AKI: Workup & Management

• Stage with KDIGO (creatinine/urine output); causes split into pre-renal, post-renal (bladder scan + ultrasound), and intrinsic (ATN, AIN, GN, vascular).
• Review every drug in AKI: stop avoidable nephrotoxins and hold ACEi/ARB during hypovolaemia, hypotension or significant hyperkalaemia. Re-dose as kidney function changes; do not withhold essential contrast imaging just because of AKI. Aim for euvolaemia.
• Dialysis triggers (AEIOU): Acidosis, Electrolytes (K⁺), Ingestions, Overload, Uremic complications.
• AIN: stop the culprit drug (PPIs, antibiotics, NSAIDs) ± corticosteroids. Diagnosis is clinical, supported by urine microscopy; kidney biopsy is the gold standard when uncertain.
• With no urgent indication, watchful waiting on KRT is often right — but reassess persistent severe AKI rather than waiting indefinitely. CRRT should deliver 20–25 mL/kg/h, with regional citrate preferred when suitable.

First tests: Sodium, potassium, bicarbonate, urea and creatinine, Urine output and fluid balance, Urinalysis and microscopy.

Only if indicated: Renal tract ultrasound, Arterial blood gas, Targeted immune/hemolysis studies, Creatine kinase.

Repeat monitoring: Sodium, potassium, bicarbonate, urea and creatinine, Urine output and fluid balance.

• Distinguishing the Three Categories of Acute Kidney Injury
• Managing Prerenal Causes of Acute Kidney Injury