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
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)