Abstract

More than half of deaths among hemodialysis patients are due to cardiovascular disease. This study examined whether intravenous administration of ferric carboxymaltose (FCM) has an impact on cardiovascular events in iron-deficient hemodialysis patients. We performed a retrospective study concerning patients undergoing hemodialysis in our center from September 2016 to December 2019. We identified those who began FCM therapy (FCM group) during this period and those who did not (control group). We analyzed clinical, echocardiographic and laboratory parameters at the beginning (t0) and after one year (t1), to detect differences between the two groups. We identified 53 patients for the FCM group and 19 for the control group. Median follow-up was 1 year±3 months for both groups. In the FCM group, we observed a reduction in the doses of erythropoiesis-stimulating agents (ESA) (p<0.001) and a significative difference in cardiovascular events (p<0.01), but no differences in echocardiographic parameters. Patients who received FCM reached satisfactory values of transferrin saturation and ferritin, presented fewer coronary artery events and cardiovascular events, and could reduce doses of ESA.

Highlights

  • Patients with end stage renal disease (ESRD) are among the highest risk populations for cardiovascular disease (CVD)

  • We analyzed the effects of intravenous ferric carboxymaltose (FCM) on the anemia profile and whether it had an impact on the reduction of cardiovascular events (CVE) in our HD population, on reducing erythropoiesis-stimulating agents (ESA)

  • We split our population into two groups: the study group (53 patients) that received FCM and the control group (19 patients) that did not receive iron replacement therapy for clinical reasons

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Summary

Introduction

Patients with end stage renal disease (ESRD) are among the highest risk populations for cardiovascular disease (CVD). In anemic patients with chronic kidney disease (CKD), iron replacement is an established part of disease management, resulting in increased hemoglobin levels, decreased concomitant therapy with erythropoiesis-stimulating agents (ESA), and stabilized renal function [5,6,7]. According to a few studies, ID directly affects human cardiomyocyte function, impairing mitochondrial respiration, and reducing contractility and relaxation; restoration of intracellular iron levels can reverse these effects [13, 14]. We analyzed the effects of intravenous FCM on the anemia profile and whether it had an impact on the reduction of CVE in our HD population, on reducing ESA dose or on determining some cardiac modifications in a period of one year

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