Renal artery stenosis and mean platelet volume
1Departments of Cardiology, Faculty of Medicine, Bülent Ecevit University; Zonguldak- Turkey
2Radiology, Faculty of Medicine, Bülent Ecevit University; Zonguldak- Turkey
3Department of Cardiology, Karadeniz Ereğli State Hospital; Zonguldak- Turkey
4Department of Cardiology, Çaka Vatan Hospital; Kahramanmaraş- Turkey
Anatol J Cardiol 2016; 16(3): 197-201 PubMed ID: 26467381 PMCID: 5336806 DOI: 10.5152/AnatolJCardiol.2015.6102
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Abstract

Objective: Increased mean platelet volume (MPV) has been reported in various atherosclerotic diseases. The aim of our study was to investigate the relationship between the atherosclerotic renal artery stenosis (ARAS) and various hematological parameters including MPV.
Methods: This study was performed with a retrospective review of the angiographic images of patients who underwent renal angiography at Bülent Ecevit University catheter laboratory between January 2004 and December 2009. The patients were trichotomized into three groups based on the presence and severity of renal artery stenosis (RAS). Group 1 included patients with a critical RAS (33 patients; 18 female (F), 15 male (M); mean age 61.6±11.5 years), group 2 consisted of patients with non-critical RAS (26 patients; 15 F, 11 M; mean age 58.1±11.3 years), and group 3 was composed of patients without RAS (69 patients; 38 F, 31 M; mean age 53.5±11.9 years). Demographic data, complete blood count, and biochemical parameters were compared between the groups.
Results: Comparison of the hematological parameters revealed that MPV and platelet distribution width were significantly higher in group 1 than in group 2 and 3 (8.96±0.99 fL versus 8.35±0.76 fL, 8.31±0.79 fL, respectively; p=0.001; 16.53±0.58% versus 16.19±0.56%, 16.29±0.53%, respectively; p=0.04).
Conclusion: MPV levels are higher in patients with ARAS. Considering both the effect of platelets on atherosclerosis and their close association with other risk factors, MPV level may be an important factor in pathogenesis of ARAS. (Anatol J Cardiol 2016; 16: 197-201)