Acute kidney injury

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

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 μmol/L within 48hrs or increase ≥ 1.5 - 1.9 BL

<0.5 mL/kg/hr for > 6 consecutive hrs

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

Stage 3 Increase ≥3 BL or increase ≥ 354 μmol/L or commenced on RRT

<0.3 mL/kg/ hr for > 24 hrs or anuria for 12 hrs

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 hypoperfusionSystemic 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, GentamicinSecondary renal disease

– Diabetes, SLE, myeloma, etc.Secondary ATN (acute tubular necrosis)

– Established after pre-renal injury

Post-renal causes

ObstructionIntrinsic- 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 RRTStarting 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 > 7o Intoxication with certain substances (salicylic acid, lithium,

etc.)o Overload of fluid when diuretics are of no useo Uraemic effects: seizure and coma (encephalopathy);

Pericardititis