Neonatal acute kidney injury — formative SAQs

SAQ 1 (10)

A 3-day-old, 26-week, 750-gram infant ventilated for respiratory distress syndrome is on indomethacin for a patent ductus arteriosus. The serum creatinine has risen from 0.9 to 1.5 mg/dL and the urine output is 0.5 mL/kg/h. The potassium is 5.8 mmol/L. [2]

1. Define neonatal acute kidney injury using the neonatal modified KDIGO criteria. (3) [2]
2. Explain why this infant is at particularly high risk of AKI. (3) [3]
3. Outline your stepwise management of his AKI, including how you would manage his potassium. (4) [3] [4]

Model answer

1. Neonatal AKI is defined by the neonatal modified KDIGO (neoKDIGO) criteria: a serum creatinine rise of 0.3 mg/dL or more, or a rise of 50% or more from the previous lowest value, and/or urine output below 1 mL/kg/h on postnatal days 2 to 7. Severity is staged from Stage 1 (mild) through Stage 2 (moderate) to Stage 3 (severe). This infant meets the criteria with a 0.6 mg/dL rise and oliguria below 1 mL/kg/h, placing him at approximately Stage 2. [2]
2. This infant has multiple compounding risk factors: extreme prematurity (26 weeks) means nephrogenesis is incomplete with fewer nephrons and a very low GFR (20–40 mL/min/1.73 m²); indomethacin for PDA causes renal vasoconstriction via prostaglandin inhibition; the PDA itself diverts systemic perfusion; respiratory distress syndrome and mechanical ventilation add haemodynamic stress; and he is in the highest-risk gestational age group — the AWAKEN study showed AKI in nearly 48% of infants below 29 weeks. [3]
3. My management is stepwise: first, assess volume status — if hypovolaemic, give 10–20 mL/kg isotonic crystalloid; if volume-replete, restrict fluids to insensible losses plus urine output. Stop or minimise nephrotoxins (review aminoglycoside and indomethacin dosing). Address the PDA, as the underlying haemodynamic lesion may need closure or ligation. For his potassium of 5.8 mmol/L (not yet at emergency threshold): restrict potassium intake, use calcium resonium enterally, and monitor with daily ECG. If potassium rises above 6.5 or ECG changes appear: give calcium gluconate 10% at 0.5 mL/kg slowly, then insulin–dextrose and salbutamol. Dose-adjust all renally cleared drugs. If the AKI progresses with refractory hyperkalaemia, severe acidosis or fluid overload above 10%, initiate renal replacement therapy with peritoneal dialysis as first-line. [3] [4]

SAQ 2 (10)

A term infant with severe perinatal asphyxia and hypoxic-ischaemic encephalopathy is receiving therapeutic hypothermia. On day 2 of life, his creatinine has risen from 1.1 to 2.2 mg/dL, his urine output is 0.2 mL/kg/h, his potassium is 7.3 mmol/L with peaked T waves, and he has fluid overload of 11% above birth weight. [3]

1. What are the indications for renal replacement therapy in neonatal AKI? (3) [3]
2. Describe your immediate management of this infant's hyperkalaemia. (4) [3]
3. Discuss the evidence for pharmacological prevention of AKI in the asphyxiated neonate, and outline your approach to long-term follow-up. (3) [5] [6]

Model answer

1. The indications for renal replacement therapy in neonatal AKI are: potassium above 7.0 mmol/L refractory to medical therapy; severe metabolic acidosis (pH below 7.1) refractory to bicarbonate correction; fluid overload exceeding 10% of birth weight with respiratory compromise; progressive uraemia (urea above 30–40 mmol/L); and anuria with progressive biochemical deterioration. This infant meets multiple criteria (refractory hyperkalaemia, fluid overload above 10%, oligoanuria). [3]
2. My immediate management of the hyperkalaemia with ECG changes: first give calcium gluconate 10% at 0.5 mL/kg (0.11 mmol/kg) slowly intravenously to stabilise the myocardial membrane and prevent arrhythmia — this is the first and most urgent step when there are ECG changes. Then shift potassium intracellularly with insulin–dextrose (0.1 units/kg insulin with 2–4 mL/kg of 10% dextrose) and nebulised or intravenous salbutamol. Give sodium bicarbonate if there is acidosis, which also promotes intracellular potassium shift. These are temporising measures — this infant needs definitive treatment with renal replacement therapy (peritoneal dialysis) because his AKI is severe and the hyperkalaemia and fluid overload are refractory. [3]
3. Adenosine antagonists — theophylline and aminophylline — block the vasoconstrictive effect of adenosine on the afferent arteriole and have shown promise in randomised trials and meta-analyses (Bhatt 2019) for preventing AKI in asphyxiated neonates, though the evidence is still maturing in the era of therapeutic hypothermia (Chock 2021). Caffeine, a related methylxanthine, is associated with lower AKI rates in preterm infants. For long-term follow-up: every AKI survivor carries a lifelong risk of CKD and hypertension from permanent nephron loss and hyperfiltration injury. I would arrange blood pressure and renal function (creatinine, eGFR) monitoring at 3 to 6 monthly intervals for the first years of life, with paediatric nephrology involvement for any hypertension or declining function. [5] [6]