Neonatal acute kidney injury — viva

Stem

The examiner hands you the chart of a 3-day-old, 26-week, 750-gram infant ventilated for respiratory distress syndrome, on indomethacin for a patent ductus arteriosus. The serum creatinine has risen from 0.9 to 1.5 mg/dL, the urine output is 0.5 mL/kg/h, and the potassium is 5.8 mmol/L. ^[1]

Examiner: What is your opening assessment of this infant? ^[1]

Strong answer: I would classify this as neonatal AKI (neoKDIGO Stage 2) in an extremely preterm infant — the creatinine has risen by 0.6 mg/dL (well above the 0.3 mg/dL threshold) and the urine output is below 1 mL/kg/h, both meeting the neonatal modified KDIGO criteria for AKI. This infant is in the highest-risk category: the AWAKEN study showed an AKI incidence of nearly 48% in infants below 29 weeks. The likely mechanism is prerenal hypoperfusion from the PDA combined with indomethacin-induced renal vasoconstriction. My immediate priorities are to assess volume status, stop or minimise nephrotoxins, address the PDA, restrict fluids if volume-replete, monitor potassium closely, and dose-adjust all renally cleared drugs. ^{[1] [4]}