Vascular calcification is not related to serum fetuin-A and osteopontin levels in hemodialysis patients

Abstract

Introduction: Vascular calcification (VC) in hemodialysis (HD) patients is a sign of severe cardiovascular disease and can predict cardiovascular outcomes. Fetuin-A and osteopontin (OPN) inhibit VC. Serum fetuin-A levels are lower in patients with end-stage kidney disease (ESKD) and in those who are on chronic HD therapy. However, there are limited data concerning OPN in patients who are on dialysis. The aim of our study was to determine VC in HD patients, the relationship between VC and 25-OH-vitamin D, fetuin-A, and OPN levels, and independent predictors of VC. Materials and methods: Ninety-three patients with ESKD on HD therapy were recruited. Among these patients, 44 were male and 49 were female. The patient group was compared with a group of 20 healthy controls of similar age and sex. A plain radiograph of the hand was taken using a mammography machine for the evaluation of VC. Serum fetuin-A, OPN, and 25-OH-vitamin D levels of both patients and controls were measured. Results: VC was detected in 45 (48.4%) HD patients. When patients were compared with healthy controls, fetuin-A levels (p < 0.029) were significantly lower in patients, whereas OPN (p < 0.000) and VC (p < 0.002) were significantly higher in the patient group. Age [odds ratio (OR) 1.036], the presence of diabetes mellitus (DM) (OR 17.527), and high parathyroid hormone (PTH) levels (OR 1.002) were independent predictors of VC in a logistic regression model including the following factors: age, the presence of DM, HD duration, and serum albumin, phosphate, PTH, 25-OH-vitamin D, fetuin-A, OPN, and calcium levels. No significant correlation was found between patients with VC and patients without VC in terms of fetuin-A, OPN, and 25-OH-vitamin D levels. Conclusions: VC is a frequent sign in patients undergoing HD and is not related to serum fetuin-A and osteopontin levels. Age, the presence of DM, and high PTH levels were independent predictors of VC in patients undergoing HD. Further studies are warranted to understand the mechanism underlying and the factors contributing to VC.