الفهرس 
IntroductionOnly 14 pages are availabe for public view
 |  | from | 131 |  |  |
| | | from | 131 | | |
Abstract
Perinatal asphyxia (PA) is an insult to the fetus or the newborn due to lack of oxygen (hypoxia) and/or lack of perfusion (ischemia) to various organs of sufficient magnitude and duration to produce more than fleeting functional and/or biochemical changes.
It is estimated that around 23% of all newborn deaths are caused by birth asphyxia, with a large proportion of stillbirths.
Asphyxia can occur before, during, or after birth due to various causes e.g maternal placental abruption , umbilical cord prolaps , anemia or shock to the newborn.
Perinatal asphyxia can result in multisystem organ damage in a neonate, like kidneys (50%), central nervous system (28% cardiovascular system (25%) and lungs (23%).Perinatal hypoxic-ischemic encephalopathy (HIE) occurs in one to three per 1000 live full-term births, hypoxia-ischemia in the perinatal period is an important cause of cerebral palsy and associated disabilities in children.
Kidneys are very sensitive to oxygen deprivation and irreversible cortical necrosis may occur due to prolonged renal insufficiency of hypoxic-ischemic episode. Perinatal asphyxia contributes to most of the neonatal renal failure. It may cause alterations in urinary protein excretion.
Acute kidney injury is a complex disorder that occurs with variable severity and in many clinical scenarios. Until recently, lack of universally recognized definition of AKI limited our ability to compare studies predict clinical courses, and improve outcomes.
Summary and conclusion The diagnosis of AKI is problematic, as current diagnoses rely on functional abnormalities; functional changes in serum creatinine [marker of glomerular filtration rate (GFR)] and oliguria. Both these are late consequences of injury and not markers of the injury itself.
Early recognition of renal failure and the implementation of therapies aim at preventing or treating predicable complications .
Biomarkers are currently being explored to differentiate between different causes of established AKI to detect AKI early, and to prognosticate outcomes.
Urinary β2-microglobulin, specific urinary marker of renal tubular damage, can identify renal damage from asphyxia within 48 hours of the insult.
β2 microglobulin is a low molecular weight protein normally filtered readily at the glomerulus and is totally reabsorbed and degraded by proximal tubular cells of the kidney, so elevation of urinary β2 microglobulin is sensitive and reliable early marker of tubular dysfunction.
Neonates with acute kidney injury are at risk of developing chronic kidney disease.
The aim of the present study is to evaluate incidence of renal affection in asphyxiated newborn and to detect renal insult early by measuring urinary β2 microglobulin.
This work included 50 term asphyxiated neonates along with 35 gestation and weight matched normal neonates as controls.
All cases and controls were subjected to the following.