The partnership between renalase and ejection fraction as a risk factor for increased cardiac remodeling biomarkers in chronic heart failure patients. (2nd June 2020)

• Record Type: Journal Article
• Authors: Stojanovic, Dijana; Mitic, Valentina; Stojanovic, Miodrag; Petrovic, Dejan; Ignjatovic, Aleksandra; Stefanovic, Nikola; Cvetkovic, Tatjana; Kocic, Gordana; Bojanic, Vladmila; Deljanin Ilic, Marina
• Is Part Of: Current medical research and opinion. Volume 36:Number 6(2020)
• Page Start: 909
• Page End: 919
• Publication Date: 2020-06-02
• Subjects: Renalase -- cardiac remodeling biomarkers -- BNP -- heart failure -- EF; Clinical medicine -- Periodicals; Therapeutics -- Periodicals; 615.5
• DOI: 10.1080/03007995.2020.1756233
• Languages: English
• ISSNs: 0300-7995

Abstract

Abstract: Objective: Heart failure (HF) represents a huge socio-economic burden. It has been demonstrated, experimentally, that renalase, a newly discovered protein, prevents cardiac hypertrophy and adverse remodeling, which is seen in HF. We postulated the following aims: to investigate associations of renalase with biomarkers of cardiac remodeling: galectin-3, soluble suppression of tumorigenicity, (sST2), growth differentiation factor 15 (GDF-15) and syndecan-1, myocardial stretch (BNP) and cardio-renal axis (cystatin C) in HF patients with reduced ejection fraction (HFrEF) and preserved ejection fraction (HFpEF) to determine whether renalase, in combination with left ventricular ejection fraction (LVEF), represents a risk factor for plasma elevation in biomarkers. Methods: We classified HF patients ( n = 76) according to LVEF (preserved/reduced), applied a median plasma renalase (113 ng/mL) as a cut-off value (low/high) and created four subgroups of HF patients: HFpEF/low renalase ( n = 19), HFrEF/low renalase ( n = 19), HFrEF/high renalase ( n = 32) and HFpEF/high renalase ( n = 6). A control group ( n = 35) consisted of healthy volunteers. Results: Plasma concentrations of evaluated biomarkers were determined using an ELISA technique and were highest in HF patients with reduced EF ( p < .001, respectively), and renalase's positive correlations were obtained relating to all biomarkers: galectin-3 ( r = 0.913; p < .001), sST2 ( r = 0.965; p < .001), GDF-15 ( r = 0.887; p < .001), syndecan-1 ( r = 0.922; p < .001), BNP ( r = 0.527; p < .001) and cystatin C ( r = 0.844; p < .001) and strong and negative correlation with LVEF ( r = −0.456, p < .001). Increased renalase, regardless of the EF (preserved/reduced), was shown to be an independent risk factor for an increase in all evaluated cardiac remodeling biomarkers, p < .001, respectively. However, increased renalase and reduced EF was the only independent risk factor for BNP and cystatin C elevation, p < .001, respectively. Results after multivariable adjustments (age/gender) were identical. Conclusion: When elevated plasma renalase and HF are present, regardless of EF being reduced or preserved, that represents a significant risk factor for increase in cardiac remodeling biomarker plasma concentrations. However, only elevated renalase and reduced EF demonstrated significance as a risk factor for BNP and cystatin C plasma elevation. Renalase may be considered a promising molecule for the improved predictive abilities of conventional biomarkers and is worthy of further investigation.