Associations of the inhibitory and stimulatory factors of vascular calcification with arterial stiffness in chronic kidney disease patients

Associations of the Inhibitory and Stimulatory Factors of Vascular Calcification with Arterial Stiffness in Chronic Kidney Disease Patients Background: Patients with end-stage renal disease treated by hemodialysis have an impressive mortality, and more than half of this mortality is attributable to cardiovascular disease. It is thought that apart from traditional risk factors; uremia-related risk factors also play an important role for the development of cardiovascular disease. Arterial stiffness and vascular calcification, independent and strong predictors of cardiovasclar risk, are often found in hemodialysis patients. The aim of the present study was to investigate the associations of the inhibitory and stimulatory factors of vascular calcification with arterial stiffness in hemodialysis patients. Methods: Eighty patients with moderate to severe SHPT were enrolled into the study. All patients had normalized total serum calcium concentration < 10.5mg/dL, serum Ca × P<75 and PTH level ≥ 300pg/ml at the begining of follow-up period. Co-morbidities, traditional cardiovascular risk factors, inflammatory markers and mineral-bone disease serology parameters were also recorded We measured pulse wave velocity (PWV) reflecting arterial stiffness as well as serum levels of inhibitory and stimulatory markers of vascular calcification. Results: Patient groups were as follows; paricalcitol group (n: 40) and calcitriol group (n: 40). Demographical, clinical and biochemical characteristics were similar at basal evaluation. We observed significantly superior control of PHT, less hyperphosphatemia and elevated CaxP level and interruption vitamin D treatment in paricalcitol group. FGF-23 and osteocalcin levels were significantly lower and Klotho, Fetuin A and 25(OH)D3 levels were significantly higher in paricalcitol group compared to calcitriol group. There was no significant change in pulse wave velocity measurement in paricalcitol group, while PWV significantly increased in calcitriol group during the follow-up period (p<0.002). In multilinear regression analysis FGF-23 was independently associated with percentage change of PWV (p<0.004). Conclusion: We observed that, compared with calcitriol therapy, paricalcitol therapy reduced the PTH concentrations more effectively without causing hyperphosphatemia and elevated CaxP and might have a substantial beneficial effect on the development of vascular calcification.