RELATIONSHIP BETWEEN UROTENSIN II AND CARDIOVASCULAR COMPLICATIONS IN PATIENTS WITH CHRONIC KIDNEY DISEASE

Introduction: Increased cardiovascular (CV) events are common causes of increased mortality in chronic kidney disease (CKD) patients. The aim of our study was to investigate the relationship between urotensin II (UT II) and left ventricular (LV) hypertrophy (LVH), arterial stiffness (AS), and atherosclerosis in predialysis CKD patients. Material and methods: In this cross-sectional study, predialysis stage 3-5 CKD patients who were followed up in the nephrology outpatient clinic and did not receive renal replacement therapy were evaluated. The patients were compared with 55 age and sex-matched healthy control groups with no known comorbidities. The laboratory values, demographic characteristics (gender, age, body mass index), comorbid diseases and antihypertensive drugs of patients were recorded. LV ejection fraction (LVEF), LV end-diastolic diameter (LVEDD), LV end-systolic diameter (LVESD), LVH and LV mass index (LVMI) were determined with M-mode echocardiogram. LVH was labeled when the LVMI was 134 g/m(2) in men and 110 g/m2 in women on echocardiogram. Brachial-ankle pulse wave velocity (baPWV) was used to determine presence of AS and ultrasonographic carotid artery intima-media thickness (CA-IMT) was used to determine presence of atherosclerosis. BaPWV value of =8.1 m/sec was considered as AS development and CA-IMT value of =0.9 mm was considered as development of atherosclerosis. Renal function was determined by; serum creatinine and spot urine protein-creatinine ratio measurement. UT II levels were determined by enzyme-linked immunosorbent assay. Results: The study was performed with 110 (59 stage 3, 40 stage 4, 11 stage 5) patients with predialysis CKD. Increased development of LVH, AS and atherosclerosis and lower plasma UT II levels were observed in patients compared to healthy individuals. No correlation was observed between UT II and renal function in the correlation analysis. Increased development of LVH, AS and atherosclerosis was observed in those with low plasma UT II levels compared to those with high plasma UT II levels. In multivariate analysis, a significant inverse relationship was observed between UT II and development of LVH, AS and atherosclerosis independent of other CV risk factors. Conclusions: The present findings show that low plasma UT II levels can be used as predictors of adverse CV events in predialysis CKD patients.