Indexed on: 21 Jul '11Published on: 21 Jul '11Published in: Comparative Clinical Pathology
Vascular calcifications are recognized as important risk factors for uremia-induced cardiovascular disease. Yet some patients with chronic kidney disease (CKD) do not develop calcification despite exposure to the same uremic conditions. Physiological inhibitors of calcification such as fetuin A, which is an extraosseous calcification inhibitor, and osteoprotegerin (OPG), which is a regulator of bone resorption, may prevent the development and progression of vascular calcification. The aim of this work is to study the serum levels of fetuin A and OPG to understand their role in vascular calcification in patients with chronic renal impairment. A total of 80 subjects (60 CKD patients and 20 age- and sex-matched healthy controls) were studied. Fetuin A and osteoprotegerin were measured by ELISA; in addition to standard biochemical analysis, ECG and echocardiography were done to evaluate cardiovascular calcification. Fetuin A levels were significantly lower; OPG levels were significantly higher in the patients group compared to the controls. There was an inverse association between fetuin A and vascular calcifications in the patients group (P = −0.498, r = −0.001), while OPG showed a positive association (P = 0.510, r = 0.003). Serum fetuin A and osteoprotegerin levels were related to vascular calcification in CKD stages III, IV, and V. Decreased serum fetuin A may have a role in enhancing the cardiovascular morbidity and mortality in those patients by promoting a process of accelerated vascular calcification; elevated serum OPG levels increase with the progression of CKD, so these can be used as markers in the follow-up of those patients.