الفهرس 
Hypoxic–Ischemic EncephalopathyOnly 14 pages are availabe for public view
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Abstract
Neonatal hypoxic–ischemic encephalopathy (HIE), HIE is a major cause of long-term neurodevelopmental disability in term infants. Despite the difficulties of adapting the diagnosis criteria of perinatal asphyxia to preterm newborns, it is accepted that neonatal hypoxic–ischemic encephalopathy can also occur in this population, leading to significant mortality and neurologic morbidity. Hypoxia–ischemia is also one of the main upstream mechanisms associated with the encephalopathy of prematurity, characterized by a combination of cerebral gray and white matter damage in preterm infants. AKI is increasingly recognized as an important and independent risk factor of morbidity and mortality in critically ill neonates. Small increases of serum creatinine levels in hospitalized patients are associated with substantial morbidity and mortality so we need to diagnose before actual increase of serum urea and creatinine levels . Erythropoietin is a glycoprotein hormone that controls erythropoiesis. Human EPO has a molecular weight of 34 kDa; it is produced primarily from the kidney and to a lesser extent from liver. In addition to erythropoiesis, EPO appears to have neurotropic and neuroprotective properties that could be useful in the prevention and repair of brain injury. Erythropoietin is potential marker for central nervous system injury in neonates with IVH, asphyxia and meningitis. The present study was designed to evaluate the role of urine Erythropoietin level as an early predictor of AKI in the neonates with HIE.