AKI, CKD and renal replacement therapy Flashcards

1
Q

Define AKI

A

A significant deterioration in renal function, which is potentially reversible, over a period of hours or days

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2
Q

What is the RIFLE criteria?

A

Classification of the severity of AKI:

Risk = 1.5x increase in Creatinine, 25% decreased GFR and less than 0.5ml/kg urine output for 6 hours
Injury = 2x increase in Creatinine, 50% decreased GFR and less than 0.5ml/kg urine output for 12 hours
Failure = 3x increase in Creatinine, 75% decreased GFR and less than 0.5ml/kg urine output for 24hrs (or anuria for 12 hours)
Loss (of kidney function) = requires RRT for >4 weeks
End (stage kidney failure) = requires RRT for >3months

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3
Q

What is the AKIN criteria?

A

Modified classification of AKI (from RIFLE) designed to increase sensitivity and specificity of AKI:

Stage 1 = Creatinine >26.4 (1.5-2x increase) and less than 0.5ml/kg urine output for 6 hours
Stage 2 = 2-3x increase in Creatinine and less than 0.5ml/kg urine output for 12 hours
Stage 3 = Serum Creatinine >354 (>3x increase) and less than 0.3ml/kg urine output for 24 hours (or anuria for 12 hours)

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4
Q

How can the causes of AKI be classified?

A

Pre-renal failure
Intrinsic renal failure
Post-renal failure

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5
Q

What can cause pre-renal failure?

A
Renal hypoperfusion (reduced blood supply/ pressure to the kidneys) 
Can be caused by systemic hypotension (e.g. hypovolaemia caused by bleeding or dehydration, sepsis) or local (e.g. renal artery stenosis or drugs e.g. ACEi or NSAIDs) 

[Approx. 85% of AKIs are pre-renal]

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6
Q

What can cause intrinsic renal failure?

A
  1. Primary renal disease (e.g. glomerulonephritis)
  2. Secondary renal disease (e.g. diabetes, myeloma)
  3. Interstitial nephritis (usually drug-induced)
  4. Secondary acute tubular necrotis (caused by prolonged renal hypoperfusion)
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7
Q

What can cause post-renal failure?

A

Obstruction or blockage of drainage from the kidneys

[Nb. important to distinguish where blockage is above anatomically e.g. above bladder - identified through ultrasound and also whether blockage is in the lumen, tubular walls or outside of the walls]

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8
Q

What can cause blockages in various layers of the urinary tract walls?

A

Lumen = stones
In wall = tumour
External = compression from other anatomical structures

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9
Q

What clinical features would you want to establish when taking a history from someone with AKI?

A
Onset
Precipitating factors 
Urinary symptoms 
Chronic symptoms
Systemic features (e.g. autoimmune disease) 
Relevant PMH/FH 
Drug history
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10
Q

What clinical features would you want to establish on examination of someone with AKI?

A

Fluid status (e.g. peripheral perfusion or oedema, JVP, pulse rate/rhythm/volume, lying and standing BP, tissue turgor)
Signs of sepsis (e.g. fever, tachycardia, tachypnoea)
Abdominal (e.g. ascites, masses, bladder)
Respiratory (pulmonary oedema/ effusion)
Cardiac (pericardial rub)
CNS (drowsiness, confusion)
Skin (e.g. rashes)

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11
Q

What tests should be done when investigating renal function?

A
Bloods (biochemistry - Cr, eGFR, Na, K, Bic, Ca, CRP; haematology - Hb; immunology) 
Urine test (dipstick, output, albumin-creatinine ratio - ACR) 
Radiological (Renal USS, CXR, CT renal angiogram)
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12
Q

What is the initial management for a patient with AKI?

A
Rectify life-threatening effects 
Generic (e.g. fluid, electrolytes) 
Review medication 
Close observation 
Diagnose cause and treat/ seek specialist advice
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13
Q

What are the life-threatening consequences of AKI?

A

Hyperkalaemia (causes arrhythmias and cardiac arrest)
Fluid overload (can lead to respiratory arrest)
Hypotension (can lead to cardiac arrest)
Acidosis

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14
Q

What ECG changes will be seen in patients with hyperkalaemia?

A
Peaked ("tented") T waves 
Prolonged P-R interval 
Prolonged QRS duration 
Loss of P waves
VF/ Asystole
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15
Q

What is the difference between AKI and CKD?

A
AKIs = acute (hours or days) and reversible 
CKD = months/ years and irreversible
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16
Q

What are the possible complications of CKD?

A
CVD 
Hypertension 
Anaemia
Bone-mineral metabolism 
Poor nutritional and functional status 
Progression of CKD 
AKI
17
Q

How is CKD measured?

A

Test for renal excretory functions (e.g. Creatinine, Cystatin C, eGR)
Test for albuminuria (proteinuria)

18
Q

What is classed as significant progression of CKD?

A

Sustained decrease in GFR of 25% or more and a change in GFR category within 12 months

OR

Sustained decrease in GFR of 15ml/min/1.73m per year

19
Q

What factors are associated with progression of CKD?

A
Hypertension (associated with level of eGFR) 
Diabetes Mellitus 
Albuminuria 
CVD 
Smoking 
Ethnicity 
NSAIDs
20
Q

What are the consequences of late presentation in patients with CKD?

A

Higher mortality, morbidity, hospital stay, costs etc.
Lack of vascular access
No possibility of pre-emptive transplantation

21
Q

What is established renal failure?

A

Stage of CKD where RRT is required to safely sustain life

22
Q

What are the options for renal replacement therapy?

A
  1. Haemodialysis
  2. Peritoneal dialysis
  3. Transplantation (from deceased or living donor) - best option
  4. Conservative care
23
Q

What is the disadvantage of haemodialysis as RRT?

A

Time consuming (requires 3 x 4hrs in hospital per week)

24
Q

What is the advantage of peritoneal dialysis as RRT?

A

Can be done at home

25
Q

What factors should be considered when discussing RRT modalities with patients with CKD?

A
Physical/ social factors (dexterity, mobility, support, employment) 
Medical factors (abdominal surgery, vascular disease, hypotension) 
Geographical factors (distance from haemodialysis unit, home environment)