Paeds SAQs · fetal-neonatal-and-perinatal
Neonatal acute kidney injury — formative SAQs
Formative SAQs.
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Prompt
Neonatal acute kidney injury
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]
- Define neonatal acute kidney injury using the neonatal modified KDIGO criteria. (3) [2]
- Explain why this infant is at particularly high risk of AKI. (3) [3]
- Outline your stepwise management of his AKI, including how you would manage his potassium. (4) [3] [4]
Model answer
- 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]
- 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]
- 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]
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- [1]Jetton JG, Boohaker LJ, Sethi SK, et al. Incidence and outcomes of neonatal acute kidney injury (AWAKEN): a multicentre, multinational, observational cohort study. Lancet Child and Adolescent Health, 2017.PMID 29732396
- [2]Askenazi D, Abitbol C, Boohaker L, et al. Optimizing the AKI definition during first postnatal week using Assessment of Worldwide Acute Kidney Injury Epidemiology in Neonates (AWAKEN) cohort. Pediatric Research, 2019.PMID 30643188
- [3]Starr MC, Charlton JR, Guillet R Advances in neonatal acute kidney injury. Pediatrics, 2021.PMID 34599008
- [4]Kent AL, Charlton JR, et al Neonatal acute kidney injury: a survey of neonatologists' and nephrologists' perceptions and practice management. American Journal of Perinatology, 2018.PMID 28709164
- [5]Charlton JR, Boohaker L, Askenazi D, et al. Late onset neonatal acute kidney injury: results from the AWAKEN Study. Pediatric Research, 2019.PMID 30546043
- [6]Harer MW, Askenazi DJ, et al Association between early caffeine citrate administration and risk of acute kidney injury in preterm infants. JAMA Pediatrics, 2018.PMID 29610830