Association of arterial stiffness measured by heart-ankle vascular index with inflammatory and atherosclerotic parameters in autosomal dominant polycystic kidney disease patients

İntroduction Autosomal Dominant Polycystic Kidney Disease is an inherited disease characterized by progressive cyst formation in bilateral kidneys and is one of the common causes of end-stage renal disease. The presence of non-traditional risk factors (inflammation, vascular calcification, etc.) in addition to traditional cardiovascular risk factors in patients with chronic kidney disease leads to higher cardiovascular morbidity and mortality. Recently, the cardio-ankle vascular index (CAVI) has been used as an early predictor of arterial stiffness and cardiovascular disease, independent of blood pressure. In this study, it was aimed to examine the relationship of CAVI with atherosclerotic and inflammatory parameters in hypertensive and normotensive ADPKD patients with preserved renal function. Methods 57 patients with ADPKD (mean age 39.59 years, 61% females) and 26 healthy volunteers followed up in Pamukkale University Faculty of Medicine, Department of Internal Medicine, Nephrology Clinic between October 2021 and March 2022 were included in our single-center prospective study. The CAVI measurement of all subjects included in the study was made with the Fukuda Denshi model VS-1500N device. Following a 12-hour fasting in all patients, FGF-23,s-Klotho, MCP-1, Salusin A, Salusin B, pro-BNP, homocysteine, creatinine (Cr), magnesium, Sodium, Potassium, Phosphorus, uric acid, LDL, HDL, triglyceride, total cholesterol, glucose, albumin, PTH, vitamin D and spot urine microalbumin/Cr ratio were studied. For statistical evaluation, data are provided by SPSS Version 28.0, Inc. Analyzed by the Chicago, IL, USA program. Findings While 29 (50.8%) of the patients with ADPKD were hypertensive, 28 (49.2%) were normotensive, 26 participants were in the healthy group. CAVI measurements were found to be significantly higher in hypertensive (8.19±1.08) and normotensive (7.24±0.86) ADPKD patients compared to the control group (6.38±1.3), respectively (p=0.000; p=0.000). FGF-23 measurements were significantly higher in the ADPKD group (365.6±46.38) compared to the control group (171.04±4.85) (p=0.033). MCP-1 measurements were found to be significantly higher in the ADPKD group (290.46±39.97) compared to the control group (99.95±3.61) (p=0.026). Salusin A was significantly higher in the ADPKD group (562.61±84.14) compared to the control group (201.19±9.73) (p=0.002). Salusin B levels were found to be significantly higher in the ADPKD group (415.12±58.85) compared to the control group (182.28±8.68) (p=0.011). Pro-BNP measurements were significantly higher in the ADPKD group (78.51±10.06) compared to the control group (46.1±8.23) (p=0.026). Homocysteine levels were found to be significantly higher in the ADPKD group (16.45±1.37) compared to the control group (12.81±0.54) (p=0.030). Age, mean blood pressure, CKD-EPI, BUN, creatinine, PTH, Pro-BNP, MCP-1, FGF-23, and Salusin B measurements in patients with a high CAVI score (≥8.0) were compared to patients with a low CAVI score (<8.0) significantly higher (p=0.026, p=0.000, p=0.003, p=0.006, p=0.032, p=0.057, p=0.005, p=0.000, p=0.007, p=0.016, respectively). Results Although CAVI has been found to be high in early-stage normotensive and hypertensive ADPKD patients, it has also been shown that MCP-1, diastolic blood pressure, CKD-EPI and magnesium can be used as markers to predict high CAVI. However, there is a need for multicenter and larger series studies on this subject. Keywords: ADPKD, CAVI, Arterial Stiffness, MCP-1