The relationship between disease stage and serum endotrophin levels in autosomal dominant polycystic kidney patients

Aim: Autosomal dominant polycystic kidney disease (ADPKD) is the most common inherited kidney disease. Due to the pressure of renal cysts, endothelial dysfunction, inflammation, and renal damage develop. Endotrophin, a fragment derived from the C-terminal of the α3 chain of collagen type VI, has been shown to be a risk factor for renal fibrosis and the development of chronic kidney damage. In our study, we aimed to evaluate the relationship between serum endotrophin levels in ADPKD patients and total kidney volume (TKV), endothelial dysfunction, inflammation, and cardiac morphology. Material and Method: A total of 70 ADPKD patients (38 female, mean age 45,27±11,4 years) and 55 healthy controls (31 female, mean age 43,1±7,1 years) were included in the study. The ADPKD group was divided into two groups: preserved renal functions (Group 1) and impaired renal functions (Group 2). Carotid artery intimamedia thickness (CIMT), flow-mediated vasodilation (FMD) measurements, and echocardiographic evaluation were performed. TKV of patients were calculated using the manual tracing method on MR images. Endotrophin levels were measured by ELISA. The correlation analysis between endotrophin, TKV, FMD, renal function, echocardiographic parameters, and inflammatory markers was evaluated. Results: Endotrophin levels did not differ statistically significantly between the patients [16,4(14,3-21,2) ng/mL] and the controls [18,2(13,0-48,9) ng/mL] (P= 0,524). FMD was lower in the patient group [6,3% (3,1-10,1)] compared to the control group [9,4% (6,1-17,9)] (P= 0,001). CIMT was statistically significantly higher in the patients (0,65±0,11 mm) compared to the controls (0,53±0,06 mm) (P< 0,001). Left ventricular mass (LVM) and left ventricular mass index (LVMI) were statistically significantly higher in the patients compared to the controls (P< 0,001, P= 0,013 respectively). There was no statistically significant difference in terms of serum endotrophin levels between Group 1 and Group 2 [respectively, 17,3(14,9-22,5) ng/ml, 16,0 (14,1-19,9) ng/ml, P= 0,472]. CIMT was statistically significantly higher inVII Group 2 (0,71±0,12 mm) compared to Group 1 (0,64±0,10 mm) (P= 0,043). There were no differences between two groups according to FMD levels (P= 0,736). TKV was statistically significantly higher in Group 2 [1299,0 (1124,0-2986,0) mm3] compared to Group 1 [933,0 (526,5-1653,0)mm3] (P= 0,044). There were no statistically significantly differences in LVM and LVMI values between the two groups. There was a positive statistically significant correlation between serum endotrophin and CRP (P= 0,038). There was a positive statistically significant correlation between TKV and age and proteinuria (P= 0,017, P= 0,013 respectively), and a negative correlation with glomerular filtration rate (P= 0,002). Conclusion: Serum endotrophin levels increase from the early stages of ADPKD. While there is a positive significant correlation between serum endotrophin levels and inflammation, there is no significant correlation between TKV, cardiac morphology, endothelial dysfunction, and subclinical atherosclerosis. Keywords: Endotrophin, Endothelial Dysfunction, Total Kidney Volume, Autosomal Dominant Polycystic Kidney Disease