The relationship of serum salusin α and β level with subclinic athosclerosis in autosomal domi̇nant polycysti̇c ki̇dney di̇sease

Introduction: Endothelial dysfunction and atherosclerosis secondary to renal parenchymal and vascular compression of cysts are the most important factors determining disease progression in autosomal dominant polycystic kidney disease (ADPKD). Salusin α and β are biomolecules that have an important role in the process of atherosclerosis. In this study, we aimed to evaluate the relationship between serum salusin levels and atherosclerosis, endothelial dysfunction and cardiac morphology in ADPKD. Material and Method: The study was started after the approval of the local ethics committee (date and no: 19.06.2019-18). Eighty three patients with ADPKD who did not receive renal replacement therapy and 53 healthy controls were included in the study. Salusin α and β levels measurement were performed by ELISA method. Echocardiography, flow-mediated vasodilatation (FMD) and Carotid Artery Intima-Media Thickness (CIMT) measurements were performed in all of the patient and control group. The relationship between salusin α and β levels with FMD, CIMT, echocardiographic and inflammatory parameters (CRP and absolute neutrophil count/absolute lymphocyte count (NLR)) was evaluated by correlation analysis. Results: Serum salusin α was found to be statistically significantly lower in the patients compared to the controls [2,64 (1,83-3,30 pg/mL, 3,19 (2,38-6,79) pg/mL, P=0,002, respectively], and the salusin β/α ratio was higher [2,81(2,30-3,54), 2,57(1,90-3,19), respectively, P=0,041]. Salusin β was not different between the patient and control groups. In the patient group, the percentage of FMD was statistically significantly lower [6±0.5% and 8±0.5%, respectively (P= 0,008)], and CIMT was higher (0.63±0.17 mm, 0.53±0.07 mm, respectively P< 0,001) than the controls. According to their renal functions, the patient group was divided into two groups as GFR≥60 ml/min/1.73 m2, Group 1 and GFR=59-15 ml/min/1.73 m2, Group 2. Salusin α levels were 2,31 (1,73-3,24) pg/mL in Group 2, 2,72 (1,94-3,32) pg/mL in Group 1, and 3,20 (2,55-7,87) pg/mL in the controls. Salusin α levels of Group 1 and 2 were statistically significantly lower than the controls (P= 0,003). Serum salusin α levels were not different between Group 2 1and 1 (P= 0,504). The serum salusin β and β/α ratio were not different between the groups (P=0,225, P=0,428, respectively). LAD and LVMI were higher and the E/A ratio was lower (P<0,001) in Group 2 compared to the controls and Group 1 (P=0,012, P=0,035, respectively). There was a positive correlation between salusin α and E/A ratio in correletion analysis. In the ROC analysis, NLR was statistically significant in the differentiation of ADPKD and the control group. Discussion: Antiatherogenic capacity decreases in ADPKD from the early stage of the disease. Subclinical atherosclerosis and endothelial dysfunction develops from the early stage of ADPKD. In the advanced stage of the disease, cardiac morphology changes and left ventricular mass increases Keywords: Autosomal dominant polycystic kidney disease, Salusin α, Salusin β, Subclinical atherosclerosis, Endothelial dysfunction