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]

Branch 1 — Definition and epidemiology

Examiner: How do you define neonatal AKI, and what do the AWAKEN data tell us about its incidence and outcomes? [2]

Strong answer: Neonatal AKI is defined by the neonatal modified KDIGO criteria: a serum creatinine rise of 0.3 mg/dL or 50% from the previous lowest value, and/or urine output below 1 mL/kg/h on postnatal days 2 to 7. The neonatal creatinine reflects maternal function at birth and should decline over the first weeks, so the trend from the previous lowest value — not an absolute number — is the diagnostic trigger. The AWAKEN study was a multicentre, multinational cohort of over 2,000 NICU admissions that found an overall AKI incidence of 29.9%, varying by gestational age from 47.9% in infants below 29 weeks to 18.3% in the 29 to 36-week group. Crucially, AKI was independently associated with a two- to four-fold increase in mortality and longer hospital stay, even after adjusting for confounders. [2] [3]

Examiner probe: Why is the neonatal kidney so vulnerable? [4]

Strong answer: Three developmental factors create a narrow renal reserve. First, nephrogenesis is incomplete until 34 to 36 weeks, so preterm infants have fewer nephrons for life — a permanent deficit with no capacity for regeneration. Second, the neonatal GFR is low at 20 to 40 mL/min/1.73 m², limiting the ability to handle stress. Third, tubular function is immature, with impaired sodium reabsorption, poor concentrating ability and reduced acid-base handling. So the same insult that an adult kidney tolerates overwhelms the neonatal kidney. [4]

Branch 2 — Classification and management ladder

Examiner: Classify this infant's AKI and give me your management ladder. [4]

Strong answer: I classify it pathophysiologically as prerenal — the PDA diverts systemic perfusion and indomethacin causes afferent arteriole vasoconstriction, reducing GFR without yet causing structural damage. By KDIGO staging, it is Stage 2: the creatinine has risen more than 200% from baseline and the urine output is below 0.5 mL/kg/h. My management ladder is: first, reverse the cause — assess volume status, give 10 to 20 mL/kg of isotonic crystalloid if hypovolaemic, address the PDA, and minimise nephrotoxins. Second, if volume-replete, restrict fluids to insensible losses plus urine output. Third, manage electrolytes — his potassium of 5.8 is not yet at the emergency threshold, but I would restrict potassium intake, use calcium resonium, and monitor with daily ECG; if it rises above 6.5 or ECG changes appear, I give calcium gluconate, insulin–dextrose and salbutamol. Fourth, dose-adjust all renally cleared drugs. Fifth, if the AKI progresses to refractory hyperkalaemia, severe acidosis or fluid overload above 10%, initiate renal replacement therapy with peritoneal dialysis as first-line. [4] [5]

Examiner probe: How would you distinguish prerenal from intrinsic AKI at the bedside? [5]

Strong answer: The fractional excretion of sodium (FENa) is the most useful index in neonates — below 2.5% suggests prerenal sodium conservation, above 2.5% suggests intrinsic tubular damage with sodium wasting. Urine osmolality above 400 mOsm/kg suggests prerenal concentration, while isosthenuria at 300 mOsm/kg suggests intrinsic disease. The response to a fluid challenge is the clinical test: prerenal AKI recovers with volume, while intrinsic AKI does not. These indices are less reliable in the diuretic- or indomethacin-exposed neonate, so the clinical context always matters. [5]

Branch 3 — Severe AKI and renal replacement therapy (a trap)

Examiner: The infant is now 5 days old. The creatinine is 2.8 mg/dL, potassium is 7.4 mmol/L with peaked T waves, pH is 6.95, and the fluid overload is 13% of birth weight with worsening respiratory status. What do you do? [4]

Strong answer: This infant now meets multiple indications for renal replacement therapy — refractory hyperkalaemia, severe acidosis, and fluid overload above 10% with respiratory compromise. The immediate first step is to give calcium gluconate 10% at 0.5 mL/kg slowly to stabilise the myocardium, followed by insulin–dextrose and salbutamol to shift potassium intracellularly, and bicarbonate for the acidosis. But these are temporising measures — I would simultaneously prepare for peritoneal dialysis, which is the first-line modality in neonates because it requires no vascular access and no anticoagulation, making it safest for the smallest infants. I would involve the neonatal nephrology team urgently. [4]

Examiner probe: What about late-onset AKI? Does it differ from early AKI? [6]

Strong answer: Yes. The AWAKEN late-onset AKI analysis found that AKI occurring after postnatal day 7 affected approximately 9% of neonates and carried independently higher odds of death — adjusted OR of 2.1 — and longer length of stay. The risk factors differ from early AKI: intubation, oligohydramnios, congenital heart disease, necrotising enterocolitis, diuretic and vasopressor exposure, and NSAID use. This means surveillance must extend beyond the first week in the sick NICU infant — a single normal creatinine in the first days does not clear the risk. [6]