الفهرس 
Amino AcidsOnly 14 pages are availabe for public view
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Abstract
Increased cardiovascular mortality and morbidity is well recognized in adults with CRF. The adverse impact of CRF on cardiovascular mortality and morbidity in the young is however even greater with a 500 times higher rate of cardiovascular deaths than a control population. The initiation of vascular damage begins very early during the course of CRF, and involves the vascular endothelium. L-arginine has been used to improve endothelial function by increasing NO bioavailability.
The aim of this work was to detect the abnormalities in plasma amino acids in pediatric patients with CRF on regular hemodialysis. Assessment of the vascular function in children with CRF following oral L-arginine supplementation. And aassessment of the vascular function in children with CRF and correlate it with L-arginine aminoacid.
This study was conducted on 21 CRF patients (12 males and 9 females). Their age ranged from 5 - 18 years with a mean value of 13.99 ± 2.794) on regular hemodialysis 3 times / week for at least 6 months at the Pediatric Nephrology Unit, Children’s Hospital, Ain Shams University, Cairo, Egypt, during the period from April 2008 to February 2009.
A control group included 13 age and sex matched healthy children (6 males, and 7females). Their age ranged from 5.5 - 18 years with a mean value of 12.15 ± 3.721.
All children enrolled in the study were subjected to history taking, physical examination, and laboratory investigations including determination of serum calcium, phosphate, alkaline phosphatase, albumen, complete blood count, createnine (for the controls only) and amino acid analysis. Evaluation of the vascular function by measuring brachial artery basal flow, EDD and ENDD.
In the 2nd part of the study, all patients with low L-Arginine (< 44 umol/L) were supplemented with oral L-Arginine (2 gm daily for 1 week was given). The vascular function was reassesed to determine if L-arginine supplementation had an effect on the vascular function in HD children.
Results of our study showed that HD patients had a significantly lower concentration of threonine, valine, methionine, leucine, tyrosine, phenylalanine and tryptophane than the control group. HD patients had lower mean L-arginine levels than the mean of the controls with no significant difference.
L-arginine concentration was not significantly different between HD patients with and without history of thromboembolic manifestations. HD patients without history of thromboembolic manifestations had significantly higher basal brachial artery flow, phenylalanine concentrations and lower glutamic acid concentrations than HD patients with history of thromboembolic manifestations. There was no significant difference between them as regard EDD or ENDD.
There was no significant difference between HD patients with low arginine and with normal arginine as regard basal, EDD or ENDD. Moreover, oral L-arginine supplementation did not significantly improve brachial artery basal flow, EDD and ENDD in HD children with low L-arginine after supplementation.
HD patients with low arginine concentration had significantly lower concentrations of tyrosine and phenylalanine amino acids than those with normal arginine concentration.
from the present study it can be concluded that several abnormalities in AA were present in HD patients compared to controls. HD patients without history of thromboembolic manifestations had significantly higher basal brachial artery flow, higher phenylalanine concentrations and lower glutamic acid concentrations than HD patients with history of thromboembolic manifestations. There was no significant change in basal brachial artery flow, EDD and ENDD after L-arginine supplementation to HD children with low L-arginine.
from this study we recommend measuring the basal brachial artery flow, glutamic acid and phenylalanine concentration as an indicator for HD patients with risk of thrombosis. we also recommend the conduction of a trial giving L-arginine in different doses and durations, and mutistep trial aiming at normalization of the different risk factors implicated in endothe lial dysfunction.