Evaluation of the Risk Factors for Acute Kidney Injury in Neonates Exposed to Antenatal Indomethacin.

Abstract

Evidence is limited about important maternal and neonatal risk factors that affect neonatal renal function. The incidence of acute kidney injury (AKI) and identification of associated risk factors in neonates exposed to antenatal indomethacin was studied. A retrospective cohort of neonates exposed to antenatal indomethacin within 1 week of delivery was analyzed for development of AKI up to 15 days of life. Adjusted hazard ratios (HRs) and 95% CIs for AKI risk were calculated in time-dependent Cox proportional hazards models. Among 143 neonates with mean gestational age of 28.3 ± 2.4 weeks, AKI occurred in 62 (43.3%), lasting a median duration of 144 hours (IQR, 72-216 hours). Neonates with AKI had greater exposure to postnatal NSAIDs (48.4% vs 9.9%, p < 0.001) and inotropes (37.1% vs 3.7%, p < 0.001) compared with neonates without AKI. In multivariable-adjusted models, increased AKI risk was observed with antenatal indomethacin doses received within 24 to 48 hours (HR, 1.6; 95% CI, 1.28-1.94; p = 0.036) and <24 hours (HR, 2.33; 95% CI, 1.17-4.64; p = 0.016) prior to delivery. Further, postnatal NSAIDs (HR, 2.8; 95% CI, 1.03-7.61; p = 0.044), patent ductus arteriosus (HR, 4.04; 95% CI, 1.27-12.89; p = 0.018), and bloodstream infection (HR, 3.01; 95% CI, 1.37-6.60; p = 0.006) were associated significantly with increased risk of AKI following antenatal indomethacin. Neonates with AKI experienced more bloodstream infection, severe intraventricular hemorrhage, patent ductus arteriosus, respiratory distress syndrome, and longer hospitalization. Extended risk of AKI with antenatal indomethacin deserves clinical attention among this population at an already increased AKI risk.