Sharp rises in FGF23 and hypophosphatemia after intravenous iron administration do not cause myocardial damage
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LETTER TO THE EDITORS
Sharp rises in FGF23 and hypophosphatemia after intravenous iron administration do not cause myocardial damage Vincent Brandenburg1 · Gunnar H. Heine3 · Nikolaus Marx2 · Robert Stöhr2 Received: 4 December 2019 / Accepted: 10 March 2020 © The Author(s) 2020
Sirs: Current guidelines recommend intravenous iron replenishment (specifically by ferric carboxymaltose [FCM]) in iron-deficient patients with heart failure and reduced ejection fraction (HFrEF). We have previously shown that the administration of FCM in HFrEF patients with normal kidney function leads to an acute increase in circulating intact FGF23 (iFGF23) with a significant and concurrent hypophosphataemia that persists over the span of several weeks [IRON-TURTLE trial (NCT03079518)] [1]. Numerous human cohort studies have postulated an independent association between elevated serum levels of FGF23 and an increased risk for cardiovascular disease and mortality [2]. Current hypotheses suggest that this association is caused by the direct effects of FGF23 on inducing myocardial hypertrophy [3]. Thus, FCM-induced increases in FGF23, paralleled by relevant hypophosphatemia, may compound to cause (additional) myocardial damage in patients with heart failure before the beneficial long-term effects of iron replenishment occur [4]. Furthermore, data suggest, that FGF23 may influence inflammation by directly stimulating the production of inflammatory markers from the liver [5, 6]. Still, to date, no data exist on such potentially harmful short-term effect of FCM in patients. The IRON-TURTLE trial included 23 patients with iron deficiency and HFrEF, all of whom received 1000 mg FCM. As reported before, FCM infusion significantly increased iFGF23 levels up to 11-fold within one day, returning back to baseline levels after four weeks, in a subgroup of 11 * Robert Stöhr [email protected] 1
Rhein-Maas-Klinikum, Würselen, Germany
2
Department of Internal Medicine I, University Hospital RWTH Aachen, Pauwelstrasse 30, 52074 Aachen, Germany
3
AGAPLESION MARKUS KRANKENHAUS, Frankfurt am Main, Germany
patients with normal renal function (eGFR 74.8 ± 12.8 ml/ min/m2). In parallel to this iFGF23 rise, 60% of these patients developed significant hypophosphatemia (mean decrease 28% ± 16% from baseline) [1]. Thus, FCM-induced increases in FGF23, paralleled by a relevant hypophosphataemia, may compound to cause (additional) myocardial damage in patients with heart failure constituting a previously underestimated (transient) post-infusion risk in these patients before the beneficial long-term effects of iron replenishment occur. We, therefore, measured levels of various established biomarkers of myocardial damage and heart failure [NTproBNP, MR-proANP, Copeptin-proAVP, Big Endothelin and MR-proadrenomedulin (MR-proADM)] [7, 8] as well as markers of renal function (GFR, Cystatin C, NGAL and KIM1) and markers of inflammation (TNF-alpha, Interleukin-6 (IL-6) and C-reactive protein (CRP)) in the aforementioned subgroup of patients with normal renal
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