Neonatal acute kidney injury — case

Case summary

A 3-day-old, 26-week, 750-gram male infant is ventilated for respiratory distress syndrome and on indomethacin for a haemodynamically significant patent ductus arteriosus. His serum creatinine has risen from 0.9 mg/dL on day 1 to 1.5 mg/dL on day 3, and his urine output is 0.5 mL/kg/h. His potassium is 5.8 mmol/L. The parents are anxious about his kidney function and whether there will be long-term consequences. [1]

Candidate tasks

1. Take a focused history and assess the clinical data; formulate a one-line problem representation. [1]
2. Outline your immediate and stepwise management of the AKI and the PDA. [2]
3. Counsel the parents about the cause, the management plan, and the longer-term outlook including follow-up. [2]

Focused history and assessment

• Antenatal: maternal pre-eclampsia, antenatal steroids, emergency caesarean for fetal distress, chorioamnionitis. [2]
• Perinatal: 26 weeks gestation, birthweight 750 g (10th centile, SGA), Apgar scores 3 and 6, cord pH 7.1, intubated in the delivery room. [2]
• NICU course: respiratory distress syndrome requiring surfactant and mechanical ventilation, a haemodynamically significant PDA started on indomethacin on day 2, caffeine started for apnoea of prematurity prophylaxis. [5]
• Drug exposures: gentamicin (day 1–3), indomethacin (day 2 onwards), caffeine (day 1 onwards). [3]
• Current biochemistry: creatinine rising (0.9 → 1.5 mg/dL), urine output 0.5 mL/kg/h, potassium 5.8 mmol/L, sodium 132 mmol/L, normal calcium and phosphate. [4]

One-line summary: "A 3-day-old, 26-week, 750-gram extremely preterm infant with RDS and a PDA on indomethacin, whose creatinine has risen by 0.6 mg/dL with oliguria — neonatal AKI (neoKDIGO Stage 2) from prerenal hypoperfusion (PDA) compounded by indomethacin nephrotoxicity, in the highest-risk gestational age group." [1]

Immediate and stepwise management

• Reverse the cause: assess volume status, give 10–20 mL/kg isotonic crystalloid if hypovolaemic; address the PDA — continue, switch or consider surgical ligation if the PDA remains haemodynamically significant. [2]
• Minimise nephrotoxins: review gentamicin dosing (use extended-interval dosing, check levels), consider alternatives; weigh the benefit of indomethacin against the renal risk. [3]
• Fluid management: once volume-replete, restrict fluids to insensible losses (60–80 mL/kg/day for a preterm) plus urine output and other measured losses; daily weights and strict I/O charts. [2]
• Electrolyte management: his potassium of 5.8 is not yet at the emergency threshold — restrict potassium intake, use calcium resonium enterally, monitor with daily ECG; if above 6.5 or ECG changes, give calcium gluconate 10% 0.5 mL/kg, insulin–dextrose and salbutamol. [2]
• Drug dose adjustment: dose-adjust all renally cleared drugs to current GFR — a patient-safety issue. [3]
• Escalation: if AKI progresses to refractory hyperkalaemia (above 7.0), severe acidosis (pH below 7.1), or fluid overload above 10% with respiratory compromise, initiate renal replacement therapy — peritoneal dialysis as first-line in neonates. [2]

Counselling the parents

• Explain clearly that their baby's kidneys are working harder than they can manage right now because the baby was born very early — the kidneys are still developing (nephrogenesis is not complete until 34 to 36 weeks), so they have fewer nephrons and less reserve. The PDA (a blood vessel that has not closed yet) is diverting blood flow away from the kidneys, and the indomethacin medicine that helps close the PDA also reduces blood flow to the kidneys temporarily. [2]
• Set immediate expectations: the team is actively managing the fluid balance and the potassium, stopping or reducing the kidney-harming medicines where possible, and treating the PDA. Most prerenal AKI improves when the perfusion is corrected, but the team is monitoring closely and is ready to provide kidney support (peritoneal dialysis) if needed. [3]
• Be honest about the longer view: most infants recover from an AKI episode, but because nephrons cannot regenerate, there is a lifelong risk of high blood pressure and chronic kidney disease. The team will monitor blood pressure and kidney function at regular intervals after discharge — this surveillance is mandatory, not optional, because early detection of any problem changes the trajectory. [2]
• Acknowledge the anxiety, invite questions, check understanding, and offer a follow-up meeting with the neonatal team and a renal specialist if the parents wish. Provide written information and clear safety-netting on the signs that would prompt escalation. [2]