الفهرس 
Material and methodsOnly 14 pages are availabe for public view
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Abstract
Renal impairment in the neonates usually occurs following complicated
labor and delivery with perinatal hypoxia, and it is usually in form of tubular
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insult.
SUMMARY
The clinical presentations of renal impairment in neonates is often
subtle, lack of recognition of its occurrence has made this especially true
when renal impairment follows perinatal anoxia.
In this work 24 neonates (13 males + 11 females), who suffered
perinatal asphyxia and needed admission to the neonatal intensive care unit,
were studied for occurrence of acute renal impairment.
12 normal infants were included in the study as controls.
Mean patients serum urea was (72.94 + 43.24 mg/dl) which was not
significantly different than that of controls (58.32 ± 52.91 mgldl) which may
be due to small number of the patients.
Mean serum creatinine of patients (1.7 + .88 mgldl) was significantly
higher than that of the controls (0.7 + 0.33 mg/dl).
Mean serum Na in patients (141.6 + 2.49 meq/l) was not significantly
in value but lower than controls (142.81 ± 2.48 meq/l).
The possible development of inappropriate secretion of antidiuretic
hormone in perinatal hypoxia often results in hyponatremia which is not
recognized in our patients may be due to small number of patients.
The present study revealed mild hyperkalemia in asphyxiated newboru
as compared to healthy controls in mean.
Mean serum K in patients (4.98 ± .66 meq/l) was not significantly
higher than that of the controls (4.1 ± .51 meqll).
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Mean serum CL in patients (110.0 + 3.50 meq/l) did not differ
significantly from that of the controls (110.36 + 5.08 meq/l).
Routine urinalysis of cases with perinatal hypoxia revealed proteinuria
in 41.7% in patients.
Many epithelial cells were found in 53.5% ofthe cases with perinatal
asphyxBiaa. sed on the findings of the pathological sediment in the urine it is
postulated that renal lesions are common as a result of perinatal asphyxia with
tubular insult.
Mean urine analysis for R.B.Cs of patients (6.33 RBCsIHP
F
+ 4.02
RBCsIHP
F
) which was significantly higher than that of controls (
4
.16
RBCsIHPF ± 2.69 RBCsIHPF).
Mean urine analysis for pus cells of patients (2.84 pus cellsIHPF ± 1.59
pus cellslHPF) which was not significantly different than that of controls
(3.08 pus cellsIHPF + 3.87 pus cellsIHPF).
Mean urinary B2 micro globulin concentration in patients (218.30 ng/mI
+ 100.93 ng/
ml
) was significantly higher than that of controls (144.316 ng/
ml
+ 126.3 ng/
ml
) which is specific for tubular renal insult in renal impairment.
Mean urinary urea in patients was (7.727 ± 3.16 meq/I) which was not
significant in relation to controls 96.80 ± 2:907 meq/l).
Mean urinary creatinine in patients was (1.30 ± 1.4 meq/l) which was
not significantly different than controls (1.22 ± 1.09 meq/l).
Based on the findings of the pathological laboratory and sediment in
the urine it is postulated that renal lesions are in form of tubular insults as a
result of perinatal asphyxia.
Among the clinical symptoms of the studied newborns, renal
impairment in the form 0’ tubular insult was detected more significallyin
cases with asphyxiated newborn.
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CONCLUSION AND RECOMMENDATIONS
The results of the present study suggested that renal impairment in form
of tubular insult should be anticipated in any hypoxic newborn infant.
An early assessment of serum creatinine and B2 micro globulin
concentration levels in urine should be performed in every newborn who
sustained - perinatal anoxia.
Elevated senun creatinine and urinary B2 micro globulin concentration
were detected in cases of perinatal asphyxia.
lt is essential that fluid restriction should be done on the first day or
two oflife to avoid fluid over load.
Appearance and composition of urine should be detennined routinely in
all hypoxic infants. Presence of epithelial cells, RBCs, albumin is indicative
of perinatal hypoxic renal insult.
Perinatal hypoxia is an important differential diagnosis 111 cases
presenting with pyuria in the newborn period.
During resuscitation, oxygenation and correction of acidosis should be
/-prompt.
Prevention and early detection of perinatal anOXia are the two
•
cornerstones on which .successful therapy of renal impairment is based.
The clinician should be aware that any infant experiencing severe
perinatal anoxia and any infant requiring·· admission to a neonatal intensive
care center is at risk for the development of renal insult in the form of tubular
insult.