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العنوان
Urotensin II as a Cardiovascular Outcome Marker in Chronic Kidney Diseases
المؤلف
Mahrose,Hany Kamal Ahmed
هيئة الاعداد
باحث / Hany Kamal Ahmed Mahrose
مشرف / Sawsan Said Hafez
مشرف / Nihal.M. El-Assaly
مشرف / Eman El-Hadidi
الموضوع
Cardiac complications in chronic kidney disease -
تاريخ النشر
2009
عدد الصفحات
125.p:
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
علم الأورام
تاريخ الإجازة
1/1/2009
مكان الإجازة
جامعة عين شمس - كلية الطب - Clinical Pathology
الفهرس
Only 14 pages are availabe for public view

from 125

from 125

Abstract

Chronic Kidney Disease (CKD) is defined as the presence of objective kidney damage and or the presence of glomerular filtration rate of 60 ml /min 1.73 m2 body surface area or less at least 3 month irrespective of the underlying etiology of the for Kidney damage.
Cardiac complications are the major complications of end-stage renal disease. Heart failure, myocardial infarction, and other cardiac events combined are the most commonly reported causes of death in these patients. Known risk factors include hypertension, hyperlipidemia, smoking and diabetes.
Human urotensin-II (U-II) is a cyclic peptide of 11 amino acids, with a molecular weight of ~1,388. U-II has been identified as an endogenous ligand for G-protein coupled receptor 14 (GPR14), which is now known as UT receptor Both U-II and UT receptor are expressed in different tissues, including the cardio vasculature, brain, kidney, atherosclerotic plaques in the coronary and carotid arteries, and abdominal aortic aneurysms.
Urotensin II (U-II) is a vasoactive substance; its vasoactivity depends on the site and caliber of the blood vessels. It leads to V.C on large vessels as pulmonary and large coronaries. But it leads to V.D in the small vessels as the abdominal and skin vessels. There is one exception for the action of UII on the skin vessels, in case of H.F and hypertension only it leads to V.C not a V.D but the cause is still unknown.
U-II may play a key role in the pathogenesis of atherosclerosis by following mechanisms: (a) Increasing the foam cell formation in macrophages by increasing the expression of mRNA transcript and increase the activity of acyl co-A: cholesterol acyl transferase I leading to convertion of the free cholesterol into cholestorl esters. (b) Synergistic effect with some mitogens as oxidized LDL, serotonin and phosphatedyl- choline. (c) Biding with UII receptors of vascular smooth muscles of coronary arteries leading to V.C by contraction and proliferation of vascular smooth muscles.