BACKGROUND: Patients with chronic kidney disease (CKD) show a risk of cardiovascular death, which is 10-100 times higher than that in the general population. This increase is not completely explained by the traditional cardiovascular risk factors. Hyperuricemia and hyperhomocysteinemia are highly prevalent in CKD. Patients suffering from these complications present accelerated atherosclerosis, determined mainly from the endothelial dysfunction that carries out a central role in the pathogenesis of cardiovascular diseases.AIM: The hypothesis was that brachial artery flow mediated dilation (FMD) and carotid intima-media thickness (cIMT) evaluation can be considered as early and systemic markers of atherosclerosis and that nontraditional risk factors, such as hyperhomocysteinemia and hyperuricemia, are associated with early endothelial dysfunction and vascular damage in patients suffering from first-and second-stage CKD.PATIENTS AND METHODS: The study comprised 50 patients, 10 for each CKD stage, and 15 age-and sex-matched healthy controls. We compared the traditional and nontraditional factors for cardiovascular diseases with alterations of vascular reactivity, such as cIMT, and brachial artery FMD, in patients affected by CKD with those in the control group.RESULTS: In our study, hyperuricemia was significantly and independently associated with brachial artery FMD reduction (p = 0.007), while hyperhomocysteinemia was significantly and independently associated with carotid intima-media thickening (p = 0.021) in patients at Stage I and II KDOQI (Kidney Disease Outcomes Quality Initiative).CONCLUSIONS: In our study, we found a progressive increase in the inflammatory indices and endothelial dysfunction at the early stages of CKD. Hyperuricemia and hyperhomocysteinemia were associated with IMT and FMD at Stage I-III KDOQI, and can be used as markers of subclinical atherosclerosis, especially in nephropathic patients with high cardiovascular risk.

Uricemia and homocysteinemia: nontraditional risk factors in the early stages of chronic kidney disease - Preliminary data

Innico, G;
2014

Abstract

BACKGROUND: Patients with chronic kidney disease (CKD) show a risk of cardiovascular death, which is 10-100 times higher than that in the general population. This increase is not completely explained by the traditional cardiovascular risk factors. Hyperuricemia and hyperhomocysteinemia are highly prevalent in CKD. Patients suffering from these complications present accelerated atherosclerosis, determined mainly from the endothelial dysfunction that carries out a central role in the pathogenesis of cardiovascular diseases.AIM: The hypothesis was that brachial artery flow mediated dilation (FMD) and carotid intima-media thickness (cIMT) evaluation can be considered as early and systemic markers of atherosclerosis and that nontraditional risk factors, such as hyperhomocysteinemia and hyperuricemia, are associated with early endothelial dysfunction and vascular damage in patients suffering from first-and second-stage CKD.PATIENTS AND METHODS: The study comprised 50 patients, 10 for each CKD stage, and 15 age-and sex-matched healthy controls. We compared the traditional and nontraditional factors for cardiovascular diseases with alterations of vascular reactivity, such as cIMT, and brachial artery FMD, in patients affected by CKD with those in the control group.RESULTS: In our study, hyperuricemia was significantly and independently associated with brachial artery FMD reduction (p = 0.007), while hyperhomocysteinemia was significantly and independently associated with carotid intima-media thickening (p = 0.021) in patients at Stage I and II KDOQI (Kidney Disease Outcomes Quality Initiative).CONCLUSIONS: In our study, we found a progressive increase in the inflammatory indices and endothelial dysfunction at the early stages of CKD. Hyperuricemia and hyperhomocysteinemia were associated with IMT and FMD at Stage I-III KDOQI, and can be used as markers of subclinical atherosclerosis, especially in nephropathic patients with high cardiovascular risk.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11577/3378163
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