Acute Kidney Injury (AKI) in perinatal asphyxia

Abstract

Background: Acute kidney injury (AKI) is a common consequence of perinatal asphyxia, occurring in upto 56% of these neonates. It is important to recognize AKI in asphyxiated neonates to facilitate administration of appropriate fluids and electrolytes in order to improve their outcome. Objectives: To determine the incidence of AKI in asphyxiated neonates and to correlate the severity and type of AKI with Apgar score and severity of hypoxic ischemic encephalopathy (HIE). Methods: 75 neonates were enrolled – 50 asphyxiated and 25 healthy neonates. Renal functions were assessed using urine output, urine microscopy, biochemical parameters and sonography. The values obtained were correlated with the severity of HIE. Neonates with AKI were managed as per unit protocol. Results: Of the 50 asphyxiated neonates, 32 (64%) had AKI: 25 (78.12 %) neonates with pre-renal AKI and the remaining 7 (21.88 %) with intrinsic AKI. Out of the 32 asphyxiated neonates with AKI, 12 (37.5%) had oliguric AKI, while the remaining 20 (62.5%) had non-oliguric AKI. Levels of blood urea and serum creatinine were significantly higher in asphyxiated neonates as compared to healthy controls (p 0.001). Biochemical derangements correlated well with the severity of HIE and Apgar scores. Serum sodium and creatinine clearance showed significantly different values in asphyxiated babies compared to controls. There was no significant difference in the urine ouput in the control and study group. Sonographic abnormalities were seen most often in oliguric babies, and indicated bad prognosis. Mortality was higher in babies with oliguric AKI. Conclusions: Perinatal asphyxia is an important cause of neonatal AKI. Majority of the babies had non-oliguric AKI and responded well to fluid challenge. Abnormalities in the renal function correlates well with the severity of HIE. Intrinsic AKI, oliguria, hyponatremia, reduced creatinine clearance and abnormal sonographic scan suggest bad prognosis in neonatal AKI secondary to perinatal asphyxia.