INFLAMMATION BUT NOT DERANGED MINERAL METABOLISM MAY EXPLAIN THE PROGRESSION OF CORONARY ARTERY CALCIFICATION IN CKD PATIENTS NOT ON DIALYSIS

INTRODUCTION AND AIMS: Coronary artery calcification (CAC) rapidly progress over time. Progression is faster in all stages of chronic kidney disease (CKD); CAC progression is independent predictor of cardiac events. In dialysis patients CAC progression appears associated to deranged mineral metabolism; this association has not been confirmed in CKD-patients not on dialysis. In contrast to dialysis patients, CAC progression is faster in CKD-patients who have lower baseline calcium score and minimally deranged mineral metabolism; this may indicate calcification within plaque more likely increases concomitantly with inflammation process. Aim of study is to evaluate role of inflammation and mineral metabolism on CAC progression in CKD-patients. METHODS: Consecutive male and not pregnant female entered study. Inclusion criteria were: age>18 years, CKD stages 2-5 not requiring dialysis, no less than 6-month follow-up before enrollment, at least two CAC-score measurements. Routine blood chemistry and serum concentrations of calcium, phosphorus, intact parathyroid hormone, homocysteine, C-reactive protein were measured. Key biomarkers of inflammation from Interleukins, TNF superfamily proteins, IFN family proteins and MMPs were assayed. Screening and scoring of CAC was performed by CT. To calculate annual progression of CAC score, following formula was used: last CAC score-baseline CAC score/days of follow-up X 365. Annual progression of CAC score was categorized as: absent (25th percentile), moderate (25th-75th percentiles), accelerated (>75th percentile). Patients were categorized as not-calcified, calcified but not progressors, progressors. RESULTS: Clinical characteristics and biochemistry of patients (n.76) are in table 1 and 2. In multivariate analysis, predictors of CAC presence were IL-6 (Beta: ,272; p=0.05) and IL-7 (Beta: ,311;p=0,04). No markers of mineral metabolism predicted presence of CAC. In multivariable analysis predictors of CAC progression was IL-7 (Beta: 1,02;p=0.001). No markers of mineral metabolism predicted CAC progression. CONCLUSIONS: CAC are present in early CKD stages and progress over time. Presence and progression of CAC are not predicted by markers of mineral metabolism. IL-7 resulted predictor of both presence and progression of CAC. This may indicate that inflammation may play more relevant role than deranged mineral metabolism in calcification process in early CKD stages. This finding should be confirmed by larger study.