Correlation between hypervolemia, left ventricular hypertrophy and fibroblast growth factor 23 in hemodialysis patients

Ünver, Suat; Kavlak, Ela; Gümüşel, Hilal Kurtoğlu; Celikbilek, Fatma; Esertas, Kenan; Müftüoğlu, Tuba; Kirilmaz, Ata

doi:10.3109/0886022x.2015.1052945

Cited by 21 publications

(23 citation statements)

References 17 publications

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“…The immediate effect of FGF23 is lowering of serum phosphate which in our study was only modest, but has been demonstrated in other studies (Table 4). A potential longer term effect of concern is that higher levels of FGF23 are associated with both cardiovascular events and death in advanced CKD [23] and that FGF23 is associated with left ventricular hypertrophy (LVH) in human studies [24]. Experimental studies have identified that the LVH associated with elevated FGF23 serum levels and mediated by its specific cardiac receptor (Type 4) can be mitigated by blocking the receptor [25].…”

Section: Discussionmentioning

confidence: 99%

Effects of intravenous iron on fibroblast growth factor 23 (FGF23) in haemodialysis patients: a randomized controlled trial

et al. 2016

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BackgroundIntravenous iron affects serum levels of intact fibroblast growth factor-23 (iFGF23) and its cleavage product c-terminal FGF23 (cFGF23) in iron-deficient people with normal renal function. We hypothesized that intravenous iron modulates iFGF23 and cFGF23 in haemodialysis patients differently according to the type of iron used.MethodsPrevalent, stable haemodialysis patients requiring protocol-based intravenous iron therapy were randomized to a single 200 mg dose of either ferric carboxymaltose (FCM) or iron sucrose (IS). The primary outcome was change in iFGF23 and cFGF23 from pre-infusion to Day 2 post-infusion. Serum hepcidin, ferritin and phosphate were also measured. Pair-wise comparisons utilised the Wilcoxon rank sum test; linear mixed models with an interaction term for treatment and time evaluated between-group effects.ResultsForty-two participants completed the study. In those randomized to FCM (n = 22), median (interquartile range) values pre-infusion and Day 2, respectively, were 843 pg/mL (313–1922) and 576 pg/mL (356–1296, p = 0.05) for iFGF23, 704RU/mL (475–1204) and 813RU/mL (267–1156, p = 0.04) for cFGF23, and 1.53 mmol/L (1.14–1.71) and 1.37 (1.05–1.67, p = 0.03) for phosphate. These parameters did not change following IS. Both serum ferritin (p < 0.001) and hepcidin (p < 0.001) increased in both groups, and the increase in hepcidin was greater in the FCM group (p = 0.03 for between-group difference).ConclusionsContrary to iron-deficient people with normal renal function, haemodialysis patients given protocol-driven intravenous FCM demonstrated a fall in iFGF23 and a rise in cFGF23, changes not evident with IS. This suggests a differential effect of intravenous iron treatment according to both formulation and renal function.Trial registrationAustralian and New Zealand Clinical Trials Register ACTRN12614000548639. Registered 22 May 2014 (retrospectively registered).Electronic supplementary materialThe online version of this article (doi:10.1186/s12882-016-0391-7) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

Effects of intravenous iron on fibroblast growth factor 23 (FGF23) in haemodialysis patients: a randomized controlled trial

et al. 2016

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“…59 In the case of FGF23, we have only indirect evidence in the form of increased cardiovascular mortality in CKD patients, including those on dialysis, with higher concentrations of FGF23 in the circulation. 60 It would, therefore, be expected that higher concentrations of sclerostin, like those of FGF-23, should increase cardiovascular risk, but there is conflicting evidence. 61 Some studies show no association between sclerostin and mortality.…”

Section: Sclerostin In Chronic Kidney Diseasementioning

confidence: 99%

Sclerostin: Intracellular mechanisms of action and its role in the pathogenesis of skeletal and vascular disorders

Pietrzyk¹,

Smertka²,

Chudek³

2017

Adv Clin Exp Med

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Sclerostin is a glycoprotein involved in the regulation of bone metabolism, exclusively secreted by osteocytes. It affects the activity of bone morphogenetic proteins (BMPs) and is an inhibitor of the Wnt/β-catenin metabolic pathway in bone cells. Osteocytes reduce the release of sclerostin in response to mechanical stimuli acting on bone, and thus promote the activation of osteogenic pathway Wnt/β-catenin in osteoblasts. This signaling pathway plays a key role in osteogenesis and bone turnover. Loss of sclerostin gene function is related to 3 different craniotubular hyperostosis processes: sclerosteosis, craniodiaphyseal dysplasia, and van Buchem disease. Additionally, experimental and clinical studies suggest that sclerostin may promote vascular calcification. Antibodies directed against sclerostin stimulate bone formation and represent a new therapeutic option in the treatment of diseases with increased bone resorption, such as osteoporosis and inflammatory diseases where there is generalized bone loss, periarticular osteoporosis, and cartilage damage, such as rheumatoid arthritis (RA), ankylosing spondylitis (AS), and glucocorticoid-induced osteoporosis (GIO). Antibody use has the potential to offer new therapeutic approaches in the therapy of mineral and bone disorders resulting from chronic kidney disease (CKD-MBD) and vascular calcifications.

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“…In addition to the traditional risk factors for heart disease such as diabetes and hypertension, patients with ESRD have risk factors that make them at greater risk for SCD, including a higher prevalence of left ventricular hypertrophy and vascular calcification [3]. Bleyer et al [4] examined the timing of SCD in a cohort of patients from five hemodialysis units in the southeastern United States and reported a 1.71 ratio of observed to expected sudden deaths in the 12 h following the onset of a hemodialysis session.…”

Section: Introductionmentioning

confidence: 99%

Dialysate content and risk of sudden cardiac death

Thornley‐Brown

Saha²

2015

Current Opinion in Nephrology and Hypertension

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Correlation between hypervolemia, left ventricular hypertrophy and fibroblast growth factor 23 in hemodialysis patients

Abstract: Our study showed that interdialytic volume overload increased both LVMI and FGF-23 values. We can consider that interdialytic volume control exerts positive effects on increased FGF-23 levels which predict the negative cardiovascular outcomes.

Cited by 21 publications

References 17 publications

Effects of intravenous iron on fibroblast growth factor 23 (FGF23) in haemodialysis patients: a randomized controlled trial

Effects of intravenous iron on fibroblast growth factor 23 (FGF23) in haemodialysis patients: a randomized controlled trial

Sclerostin: Intracellular mechanisms of action and its role in the pathogenesis of skeletal and vascular disorders

Dialysate content and risk of sudden cardiac death

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