Neonatal acute kidney injury and the patent ductus arteriosus

Patent ductus arteriosus (PDA) is a common finding in premature infants and has an established association with systemic hypoperfusion. Emerging literature has suggested that ductal patency may play a role in the pathophysiology of neonatal acute kidney injury (AKI), primarily through kidney hypoperfusion. While therapeutic interventions, including catheter closure, surgical ligation or medical therapies (non-steroidal anti-inflammatories), aim to mitigate the haemodynamic burden of the PDA, they also have negative sequelae for the neonatal kidney. The growing body of literature pertaining to AKI in prematurity emphasises arrested nephrogenesis, inherent physiological features of prematurity and severity of illness as the primary drivers of neonatal AKI. A PDA and the iatrogenic damage posed by existing management strategies can further compound both the likelihood and severity of an AKI in the premature infant. Here, we review the physiology of the PDA and discuss its implications in the field of neonatal AKI.