Abstract

Abstract Background Calcific aortic valve disease (CAVD) is the western world’s leading degenerative valve disease affecting nearly 2% of the general population. Considered for a long time as the result of a passive process, nowadays CAVD is referred as an active process mediated by different cell types and involving several molecular mediators and cellular pathways. Aim of the Study The aim of this study was to investigate the role played by renal function during the progression of CAVD. Materials and Methods – We enrolled 116 patients affected by CAVD from the Cardiology departments of the Treviso Hospital and the High Specialization Rehabilitative Hospital of Motta di Livenza (TV). For each patient at the time of the recruitment a clinical visit was carried out that included the collection of anamnestic, anthropometric and echocardiographic data. Blood samples were collected from each subject at the recruitment to measure the following biochemical parameters: creatinine, lipidic profile, phospho–calcium metabolism. The GFR was estimated by using the CKD–EPI 2009 equation. To investigate the predictive role of renal function in the progression of CAVD, only patients (n = 49) with at least two transthoracic echocardiograms (TTE) were selected for the prospective analysis. These patients were followed for an average of 18.9 ± 11 months. The rate of progression of valvular disease was assessed in terms of difference in indexed valve area per month (ΔAVA/month). Results We observed that fast progressors had a significant reduction of eGFR at baseline as compared to slow progressors (60.62 ± 18.83 ml/min/1.73m2 vs. 77.22 ± 11.46 ml/min/1.73m2, p = 0.001). An increased risk of rapid progression of valvulopathy was found in patients with eGFR < 60 ml/min/1.73m2 (RR = 2.64, IC95%=1.50–4.60, p = 0.001) compared to subjects with normal renal function. A close to significance correlation was also found between values of circulating Pi and ΔAVA/month (r = –0.252, p = 0.084). Conclusions The present study showed that reduction of renal function, and in particular the presence of CKD (eGFR values <60 ml/min/1.73m2), is significantly associated with an increased risk of rapid progression of calcified aortic valvulopathy; this risk is further increased by the concomitant presence of increased levels of phosphatemia. Overall, these data indicate the potential predictive role of eGFR on the risk of accelerated calcific valvulopathy in non–dialysed patients.

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