Fibroblast growth factor-23 and Klotho in chronic kidney disease

Marc G. Vervloet*, Tobias E. Larsson

*Corresponding author for this work

Research output: Contribution to journalReview articleAcademicpeer-review


The well-established increased cardiovascular risk that is a hallmark of chronic kidney disease (CKD) has directed research to metabolic changes that are typical of CKD. Epidemiological data point to derangements of mineral metabolism to be involved in this risk profile. Subsequently, newly discovered humoral factors - such as fibroblast growth factor (FGF)-23 - that are involved in mineral and vitamin D homeostasis turned out to be associated with clinical outcome, independently of the minerals they regulate. Additional proteins involved in FGF-23 signaling, such as Klotho, subsequently appeared to have FGF-23-independent effects as well. In this review, the discovery, mode of action, and clinical implications of these new factors are outlined.

Original languageEnglish
Pages (from-to)130-135
Number of pages6
JournalKidney International Supplements
Issue number4
Publication statusPublished - 1 Sep 2011

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