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
Symptoms: Oliguria, Malaise, lethargy, confusion, nausea, seizure, pruritus, purpura, breathlessness, pericarditis
Signs: Reduced urine output, rash, peripheral oedema, arrhythmias, signs of heart failure
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 Biopsy: if no obvious cause located – renal vasculitis
Treatment: Medical: Establish and treat underlying cause for AKI, Fluid resuscitation, Catheter insertion, Stop nephrotoxic drugs , may require dialysis.
Complications: Hyperkalaemia, fluid overload, uraemia and a high anion gap metabolic acidosis
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
