Randomized Clinical Trial of Sevelamer Carbonate on Serum Klotho and Fibroblast Growth Factor 23 in CKD

Liabeuf, Sophie; Ryckelynck, Jean-Philippe; Esper, N. El; Ureña, Pablo; Combe, Christian; Dussol, Bertrand; Fouque, Denis; Vanhille, Philippe; Frimat, Luc; Thervet, Éric; Mentaverri, Romuald; Prié, Dominique; Choukroun, Gabriel

doi:10.2215/cjn.03030317

Cited by 36 publications

(32 citation statements)

References 37 publications

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“…In an RCT of limited extent in CKD stages 3–4, only sevelamer and not calcium acetate could decrease FGF-23 [ 318 ]. Another RCT, comparing sevelamer to placebo, however, showed no impact on FGF-23 or Klotho [ 319 ]. Another placebo-controlled study showed no difference with sevelamer in left ventricular mass, systolic and diastolic cardiac function and a difference in FGF-23, only in a subgroup analysis accounting for the compliant subpopulation [ 320 ].…”

Section: Pharmacological Treatmentmentioning

confidence: 99%

Deleting Death and Dialysis: Conservative Care of Cardio-Vascular Risk and Kidney Function Loss in Chronic Kidney Disease (CKD)

Vanholder

Laecke

Glorieux

et al. 2018

Toxins

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The uremic syndrome, which is the clinical expression of chronic kidney disease (CKD), is a complex amalgam of accelerated aging and organ dysfunctions, whereby cardio-vascular disease plays a capital role. In this narrative review, we offer a summary of the current conservative (medical) treatment options for cardio-vascular and overall morbidity and mortality risk in CKD. Since the progression of CKD is also associated with a higher cardio-vascular risk, we summarize the interventions that may prevent the progression of CKD as well. We pay attention to established therapies, as well as to novel promising options. Approaches that have been considered are not limited to pharmacological approaches but take into account lifestyle measures and diet as well. We took as many randomized controlled hard endpoint outcome trials as possible into account, although observational studies and post hoc analyses were included where appropriate. We also considered health economic aspects. Based on this information, we constructed comprehensive tables summarizing the available therapeutic options and the number and kind of studies (controlled or not, contradictory outcomes or not) with regard to each approach. Our review underscores the scarcity of well-designed large controlled trials in CKD. Nevertheless, based on the controlled and observational data, a therapeutic algorithm can be developed for this complex and multifactorial condition. It is likely that interventions should be aimed at targeting several modifiable factors simultaneously.

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Section: Pharmacological Treatmentmentioning

confidence: 99%

Deleting Death and Dialysis: Conservative Care of Cardio-Vascular Risk and Kidney Function Loss in Chronic Kidney Disease (CKD)

Vanholder

Laecke

Glorieux

et al. 2018

Toxins

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“…Most studies in CKD patients measuring the intact FGF23 assay found a decrease of FGF23 with the use of either sevelamer [124][125][126]128], or lanthanum carbonate [129][130][131] in CKD stage 2-5 patients. Ketteler and colleagues did report a 64% reduction of intact FGF23 using sucroferric oxyhydroxide (Velphoro) in patients on dialysis [132]. However, several other studies in predialysis CKD did not find a reduction of FGF23 levels with the use of sevelamer carbonate measuring intact FGF23 [133][134][135][136].…”

Section: Dietary Phosphate Restriction To Lower Fgf23mentioning

confidence: 99%

Fibroblast growth factor 23: are we ready to use it in clinical practice?

Krijger

Vervloet

2020

J Nephrol

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Patients with chronic kidney disease (CKD) have a greatly enhanced risk of cardiovascular morbidity and mortality. Over the past decade it has come clear that a disturbed calcium-phosphate metabolism, with Fibroblast Growth Factor-23 as a key hormone, is partly accountable for this enhanced risk. Numerous studies have been performed unravelling FGF23s actions and its association with clinical conditions. As FGF23 is strongly associated with adverse outcome it may be a promising biomarker for risk prediction or, even more important, targeting FGF23 may be a strategy to improve patient outcome. This review elaborates on the clinical usefulness of FGF23 measurement. Firstly it discusses the reliability of the FGF23 measurement. Secondly, it evaluates whether FGF23 measurement may lead to improved patient risk classification. Finally, and possibly most importantly, this review evaluates if lowering of FGF23 should be a target for therapy. For this, the review discusses the current evidence indicating that FGF23 may be in the causal pathway to cardiovascular pathology, provides an overview of strategies to lower FGF23 levels and discusses the current evidence concerning the benefit of lowering FGF23.

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“…16,[46][47][48] Efforts to decrease FGF23 in CKD patients by controlling phosphate or PTH, however, have met with mixed success, suggesting that additional mechanisms regulate its production. [49][50][51][52]…”

Section: Fgf23 In Ckdmentioning

confidence: 99%

Fibroblast Growth Factor 23 and Klotho in AKI

Christov

Neyra

Gupta

et al. 2019

Seminars in Nephrology

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Acute kidney injury (AKI) is associated with many of the same mineral metabolite abnormalities that are observed in chronic kidney disease. These include increased circulating levels of the osteocyte-derived, vitamin D −regulating hormone, fibroblast growth factor 23 (FGF23), and decreased renal expression of klotho, the co-receptor for FGF23. Recent data have indicated that increased FGF23 and decreased klotho levels in the blood and urine could serve as novel predictive biomarkers of incident AKI, or as novel prognostic biomarkers of adverse outcomes in patients with established AKI. In addition, because FGF23 and klotho exert numerous classic as well as off-target effects on a variety of organ systems, targeting their dysregulation in AKI may represent a unique opportunity for therapeutic intervention. We review the pathophysiology, kinetics, and regulation of FGF23 and klotho in animal and human studies of AKI, and we discuss the challenges and opportunities involved in targeting FGF23 and klotho therapeutically.

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Randomized Clinical Trial of Sevelamer Carbonate on Serum Klotho and Fibroblast Growth Factor 23 in CKD

Cited by 36 publications

References 37 publications

Deleting Death and Dialysis: Conservative Care of Cardio-Vascular Risk and Kidney Function Loss in Chronic Kidney Disease (CKD)

Deleting Death and Dialysis: Conservative Care of Cardio-Vascular Risk and Kidney Function Loss in Chronic Kidney Disease (CKD)

Fibroblast growth factor 23: are we ready to use it in clinical practice?

Fibroblast Growth Factor 23 and Klotho in AKI

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