhage
  • vomiting/diarhhoea

Relative fluid loss

  • hypotension/septic shock
  • congestive cardiac failure

Renal artery stenosis/embolus

Liver failure

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8
Q

Renal (intrinsic) AKI refers to damage …

A

within the renal parenchyma

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9
Q

Post-renal AKI refers to damage …

A

due to obstruction of urine outflow tract (i.e. ureter)

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10
Q

All types of AKI exhibit decreased GFR which stimulates what system

A

RAAS to increase Na+ and water retention and therefore urea follows which increases the blood urea nitrogen ratio to creatinine

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11
Q

Causes of renal (intrinsic) AKI (5)

A

Glomerulonephritis, e.g. crescentic (rapidly progressive) GN

Tubular injury, e.g. acute tubular necrosis (usually from ischaemia)

Nephrotoxins - e.g. drugs (NSAIDs, aminoglycosides), radiocontrast

Interstitial injury, e.g. acute interstitial nephritis (due to allergic reaction to drugs)

Multiple myeloma (blood cancer)

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12
Q

Causes of post-renal AKI (3)

A

Compression

  • of ureter, e.g. intra-abdo tumours
  • of urethra - e.g. BPH

Obstruction within lumen
-calculi within ureter, bladder or urethra

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13
Q

Most common type of AKI is

A

pre-renal, i.e. hypoperfusion of kidneys

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14
Q

If pre-renal AKI sustains, it will go on to cause what

A

renal AKI - as persistent hypoperfusion will result in ischaemia of the tubules –> acute tubular necrosis because not enough oxygen and nutrients

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15
Q

What is azotaemia

A

High nitrogen containing compounds in urine

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16
Q

Acute tubular necrosis is a cause of renal (intrinsic) AKI - what is usually the cause of this

A

Sustained hypoperfusion (in pr-renal AKI) leading to ischaemia of tubules

17
Q

Aminoglycosides (a type of antibiotic) are nephrotoxic - give an example

A

gentamicin

18
Q

Investigations of AKI (6; 1 is radiological)

A
Serum creatinine
U+Es
Urine dipstick/other urinalysis
FBC - may show anaemia
Venous blood gas - indicates metabolic acidosis from anion gap

Renal USS

19
Q

Questions to ask to confirm AKI history (4)

A

PMH of diabetes, hypertension, liver disease, congestive heart failure

Family history of congenital/systemic diseases like DM

Any nephrotoxic medication

Symptoms of uraemia

20
Q

Symptoms (7) /signs (3) of AKI (most common is pre-renal AKI)

A

Symptoms

  • oliguria
  • symptoms of azotaemia (high nitrogenous compounds in blood) - confusion, lethargy, fatigue, anorexia, nausea/vomiting
  • orthopnoea

Signs

  • tachycardia
  • hypotension (suggests pre-renal AKI)
  • dry mucous membranes, skin turgor loss
21
Q

Risk factors of AKI (6)

A
Age >65
CKD
DM
Malignant hypertension
Congestive heart failure
Nephrotoxins - aminoglycosides, NSAIDs, radiocontrast
22
Q

Principles of management of AKI (STOP ACRONYM)

A

Suspect sepsis and treat

Toxins - stop/avoid nephrotoxic drugs

Optimise BP - IV fluids if dehydrated, diuretics if overhdyrated, stop antihypertensives if on them

Prevent harm - treat complications, review U+Es daily, review medication

23
Q

Supportive management of AKI (3)

A

Fluid balance

  • IV fluids if hypovolaemic
  • restrict fluids if hypervolaemic

Optimise BP

  • IV fluids or vasopressors
  • stop antihypertensives

Stop nephrotoxic drugs - NSAIDs, aminoglycosides

24
Q

1st line treatment of renal (intrinsic) AKI

A

Treat the underlying condition with SPECIFIC THERAPY, e.g. glomerulonephritis (often steroids, other immunosuppressants), acute tubular necrosis, interstitial injury

+ supportive measures (in other flashcard)

25
1st line treatment of post-renal AKI | + then
Catheterisation - to relieve urinary retention Relief of obstruction -e.g. if stone then ureteral stent or lithotripsy
26
Dialysis is indicated in AKI if patient has... (think AEIOU complications of AKI)
severe metabolic Acidosis hyperkalaemia (Electrolyte) refractory to medication volume Overload unresponsive to diuretics - i.e. pull oedema Uraemia (severe) --> pericarditis
27
Severe electrolyte imbalance of what cation occurs in AKI
K+ --> hyperkalaemia
28
ECG changes of hyperkalaemia (3)
Tall tented T waves Broad QRS Flat p waves
29
Hyperkalaemia has a high risk of going on to cause
arrhythmias - ventricular fibrillation --> cardiac arrest
30
Acute treatment of hyperkalaemia secondary to AKI (2)
Stabilise myocardium with IV calcium gluconate Shift K+ back into cells with - insulin + glucose infusion - or salbutamol
31
Biochemical investigations of renal disorders (5)
``` U+Es - high K+, high urea Serum creatinine - increased FBC: +/- low RBCs, +/- leukocytes (infection) Urine dipstick Urine culture ```
32
1st line treatment of pre-renal AKI | + then
Volume expansion and/or blood transfusion Vasopressor if severe hypotension
33
COMMONEST CAUSE OF ACUTE KIDNEY INJURY
ACUTE TUBULAR NECROSIS (due to sustained hypoperfusion of kidneys)