Biomarkers of perinatal asphyxia: the divergent roles of erythropoietin: a cross sectional study

Abstract Background Hypoxic-ischemic encephalopathy (HIE) is a leading cause of neonatal morbidity and mortality, frequently complicated by multiorgan dysfunction, including acute kidney injury (AKI). Erythropoietin (EPO), a glycoprotein hormone, is upregulated in response to tissue hypoxia. Objective To evaluate serum EPO levels alongside serum creatinine in full-term neonates as indicators of perinatal hypoxia, HIE severity, and concurrent AKI. Methods This cross-sectional study included 80 full-term neonates (40 healthy controls and 40 asphyxiated neonates) evaluated within their first 96 h of life. Results Serum EPO levels were significantly elevated in the asphyxiated group compared to healthy controls, with the highest concentrations observed in neonates with severe HIE. AKI was diagnosed in 50% of the patient group, predominantly presenting as non-oliguric (95%). There was no significant difference in serum EPO levels between asphyxiated neonates with and without AKI. Receiver Operating Characteristic (ROC) analysis for EPO at a cut-off of > 10.5 mIU/mL demonstrated an area under the curve (AUC) of 0.700, yielding a sensitivity of 67.5% and a specificity of 82.5% for detecting perinatal injury. Conclusion Serum EPO is significantly elevated following perinatal asphyxia and is associated with severe encephalopathy, supporting its role as an adjunctive biomarker for hypoxic injury. However, its moderate sensitivity and lack of correlation with renal impairment demonstrate that EPO is not a standalone diagnostic tool or an independent predictor of AKI.