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SUMMARY AND CONCLUSIONPatients with end-stage renal disease undergoing HD are exposed to oxidative stress. Increased levels of MDA and 4-HNE were found in plasma of uremic patients indicating accelerated lipid peroxidation (LPO) as a consequence of multiple pathogenetic factors, those highly reactive metabolites are able to bind to protein, Nucleic acids, and other molecules are able to exacerbate tissue and organ damage, e.g. cardiotoxic effect.Renal anaemia was shown to promote oxidative stress. Cardiovascular injury has be shown to be the most critical factor affecting quality of life and mortality in patients with CRF. Oxidative stress has be thought to be an important risk factor for cardiovascular disorder.The work was done to evaluate the level of LPO products (MDA and HNE) in patients with CRF before and after dialysis in relation to Hb level, and lastly in relation to LVH. This study has been conducted on 20 children (8 males and 12 females) suffering from CRF before dialysis (GFR = 10 -30 cc/min/1.73 m2) and 20 children (8 males and 12 females) suffering from CRF after dialysis and EPO therapy for at least 6 months. They were selected from those uremic children attending Haemodilaysis units of Zagazig university hospital as well as Ain shams university Hospital, their age ranged from 4 to 16 years.Control group: contains 20 healthy children of comparable age and sex.We measure the MDA and HNE as marker for lipid peroxidation. We do echocardiocraphy for all subjects.The results show an increase in LPO products in CRF patients as compared with healthy subjects. Also the LPO products correlates with the state of anaemia i.e. the more the renal anaemia the more the LPO products. So correction of renal Anaemia by EPO improves the LPO. We also found that the levels of MDA and HNE significantly decreased after dialysis than before dialysis. Also there is impaired diastolic function by echocardiography in patient with CRF under HD. There is a high significant increase in LVMI, IVSST and LVPWST in CRF children. We can register LVH which may be concentric or eccentric or symmetrical hypertrophy in CRF children.Conclusions:Our experiments leads to the important conclusion that the optimized correction of renal anaemia. That means the complete correction of renal anaemia. Should cause a significant reduction of oxidative stress including lipid peroxidation because the facts known about atherogenesis and cardiotoxicity promoting effects of aldehydic lipid peroxidation products.The correction of renal anaemia will offer Benefits for the reduction of the cardiovascular risk of patients with CRF improving their quality of life and improving the prognosis of renal failure.Recommendations:Proper treatment of CRF anaemia by frequent packed red cell transfusion and EPO may improve outcome and decrease LPO. Improve of LPO will decrease the cardiovascular complication and mortality.Regular echocardiocraphic examination of all patients with end stage renal disease may minimize the cardiac changesFurther study of HD patients to identify other specific uremic toxin behind that cardiac changes.4-HNE is cardiotoxic and can be used as a good marker for severity of cardiac disease in CRF patients.REFERENCESAdamson J, Longo D (2001): anaemia and polycythemia, In: Braunwald E, Fauci AS. Isselbacher K, Kasper DL, Hauser SL, Longo DL, Jameson JL (eds). Harrison’s principles of internal medicine 15th ed McGrow Hill. New York, 1551– -1561.Adamson JW and Eschbach JW (1998): Erythropoietin for end – stage renal disease. N Engl J Med; 339 (9) : 625-627.Akubue PI, Bagchi D, Ihm WJ, Stohs SJ. (1994): Excertion of malondial dehyde, formaldehyde, actaldehyde, acetone and methyl ethylketone in the urine of rats given an acute dose of malondialdehyde. Toxicoogy 1994; 68:338-341.Al-Ezzy YA, AL-Barraq Ao, AL-Hamoty NA,Haza’ak, Thoniasy. AL-saidy FA. (2003): Cardio vascular manifestation in CRF patients on Haemolialysis Saudi Med J. 24(6): 652-5. Department of medicine, Sana’a University, Sana’a Yemen.Andre JL,Bourquard R,Guillemin F, Krier MJ and Briancon S.(2003):Final height in children with chronic renal failure who have not received growth hormone. Pediatric Ne
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