No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher.ĭrug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. These findings do not provide evidence for a relevant clinical role of either FGFR4 stimulation or soluble form of Klotho deficiency in LVH development.Ĭopyright: All rights reserved. Discussion/Conclusion: rs351855 and rs9536314 were not associated with LVMI or cardiac events. Time to cardiac decompensation (rs351855: p = 0.316 rs9536314: p = 0.765) and ASCVD ( p = 0.508 and p = 0.800, respectively) did not differ between carriers of different alleles. Hundred and four patients suffered cardiac decompensation, and 144 patients had ASCVD. Results: Carriers of the different alleles did neither differ in baseline LVMI (rs351855: p = 0.861 rs9536314: p = 0.379) nor in LVMI changes between baseline and follow-up (rs351855: p = 0.181 rs9536314: p = 0.995).
Patients were followed for 5.1 ± 2.1 years for the primary endpoints of cardiac decompensation and atherosclerotic cardiovascular disease (ASCVD). Echocardiographic examinations at baseline and 5 years later assessed prevalence of LVH by measurement of left-ventricular mass index (LVMI).
Methods: The prospective Cardiovascular and Renal Outcome in CKD 2–4 Patients–The Fourth Homburg Evaluation study recruited CKD G2–G4 patients, of whom 519 consented to SNP genotyping (FGFR4: rs351855 Klotho: rs9536314). To evaluate the clinical relevance of these findings, a Mendelian randomization study analyzed the association of genetic variants of FGFR4 and Klotho with echocardiographic parameters and cardiac events in CKD patients. Experimental evidence suggests FGF receptor 4 (FGFR4) activation by FGF-23, and deficiency of the soluble form of its co-receptor Klotho promotes left-ventricular hypertrophy (LVH). Introduction: High plasma fibroblast growth factor 23 (FGF-23) predicts cardiovascular events in chronic kidney disease (CKD) patients.
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