Acute kidney injury in critically ill newborns: what do we know? What do we need to learn?

Abstract

Outcomes in critically ill neonates have improved over the past three decades, yet high residual mortality and morbidity rates exist. Acute kidney injury (AKI) is not just an innocent by-stander in the critically ill patient. Research on incidence and outcomes of AKI in the critically ill neonatal population is scarce. The objective of this publication is to (a) review original articles on the short- and long-term outcomes after neonatal AKI, (b) highlight key articles on adults and children with AKI in order to demonstrate how such insights might be applied to neonates, and (c) suggest clinical research studies to fill the gaps in our understanding of neonatal AKI. To date, observational studies suggest high rates of AKI and poor outcomes in critically ill neonates. Neonates with AKI are at risk of developing chronic kidney disease and hypertension. Large prospective studies are needed to test definitions and to better understand risk factors, incidence, independent outcomes, and mechanisms that lead to poor short- and long-term outcomes. Early biomarkers of AKI need to be explored in critically ill neonates. Infants with AKI need to be followed for sequelae after AKI.

Fig. 1

Plasma creatinine in neonates (reproduced with permission from [23])

Fig. 2

Age-related comparative yearly incidence of AKI (adapted with permission from [25])

Fig. 3

Box plot distribution showing cystatin C across age groups. The categories 24–28 weeks and 29–36 weeks refer to the gestational age of preterm babies. Preterm babies were 1 day old when the samples were drawn (reproduced with permission [45])

Fig. 4

Pattern of urinary IL-18 and NGAL levels after cardiopulmonary bypass. AKI (defined as a > 50% increase in serum creatinine) developed after 48–72 h in the AKI patients (reproduced with permission from [49])