Journal Article

FGF23 antagonism: the thin line between adaptation and maladaptation in chronic kidney disease

Markus Ketteler, Patrick H. Biggar and Orfeas Liangos

in Nephrology Dialysis Transplantation

Published on behalf of European Renal Association - European Dialysis and Transplant Assoc

Volume 28, issue 4, pages 821-825
Published in print April 2013 | ISSN: 0931-0509
Published online December 2012 | e-ISSN: 1460-2385 | DOI:
FGF23 antagonism: the thin line between adaptation and maladaptation in chronic kidney disease

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For more than 10 years, we have been convinced by overwhelming epidemiological evidence with a high biological plausibility that hyperphosphataemia imposes one of the most sustained cardiovascular and mortality risks on patients suffering from chronic kidney disease (CKD). With the discovery of the fibroblast growth factor-23 (FGF23)/klotho axis, we not only gained a new and mechanistic understanding of phosphate handling of the body, we also felt that novel therapeutic strategies may arise counteracting the deleterious consequences of phosphate retention, dysregulation and maldistribution. Two recent experimental studies shed additional and important light on what we can expect from such new insights. Faul et al. showed us that FGF23 excess may directly induce left ventricular hypertrophy (LVH) and that FGF-receptor antagonism ameliorates CKD-induced LVH in rats. Shalhoub et al. demonstrated that FGF23 antibodies successfully ameliorated the development and progression of most features of secondary hyperparathyroidism in a rat model of CKD, however, at the expense of hyperphosphataemia, progressive vascular calcification and death. Such studies not only help to continuously improve our understanding, but also especially sharpen our perception of how thin the line may be between adaptation and maladaptation in chronic disease scenarios.

Keywords: fibroblast growth factor-23; hyperphosphataemia; left ventricular hypertrophy; secondary hyperparathyroidism; vascular calcification

Journal Article.  2724 words. 

Subjects: Nephrology

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