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  • Title: Serum and tissue endothelin-1 are independent from intima-media thickness of peripheral arteries in patients with chronic kidney disease.
    Author: Nezami N, Sepehrvand N, Mirchi M, Salari B, Shokouhi B, Ghojazadeh M, Naghavi-Behzad M, Ghorashi S, Mirzaie F, Noshad H, Zomorrodi A, Gharedaghi A, Babapoor-Farrokhran S, Mirbagheri S, Tarzamni MK.
    Journal: Vascular; 2015 Aug; 23(4):382-90. PubMed ID: 25245046.
    Abstract:
    AIM: We aimed to study the relationship of peripheral arteries' atherosclerosis with serum and tissue endothelin-1 in chronic kidney disease patients. METHODS: Ninety patients were enrolled, including 35 patients with chronic kidney disease (case group), 31 patients with coronary artery diseases who were candidates for coronary artery bypass grafting (positive control group), and 24 living kidney donors (negative control group). Intima-media thickness of the common carotid and femoral arteries was determined by ultrasonography. Serum and tissue endothelin-1 were measured by ELISA method. RESULTS: The mean serum and tissue endothelin-1 levels in the donor group were significantly lower than other groups (p < 0.001 for both). The coronary artery bypass grafting group had higher carotid and femoral intima-media thickness than other groups (p < 0.001), and the chronic kidney disease group had higher carotid and femoral intima-media thickness than the donor group (p < 0.001). Regression analysis in all groups did not reveal any correlation between the carotid intima-media thickness/femoral intima-media thickness and the serum/tissue endothelin-1. There was a direct linear correlation between the carotid and femoral intima-media thickness (p < 0.001) in all groups. CONCLUSIONS: Endothelin-1 level and intima-media thickness were higher in the chronic kidney disease patients and coronary artery bypass grafting candidates, without any correlation between endothelin-1 and peripheral arteries' intima-media thickness of both groups. Perhaps endothelin-1 rises and remains high upon endothelial damage and initiation of atherosclerosis.
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