Renal and Cerebral NIRS and Early Acute Kidney Injury in Cooled Neonates With Birth Asphyxia

Overview

This prospective, single-center observational cohort study evaluated whether continuous cerebral and bilateral renal near-infrared spectroscopy (NIRS) monitoring during therapeutic hypothermia distinguishes term neonates with hypoxic-ischemic encephalopathy (HIE) who develop acute kidney injury (AKI) from those who do not. Forty-six neonates who received whole-body therapeutic hypothermia for HIE were enrolled and monitored continuously for 72 hours. Regional oxygen saturation was recorded at three sites: the cerebral cortex and both kidneys. Acute kidney injury was classified after the monitoring period using serum creatinine-based criteria, and participants were assigned to an AKI group or a non-AKI group. The primary objective was to compare regional oxygen saturation between the two groups. Serum and urinary indices of tubular function were assessed at 24, 48, and 72 hours as secondary measures.

Acute kidney injury is among the most frequent organ complications of perinatal asphyxia, and serum creatinine rises only after substantial functional loss has already occurred. Near-infrared spectroscopy provides continuous, non-invasive measurement of regional tissue oxygen saturation and may detect renal compromise earlier than conventional biochemical markers, but data in neonates undergoing therapeutic hypothermia remain limited. This single-center prospective observational cohort study was conducted in the neonatal intensive care unit of Kayseri City Training and Research Hospital, Kayseri, Türkiye. Consecutive neonates with hypoxic-ischemic encephalopathy who began whole-body therapeutic hypothermia within 6 hours of birth were enrolled. All clinical management followed the unit's pre-existing standing protocol for therapeutic hypothermia and was not assigned, modified, or withheld for research purposes. Under that routine protocol, core temperature was maintained at 33.5 °C for 72 hours with servo-controlled feedback, followed by rewarming at 0.25 °C per hour; all neonates received ampicillin and cefotaxime because of infection risk, antibiotics were discontinued after rewarming in neonates without signs of infection, and aminoglycosides were not administered to any neonate owing to their recognized renal toxicity. The investigators recorded, but did not direct, clinical care. Regional oxygen saturation was recorded continuously across the 72-hour cooling period using a cerebral/somatic oximeter. A neonatal sensor was placed on the right lateral forehead for cerebral measurement, and bilateral sensors were placed lateral to the lumbar spine at the T12-L2 vertebral level for renal measurement. Sensor position and skin integrity were checked every 4 to 6 hours. Recordings were time-synchronized with pulse oximetry and averaged into 6-hour intervals. Serum and spot urine samples were obtained at 24, 48, and 72 hours for electrolytes and creatinine, from which fractional excretion of sodium and potassium, tubular reabsorption of phosphate, and urinary calcium/creatinine and magnesium/creatinine ratios were derived. Acute kidney injury was classified after the monitoring period using modified pediatric RIFLE criteria together with a neonatal-specific serum creatinine decline-rate criterion. Participants were then assigned to an AKI group or a non-AKI group, and regional oxygen saturation was compared between them.