Acute Kidney Injury (AKI)

Vivian Phan
Acute kidney injury = Acute renal failure

A sudden (within 48h) deterioration in renal

function, that is potentially reversible

Absolute increase in:

- SCr 0.3 mg/dL (26.4 micromol/L) from baseline
- SCr 50%
- Oliguria < 0.5 mL/kg/h for > 6h
 RIFLE criteria (ADQI)
Creatinine GFR Urine

Risk 1.5x 25% <0.5ml/kg for 6h

Injury 2x 50% <0.5ml/kg for 12h

Failure 3x 75% <0.5ml/kg for 24h or

anuria for 12h

Loss Need for RRT for

>4 weeks

ESRD Need for RRT for

>3 months

Crit Care 2004; 8:R204.

 AKI: KDIGO Classification
Stage SCr criteria UOP criteria (duration of
oliguria)
Stage 1 increase 26 mol/L <0.5 mL/kg/hr for > 6
within 48hrs or consecutive hrs
increase 1.5 - 1.9 BL

Stage 2 increase 2 - 2.9 BL <0.5 mL/kg/ hr for > 12 hrs

Stage 3 Increase 3 BL or <0.3 mL/kg/ hr for > 24 hrs

increase 354 mol/L or or anuria for 12 hrs
commenced on RRT

SCr and UOP remains the best biomarkers for AKI (RA, AKI Guidelines 03.2011)
Stage 1 = AKIN/ (KDIGO) definition of AKI
 Causes
Pre-renal failure
Hypoperfusion
Intrinsic renal failure
Many causes
Acute tubular necrosis
Post-renal failure
Obstruction
 Pre-renal causes
Renal hypoperfusion
Systemic hypotension
- Hypovolaemia, hypotension (bleeding, dehydration)
- Sepsis
- Anaphylatic shock

Local = hypoperfusion of the gromerulus

- Renal artery stenosis (reduced gromerular pressure)
- Drugs: ACE inhibitors, NSAIDs
 Intrinsic renal causes
Primary renal disease
Glomerulonephritis
Interstitial nephritis usually caused by drugs e.g.
NSAIDs, Gentamicin
Secondary renal disease
Diabetes, SLE, myeloma, etc.
Secondary ATN (acute tubular necrosis)
Established after pre-renal injury
 Post-renal causes
Obstruction
Intrinsic
- Urinary tumours e.g. RCC
- Stones

Extrinsic
- Pelvic tumours (prostate, cervix, ovaries)
- TB strictures
- Retroperitoneal tumours & fibrosis
 Investigations
History & examination
Rate of onset, urinary symptoms, PMH, DH
Fluid status, signs of sepsis
Bedside
Urine tests: dipstick, MSU, ACR/PCR
Urine output
ECG: K+, arrhythmia
Bloods
Kidney function: U+E, Creat, GFR
Markers of CKD: Ca, PO4, PTH, HCO3
Imaging
USS if find problems -> CT KUB, biopsy
CXR to monitor fluid overload
 Treatment
Treat underlying cause
Generic AKI management
Pre-renal: IV fluids
Intrinsic: Treat medically
Post-renal: Relieve obstruction
Percutaneous nephrostomy (drain pus/urine from kidneys)
Stents: antegrade (kidneys to bladder) vs retrograde
(bladder to kidneys)
Monitor: EWS (early warning score)
BP, pulse, sats, U+E, weight (= fluid level)
Fluid input vs output
 Hyperkalaemia: K+ > 6mmol/L
Very common complication of AKI
ECG changes (in this sequence)
Peaked tented T waves
Prolonged P-R interval
Prolonged QRS duration
Loss of P waves
VF/asystole
Treatment (at once!)
Stabilise myocardium: Ca Gluconate
Shift K+ into cells: IV Insulin+Dextrose, Salbutamol
nebuliser, NaHCO3 if acidotic
Diuresis, Ca Resonium, (RRT/Dialysis)
 Indications for RRT
Starting RRT is a clinical decision RA Guidelines, AKI, 03.2011:
AKI and the AEIOU
o Acidaemia (PH <7.1) when correction would cause fluid
overload
o Electrolyte abnormalities e.g. K > 7
o Intoxication with certain substances (salicylic acid, lithium,
etc.)
o Overload of fluid when diuretics are of no use
o Uraemic effects: seizure and coma (encephalopathy);
Pericardititis