Platelet activating factor acetylhydrolase is associated with cardiac valvular calcification in dialysis patients

Author:

Bolat Serkan1ORCID,Fidancı Vildan2ORCID,Elçik Deniz3ORCID,Kavraz Tomar Özdem4ORCID,Murat Sani Namık5ORCID,Duranay Murat6ORCID,Yücel Doğan7ORCID

Affiliation:

1. Department of Medical Biochemistry , 63986 Sivas Cumhuriyet University Faculty of Medicine , Sivas , Türkiye

2. Department of Medical Biochemistry, University of Health Sciences , 64082 Ankara Training and Research Hospital , Ankara , Türkiye

3. Department of Cardiology , 52958 Erciyes University Faculty of Medicine , Kayseri , Türkiye

4. Department of Internal Medicine , 187438 Giresun University Faculty of Medicine , Giresun , Türkiye

5. Department of Cardiology, University of Health Sciences , 64082 Ankara Training and Research Hospital , Ankara , Türkiye

6. Department of Nephrology, University of Health Sciences , 64082 Ankara Training and Research Hospital , Ankara , Türkiye

7. Department of Medical Biochemistry , 518003 Lokman Hekim University Faculty of Medicine , Ankara , Türkiye

Abstract

Abstract Objectives The cardiovascular mortality risk is greatly increased in patients with chronic kidney disease (CKD), especially in dialysis patients, due to atherosclerosis. Platelet activating factor acetylhydrolase (PAF-AH) is an enzyme that hydrolyzes platelet activating factor (PAF). Valvular calcifications and PAF-AH are associated with atherosclerosis. However, little is known about the status of PAF-AH activity and valvular calcification in dialysis patients. Therefore, the aim of this study was to investigate the status of these parameters in CKD patients. Methods This study included 92 chronic renal failure (CRF) (dialysis group), and 86 CKD patients (non-dialysis group). Echocardiography was performed to assess valvular calcification. Results There was no significant difference between the dialysis and CKD groups in terms of PAF-AH activities. However, when comparisons were stratified according to the presence of valve calcification, higher PAF-AH activity and N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were evident in patients with calcification compared to those without. Additionally, the CRF group also exhibited elevated PAF-AH and NT-proBNP levels. While elevated NT-proBNP persisted in the CKD group, in contrast, changes in PAF-AH were not significant. Conclusions The results of this study suggest that high PAF-AH and NT-proBNP levels are associated with valvular calcification in dialysis patients. Both biomarkers may be used as a risk factor for calcification. Furthermore, inhibition of PAF-AH activity may be a treatment target to reduce calcification.

Publisher

Walter de Gruyter GmbH

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