Association of Urotensin-II with factors influencing atherogenesis in patients with chronic kidney disease

In this study, we investigated the relationship of plasma urotensin-II with cardiovascular risk factors, whether traditional or specific to chronic kidney disease, and with ADMA, homocystein and CRP, which may have an influence on those risk factors. 109 CKD patients (30 stage-3, 33 stage-4, 46 stage-5 ) and 35 healthy controls were included in the study. Serum ADMA, homocystein, CRP and plazma urotensin-II levels were measured and ultrasonographic carotid artery intima-media thickness, which has been accepted as a marker of atherosclerosis, were determined in all participants. Frequencies of nonparametric risk factors and levels of parametric risk factors were measured.We found that carotid artery intima-media thickness was significantly higher in stage 4 and 5 patients compared to stage 3 and controls and also in stage 5 compared to stage 4. Urotensin-II levels were lower in stage 3 and 5 patients compared to controls. Homocystein levels were higher in all stages of CKD, CRP in stage 5 and ADMA in stage 4 compared to control group. There was no significant correlation between urotensin-II and ADMA, CRP, homocystein and CIMT. In stage 5, CIMT of patients with hyperlipidemia were higher and Urotensin-II levels were lower in patients with a history of cardiovascular disease compared to patients without these comorbidities. Phosphate levels and calcium-phosphate product were correlated with ADMA and CRP, triglycerides wih CIMT and urotensin-II, hemoglobin with urotensin-II and CRP in stage 5 patients.In conclusion, CIMT and ADMA, CRP and homocystein levels are increased while U-II levels are decreased in renal dysfunction. This decline, in parallel with an increased rate of cardiovascular accident history, may suggest a protective role for U-II in these patients. Presence of anemia, higher CRP levels, lower BMI and serum albumin and impaired calcium and phosphate metabolism, may indicate that the interplay of uremia and inflammation sets the ground for cardiovascular diseases in dialysis patients.