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Acute kidney injury

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.

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Acute kidney injury

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  1. Acute kidney injury Vivian Phan

  2. 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

  3. RIFLE criteria Crit Care 2004; 8:R204.

  4. AKI: KDIGO Classification SCr and UOP remains the best biomarkers for AKI (RA, AKI Guidelines 03.2011) Stage 1 = AKIN/ (KDIGO) definition of AKI

  5. Causes Pre-renal failure • Hypoperfusion Intrinsic renal failure • Many causes • Acute tubular necrosis Post-renal failure • Obstruction

  6. 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

  7. 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

  8. Post-renal causes Obstruction Intrinsic • Urinary tumours e.g. RCC • Stones Extrinsic • Pelvic tumours (prostate, cervix, ovaries) • TB strictures • Retroperitoneal tumours & fibrosis

  9. 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

  10. 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

  11. 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: CaGluconate • Shift K+ into cells: IV Insulin+Dextrose, Salbutamol nebuliser, NaHCO3 if acidotic • Diuresis, Ca Resonium, (RRT/Dialysis)

  12. Indications for RRT Starting RRT is a clinical decision RA Guidelines, AKI, 03.2011: AKI and the AEIOU • Acidaemia (PH <7.1) when correction would cause fluid overload • Electrolyte abnormalities e.g. K > 7 • Intoxication with certain substances (salicylic acid, lithium, etc.) • Overload of fluid when diuretics are of no use • Uraemic effects: seizure and coma (encephalopathy); Pericardititis

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