An abrupt (<48 hours) reduction in kidney function defined as: an absolute increase in serum creatinine by >26.4 µm/l OR an increase in creatinine by >50% OR a reduction in UO

Aetiology

Pre-renal - impaired blood flow to the kidney

• Reversible volume depletion causes a reduction in perfusion to the kidneys - leads to oliguria (<0.5 mls/kg/hr) and increase in creatinine
• Hypovolaemia - haemorrhage, volume depletion (e.g. D+V, burns)
• Hypotension - cardiogenic shock, distributive shock (e.g. sepsis, anaphylaxis)
• Renal hypoperfusion - NSAIDs/COX-2, ACEi/ARBs, hepatorenal syndrome
  • ACEi result in loss of loss of efferent arteriolar vasoconstriction which is a compensatory mechanism for volume depletion → major fall in GFR
• Untreated pre-renal AKI leads to acute tubular necrosis (see below)

Renal

• Diseases causing inflammation or damage to cells causing AKI
• Vascular - vasculitis, renovascular disease
• Glomerular - glomerulonephritis
• Interstitial nephritis - drugs, infection (TB), systemic (sarcoid)
• Tubular injury - ischaemia, drugs (gentamicin), contrast, rhabdomyolysis

Acute tubular necrosis

• Tubular cell death
• Commonest form of AKI in hospital
• Due to a combination of factors leading to decreased renal perfusion
• Common causes include sepsis and severe dehydration
• Other important causes include rhabdomyolysis and drug toxicity