P0895the Relationship of Arterial Calcifications in Chronic Kidney Disease Patients With Indirect Anticoagulant Intake and Heart Morbidity

Abstract

Background and Aims In patients with chronic kidney disease (CKD), arterial calcification (AC) is a potential mechanism for the progression of cardiovascular disease. AC is common in CKD patients and is a consequence of mineral-bone disorders. Indirect anticoagulants or vitamin K deficiency lead to matrix γ-carboxyglutamate decarboxylation, which may potentiate vascular calcification formation. The impaired renal function and indirect anticoagulants intake may lead to vitamin K deficiency and increased AC. The aim of this study is to determine if oral intake of Acenocoumarol has influence on abdominal aorta calcium score (AACS) and the AC relation with atrial fibrillation (AF) and / or ischemic heart disease (IHD) morbidity. Method We observe 129 patients with CKD (glomerular filtration rate below 44 ml/min/1,73 m2, MDRD formula calculated). X - ray of the lateral abdominal aorta is performed for the AACS assessment according to L. I. Kauppila et al. method. The assessment of calcium score is formed by the involvement grade of each segment on the anterior and posterior wall of the vessel along the first four lumbar vertebrae. Calcification affecting less than 1/3 of the anterior wall of the aorta along the lumbar vertebral body receives 1 score and calcification extending over ½ of the vertebral body length receives 3 scores (total score - 24). The patients are distributed into three groups: I group with calcium score from 0 to 7, II - from 8 to 15 and III group - from 16 to 24. The data from assessed AACS are compared with Acenocoumarol intake and the presence/absence of AF and/or IHD. The results are processed with χ2 statistical analysis. Results One hundred twenty nine patients with CKD (95 males and 34 females) are included in the study. The patients data (mean, percentages, degrees, etc.) are summarized in tabl.1 and tabl. 2. Clinically significant is the correlation between the grades of AACS and Acenocoumarol intake (p < 0,05). With the calcium score increasing, the patients percentage treated with Acenocoumarol also increases (fig. 1). There is a moderate correlation (Cramer’s coefficient is 0,39) between the AACS grades and heart morbidity from AF and / or IHD (p < 0,05). The data shows that the higher calcium score is related with increased patients percentage with AF and / or IHD morbidity (fig. 2). In our study, vascular calcifications are found in the abdominal aorta walls in all of the observed patients. We found that a higher AACS is associated with an Acenocoumarol intake in CKD patients and corresponds to an increased morbidity of AF and / or IHD. Acenocoumarol intake may lead to increased AACS. The higher calcium score is associated with a higher incidence of AF and / or IHD morbidity. Conclusion The study outcome supported the hypothesis that the increased AC formation and cardiovascular morbidity high risk could be a reason for the limited vitamin K antagonists (acenocoumarol) use in CKD patients. Furthermore, vitamin K2 supplementation is reasonable and may reduce the progression of AC.