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Pathology
Rapid deterioration of renal function defined by a creatinine rise ≥ 26.4µmol/l within a 48 hour period or a urine output <0.5 ml/kg/hour sustained > 6 hours
Aetiology
Pre-Renal: Hypovolaemia: CCF, Liver cirrhosis, renal artery stenosis, blood loss
Renal: Acute tubular necrosis, Acute glomerulonephritis, Interstitial nephritis, Vasculitis
Post-Renal: Blocked catheter, enlarged prostate, retroperitoneal fibrosis
Signs
Reduced urine output, rash, peripheral oedema, arrhythmias, signs of heart failure
Symptoms
Oliguria, Malaise, lethargy, confusion, nausea, seizure, pruritus, purpura, breathlessness, pericarditis
Investigations
Bloods: FBC, U&E, blood film, blood cultures
ABG: Metabolic acidosis
ECG: Assess for underlying pathology
MSU: Urine dipstick
Imaging: Ultrasound urinary tract to exclude obstruction
Treatment
Medical: Establish and treat underlying cause for AKI, Fluid resuscitation, Catheter insertion, Stop nephrotoxic drugs , may require dialysis.
Prognosis
50-60% of patients admitted to ITU have AKI.
Significant increase in length of hospital stay and increased mortality.
Majority make good recovery; those with concurrent CKD have a poor prognosis
Hyperkalaemia, fluid overload, uraemia and a high anion gap metabolic acidosis
Key Facts
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Key References
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