• S Kaur, S Jain, A Saha, D Chawla, V R Parmar, S Basu, and J Kaur.
• Department of Pediatrics, Government Medical College and Hospital, Chandigarh, India.
• Ann Trop Paediatr. 2011 Jan 1; 31 (2): 129-34.

BackgroundAcute kidney injury (AKI) is one of the commonest manifestations of end-organ damage associated with birth asphyxia.ObjectiveTo evaluate glomerular and tubular dysfunction in neonates with moderate to severe birth asphyxia.DesignProspective cohort study.SettingNeonatal unit of a teaching hospital.MethodsSubjects were inborn neonates of ≥34 completed weeks of gestation with an APGAR score <7 at 1 min after birth. Renal function tests including serum electrolytes were measured daily until 96 hrs of life along with urinary output. Fractional excretion of sodium (FeNa), renal failure index (RFI), urinary myoglobin and creatinine clearance (CrCl) were calculated using timed urine collection. Staging of AKI was undertaken using Acute Kidney Injury Network criteria (AKIN). PRIMARY OUTCOME MEASUREMENT: Recovery of glomerular function.ResultsA total of 2196 neonates were born during the study period (September 2006 to April 2007), 44 of whom met the inclusion criteria. Data from 36 neonates were available for final analysis. AKI developed in 9·1% (1/11) infants with moderate asphyxia and 56·0% (12/25) infants with severe asphyxia, making a total incidence of 41·7%. AKI persisted in 16·6% neonates at 96 hours of life. Ten neonates (27·7%) had serum creatinine levels >1·5 mg/dl. In neonates with AKI, tubular function (Fe Na, RFI, urinary myoglobin) was significantly deranged until 72-96 hrs of life. One infant died and one who was critically ill was discharged against medical advice; both had AKI.ConclusionIt is feasible to use AKIN staging for evaluating AKI in neonates with birth asphyxia.

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