Renal System >
Acute Kidney Injury (AKI)

“Acute drop in renal function (usually reversible)”

Risk Factors
  • Age (>65)
  • Cognitive impairment
  • Pre-Renal risks:
    • Dehydration
    • Hypotension
    • Heart Failure
  • Renal risks:
    • Diabetes
    • Nephrotic medications
    • CT Contrast
    • Chronic Kidney Disease
  • Post-Renal risks:
    • Renal stones
    • Ureteric strictures
    • Enlarged Prostate / Malignancy
  • Acute illness such as infection/sepsis
  • Recent surgery or being immobile (risk of rhabdomyolysis)
  • Underlying renal disease (e.g. glomerulonephritis / interstitial nephritis)
  • Pre-Renal:
    • Inadequate perfusion of the glomerulus reduces capillary pressure
    • Reduced pressure = reduced Glomerular Filtration Rate (GFR)
    • Example: NSAIDs can cause afferent arteriole vasoconstriction, decreasing perfusion.
  • Renal:
    • Structural alterations in the tubules & glomerulus
    • Acute Tubular Necrosis (ATN) is the most common cause of renal AKI and often secondary to pre-renal AKI, leading to ischaemic ATN.
    • Ischaemia damages tubular cells & the debris is shed into the tubule, increasing tubular pressure
    • The increased tubular pressure decreases the GFR
  • Post-Renal:
    • Obstruction to the outflow or urine leads to increased tubular pressure.
    • The increased tubular pressure decreases the GFR
Clinical Presentation
  • Symptom onset occurs over several days to weeks.
  • Patients with early-onset AKI may present asymptomatic with laboratory findings.
  • Symptoms:
    • Oliguria (<0.5ml/kg/hour)
    • Pulmonary & peripheral oedema
    • Nausea (due to metabolic acidosis)
    • Arrhythmias (secondary to K+ imbalance)
    • Features of uraemia (encephalopathy, pericarditis) 
  • Bloods:
    • Full Blood Count (FBC) – Any signs of Infection?
    • Urea and Electrolytes – eGFR, urea, creatinine, K+, Na+
    • C-Reactive Protein (CRP) – Any signs of Inflammation?
    • Arterial Blood Gas – Any metabolic Acidosis?
  • Imaging:
    • Chest X-Ray – Any pulmonary oedema?
    • Renal Ultrasound – Assess for any post-renal obstruction
  • Special:
    • Urinalysis – look for any infection (leucocytes + nitrites) or any underlying nephritis (haematuria + proteinuria)
    • ECG – any signs of hyperkalaemia or arrhythmias?
  • NICE Criteria:
    • 50% rise in creatinine over the last 7 days
    • ≥26 micromole/l rise in creatinine in 48 hours
    • Urine output <0.5ml/kg/hour for >6 hours
AKI StageCreatinineUrine Output
Stage 11.5-1.9x increase<0.5ml/kg/hour for 6-12 hrs
Stage 22.0-2.9x increase<0.5ml/kg/hour for ≥12 hours
Stage 3>3x increase
<0.3ml/kg/hour for ≥24 hours
Anuria for ≥12 hours
  • Conservative: n/a
  • Medical:
    • Fluid rehydration
    • Treat underlying cause (e.g. avoid/stop nephrotoxic agents, relieve obstruction)
    • Dialysis – For severe complications (refractory metabolic acidosis/hyperkalaemia, complications from rising urea, pulmonary oedema)
  • Surgical: n/a
  • NICE estimates inpatient mortality of AKI in the UK is around 25-30%.
  • Metabolic acidosis (due to decreased HCO3- absorption and decreased H+ excretion)
  • Hyperkalaemia (arrhythmia, muscle pain, palpitation)
  • Fluid overload (decreased renal function)
  • Uraemia (can lead to encephalopathy or pericarditis)

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