Acute Kidney Injury

“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

Aetiology

• Acute illness such as infection/sepsis
• Recent surgery or being immobile (risk of rhabdomyolysis)
• Underlying renal disease (e.g. glomerulonephritis / interstitial nephritis)

Pathophysiology

• 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) 

Investigations

• 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?

Diagnosis

• 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 Stage	Creatinine	Urine Output
Stage 1	1.5-1.9x increase	<0.5ml/kg/hour for 6-12 hrs
Stage 2	2.0-2.9x increase	<0.5ml/kg/hour for ≥12 hours
Stage 3	>3x increase	<0.3ml/kg/hour for ≥24 hours Anuria for ≥12 hours

Management

• 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

Complications

• 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)