Fibroblast Growth Factor 23 and Adverse Clinical Outcomes in Type 2 Diabetes: a Bitter-Sweet Symphony
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MICROVASCULAR COMPLICATIONS—NEPHROPATHY (B ROSHANRAVAN, SECTION EDITOR)
Fibroblast Growth Factor 23 and Adverse Clinical Outcomes in Type 2 Diabetes: a Bitter-Sweet Symphony Stanley M. H. Yeung 1 & Stephan J. L. Bakker 1 & Gozewijn D. Laverman 2 & Martin H. De Borst 1
# The Author(s) 2020
Abstract Purpose of Review Fibroblast growth factor 23 (FGF23) is a key phosphate-regulating hormone that has been associated with adverse outcomes in patients with chronic kidney disease (CKD). Emerging data suggest that FGF23 plays a specific role in type 2 diabetes, partly independent of kidney function. We aimed to summarize current literature on the associations between FGF23 and outcomes in patients with type 2 diabetes with or without CKD. Recent Findings Several cohort studies have shown strong associations between plasma FGF23 and cardiovascular outcomes in diabetic CKD. Moreover, recent data suggest that FGF23 are elevated and may also be a risk factor for cardiovascular disease and mortality in type 2 diabetes patients without CKD, although the magnitude of the association is smaller than in CKD patients. Summary Diabetes-related factors may influence plasma FGF23 levels, and a higher FGF23 levels seem to contribute to a higher cardiovascular and mortality risk in patients with type 2 diabetes. Although this risk may be relevant in diabetic individuals with preserved kidney function, it is strongly accentuated in diabetic nephropathy. Future studies should clarify if FGF23 is merely a disease severity marker or a contributor to adverse outcomes in type 2 diabetes and establish if antidiabetic medication can modify FGF23 levels. Keywords Mineral metabolism . Diabetes . Kidney disease . Cardiovascular disease
Introduction Fibroblast growth factor 23 (FGF23) is a circulating hormone, predominantly produced by osteocytes, that regulates This article is part of the Topical Collection on Microvascular Complications—Nephropathy * Martin H. De Borst [email protected] Stanley M. H. Yeung [email protected] Stephan J. L. Bakker [email protected] Gozewijn D. Laverman [email protected] 1
Department of Internal Medicine, Division of Nephrology, University of Groningen, University Medical Center Groningen, P.O. Box 30.001, 9700 RB Groningen, the Netherlands
2
Department of Internal Medicine/Nephrology, Ziekenhuisgroep Twente Hospital, Almelo and Hengelo, the Netherlands
phosphate excretion by the kidneys and inhibits the synthesis of 1,25-dihydroxyvitamin-D3 [1•]. Initial studies found that deregulations in FGF23 play an important role in the development of bone and mineral disorders. Over 20 years ago, genetic mutations in the FGF23 gene were identified as the cause of autosomal dominant hypophosphatemic rickets (ADHR) [2]. Deregulated FGF23 also plays a role in the etiology of X-linked hypophosphatemic rickets (XLH), another bone disease where renal phosphate wasting plays a main role. Subsequently, novel therapies have been developed including the monoclonal antibody burosumab, which specifically targets FGF23. Clinic
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