2: Renal Haemodynamics and Acute Kidney Injury During Therapeutic Hypothermia and Re-Warming in Neonates with Hypoxic-Ischaemic Encephalopathy

Abstract

Birth asphyxia is associated with acute kidney injury (AKI); severity may correspond with degree of hypoxia. Previous work by our group demonstrated lower cardiac output in neonates undergoing therapeutic hypothermia (TH). The relevance of these changes to AKI remains unknown. To describe longitudinal renal haemodynamic changes during TH and re-warming (RW) and evaluate their relationship with cardiac output in neonates with and without AKI. Prospective observational study of 18 term and near-term infants with hypoxic-ischaemic encephalopathy (HIE) who received TH. Doppler ultrasound was used to assess left ventricular output (LVO) and renal artery (RA) blood flow parameters – systolic and end-diastolic velocity (Vs and Vd), and resistive index (RI) during cooling [TH I (24 h) and II (72 h)] and post re-warming [RW I (12 h) and II (>24 h)]. AKI was defined as anuria/oliguria (100 mmol/L; or anuria/oliguria for >36 h; or any serum creatinine >125 mmol/L; or rising serum creatinine postnatally. There was no difference in baseline demographics or severity of HIE between neonates with (n=8) vs without (n=10) AKI. All 18 infants survived till discharge. Neonates who developed AKI had higher RA RI 24 h after TH was initiated [Table 1]. There was a temporal increase in LVO in both groups (P<0.01, two-way ANOVA), without intergroup difference. Neonates in the non-AKI group only showed an increase in RI (P=0.01) and a trend towards increase in RA Vs over time (P=0.05). Early changes in end-diastolic flow (EDF) were seen in both groups, which normalized over time. Elevated RA RI at 24 h after introduction of TH is associated with and predicts AKI. The fall in cardiac output and renal systolic flow after TH is not associated with AKI.