AKI, CKD and renal replacement therapy Flashcards
Define AKI
A significant deterioration in renal function, which is potentially reversible, over a period of hours or days
What is the RIFLE criteria?
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
What is the AKIN criteria?
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)
How can the causes of AKI be classified?
Pre-renal failure
Intrinsic renal failure
Post-renal failure
What can cause pre-renal failure?
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]
What can cause intrinsic renal failure?
- Primary renal disease (e.g. glomerulonephritis)
- Secondary renal disease (e.g. diabetes, myeloma)
- Interstitial nephritis (usually drug-induced)
- Secondary acute tubular necrotis (caused by prolonged renal hypoperfusion)
What can cause post-renal failure?
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]
What can cause blockages in various layers of the urinary tract walls?
Lumen = stones
In wall = tumour
External = compression from other anatomical structures
What clinical features would you want to establish when taking a history from someone with AKI?
Onset Precipitating factors Urinary symptoms Chronic symptoms Systemic features (e.g. autoimmune disease) Relevant PMH/FH Drug history
What clinical features would you want to establish on examination of someone with AKI?
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)
What tests should be done when investigating renal function?
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)
What is the initial management for a patient with AKI?
Rectify life-threatening effects Generic (e.g. fluid, electrolytes) Review medication Close observation Diagnose cause and treat/ seek specialist advice
What are the life-threatening consequences of AKI?
Hyperkalaemia (causes arrhythmias and cardiac arrest)
Fluid overload (can lead to respiratory arrest)
Hypotension (can lead to cardiac arrest)
Acidosis
What ECG changes will be seen in patients with hyperkalaemia?
Peaked ("tented") T waves Prolonged P-R interval Prolonged QRS duration Loss of P waves VF/ Asystole
What is the difference between AKI and CKD?
AKIs = acute (hours or days) and reversible CKD = months/ years and irreversible