Acute Kidney Injury AKI Flashcards

1
Q

Definition

A

Abrupt (<48 hrs) reduction in kidney function

Can only be applied following adequate fluid resuscitation and exclusion of obstruction

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2
Q

Classification

A
  • absolute increase in serum creatinine by >26.4umol/l OR
  • reduction in urine output

Urine output decreases
Creatinine level increases

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3
Q

Who gets it

A

Common in hospitalised patents

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4
Q

Risk factors

A
Increases with age 
Diabetes 
Heart failure 
CKD
Peripheral vascular disease 
Previous AKI 
Recent contrast in imaging
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5
Q

What are the 3 main categories of causes?

A

Pre-renal
Renal
Post-renal

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6
Q

People who have AKI are at increased risk of developing CKD. True or false?

A

True

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7
Q

Drugs to avoid in patients with AKI

A
NSAIDs 
ACE inhibitor 
ARB 
Diuretics 
Gentamicin 
K+ sparing diuretics
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8
Q

PRE RENAL AKI - definition

A

Reduction in circulating volume which disrupts the kidneys

Decreased blood flow to kidneys –> decreased blood filtered –> decrease in GFR

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9
Q

PRE RENAL AKI - causes

A

Hypovolaemia

  • haemorrhage
  • volume depletion (D+V, severe burns)

Hypotension

  • shock
  • sepsis

Renal hypoperfusion
- NSAIDs
ACE inhibitors / ARBs

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10
Q

PRE RENAL AKI - clinical features

A

Decreased urine output (oliguria)

- less than 0.5ml/kg/hr

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11
Q

PRE RENAL AKI - clinical examinations

A
Blood pressure 
Heart rate 
Urine output
Cap refill
Oedema
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12
Q

PRE RENAL AKI - management

A

IV crystlloid (0.9% NaCl)
Give 250ml bolus
Reassess patient
Give up to 1000ml and if there is still no improvement, seek help

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13
Q

What can untreated pre-renal AKI result in?

A

Acute tubular necrosis

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14
Q

Acute tubular necrosis falls into which AKI category?

A

Renal AKI

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15
Q

What is the commonest form of AKI in hospital

A

Acute tubular necrosis

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16
Q

RENAL AKI - definition

A

Diseases causing inflammation or damage to the renal cells

This means the kidneys can’t filter blood effectively and reabsorption/secretion is limited

17
Q

RENAL AKI - categories

A

Blood vessels (vascular)
Glomerular disease
Interstitial injury
Tubular injury

18
Q

RENAL AKI - glomerular diseases

A

Goodpastures
Lupus nephritis
Post infectious glomerulonephritis

19
Q

RENAL AKI - interstitial injury

A

Drugs - antibiotics, PPI

Infection (TB)

20
Q

RENAL AKI - tubular injury

A

Acute tubular necrosis
- ischaemia due to pre-renal AKI where there is hypovelaemia
Contrast

21
Q

RENAL AKI - blood vessel causes

A

Vasculitis

22
Q

RENAL AKI - clinical features

A
Anorexia 
Weight loss 
Fatigue 
Nausea and vomiting 
Itch 
Oedema - fluid overload 
Pulmonary oedema 
Uraemia 
Rash (if vasculitis)
23
Q

RENAL AKI - investigations

A

U+Es
- renal function marker

FBC + coagulation screen
- abnormal clotting

Urinalysis
- haematoproteinuria

US
- size of kidneys (should be normal)

Renal biopsy

24
Q

RENAL AKI - Management

A

Fluid resuscitation
250ml bolus of 0.9% NaCl
Reassess patient and repeat until 1000ml administered
If still not achieving adequate BP then further management
- inotropes
- vasopressors
Manage underlying cause

25
Q

RENAL AKI - complications

A
Hyperkalaemia 
Fluid overload (pulmonary oedema) 
Severe acidosis
26
Q

POST-RENAL AKI - definition

A

Due to obstruction of urine flow leading to back pressure (hydronephrosis) and thus loss of concentrating ability
- i.e. the back pressure causes an increased pressure in the renal tubule so diffusion from high conc glomerulus -> low conc renal tubule no longer works and as a result, less molecules are filtered. This lowers the GFR

27
Q

POST-RENAL AKI - causes

A

Obstruction/compression

  • malignancy
  • stones
  • strictures
  • BPH
28
Q

POST-RENAL AKI - clinical features

A

Oliguria

Urine is concentrated

29
Q

POST-RENAL AKI - investigations

A

US

CT

30
Q

POST-RENAL AKI - management

A

Relieve obstruction

  • catheter
  • nephrostomy