Abstract
Patients affected by chronic kidney disease (CKD) exhibit a high risk of cardiovascular mortality that is poorly explained by traditional risk factors. There is a growing awareness about the role of derangement of mineral metabolism that is currently accepted as a trigger and sustainer of cardiovascular disease (CVD) in CKD patients. The synthetic definition of CKD mineral and bone disorder (CKD-MBD) split the concept that the indexes of mineral metabolism extend their effects beyond the bone until the vascular wall and metabolic milieu of CKD patients through complex pathways. A better understanding of the biomarkers and mechanisms of left ventricular hypertrophy, CVD, inflammation, and chronic renal damage may help with the diagnosis and treatment of the systemic impairment that occurs secondary to CKD-MBD, thus slowing the progression of renal and CVD and improving patient survival. Recent insights into fibroblast growth factor (FGF) 23 have led to marked advancement in interpreting data on CVD and CKD progression ascribing to FGF23 a pivotal role in these pathologies independent of its co-receptor klotho and well beyond mineral metabolism. This review article will discuss the current experimental and clinical evidence regarding the role of FGF23 in physiology and pathophysiology of CKD and its associated complications with an emphasis on CVD.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 83-95 |
| Number of pages | 13 |
| Journal | Contributions to Nephrology |
| Volume | 190 |
| DOIs | |
| State | Published - 2017 |
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ASJC Scopus subject areas
- Medicine(all)
- Nephrology
Cite this
Fibroblast Growth Factor 23 : Mineral Metabolism and beyond. / Grabner, Alexander; Mazzaferro, Sandro; Cianciolo, Giuseppe; Krick, Stefanie; Capelli, Irene; Rotondi, Silverio; Ronco, Claudio; La Manna, Gaetano; Faul, Christian H.
In: Contributions to Nephrology, Vol. 190, 2017, p. 83-95.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Fibroblast Growth Factor 23
T2 - Mineral Metabolism and beyond
AU - Grabner, Alexander
AU - Mazzaferro, Sandro
AU - Cianciolo, Giuseppe
AU - Krick, Stefanie
AU - Capelli, Irene
AU - Rotondi, Silverio
AU - Ronco, Claudio
AU - La Manna, Gaetano
AU - Faul, Christian H
PY - 2017
Y1 - 2017
N2 - Patients affected by chronic kidney disease (CKD) exhibit a high risk of cardiovascular mortality that is poorly explained by traditional risk factors. There is a growing awareness about the role of derangement of mineral metabolism that is currently accepted as a trigger and sustainer of cardiovascular disease (CVD) in CKD patients. The synthetic definition of CKD mineral and bone disorder (CKD-MBD) split the concept that the indexes of mineral metabolism extend their effects beyond the bone until the vascular wall and metabolic milieu of CKD patients through complex pathways. A better understanding of the biomarkers and mechanisms of left ventricular hypertrophy, CVD, inflammation, and chronic renal damage may help with the diagnosis and treatment of the systemic impairment that occurs secondary to CKD-MBD, thus slowing the progression of renal and CVD and improving patient survival. Recent insights into fibroblast growth factor (FGF) 23 have led to marked advancement in interpreting data on CVD and CKD progression ascribing to FGF23 a pivotal role in these pathologies independent of its co-receptor klotho and well beyond mineral metabolism. This review article will discuss the current experimental and clinical evidence regarding the role of FGF23 in physiology and pathophysiology of CKD and its associated complications with an emphasis on CVD.
AB - Patients affected by chronic kidney disease (CKD) exhibit a high risk of cardiovascular mortality that is poorly explained by traditional risk factors. There is a growing awareness about the role of derangement of mineral metabolism that is currently accepted as a trigger and sustainer of cardiovascular disease (CVD) in CKD patients. The synthetic definition of CKD mineral and bone disorder (CKD-MBD) split the concept that the indexes of mineral metabolism extend their effects beyond the bone until the vascular wall and metabolic milieu of CKD patients through complex pathways. A better understanding of the biomarkers and mechanisms of left ventricular hypertrophy, CVD, inflammation, and chronic renal damage may help with the diagnosis and treatment of the systemic impairment that occurs secondary to CKD-MBD, thus slowing the progression of renal and CVD and improving patient survival. Recent insights into fibroblast growth factor (FGF) 23 have led to marked advancement in interpreting data on CVD and CKD progression ascribing to FGF23 a pivotal role in these pathologies independent of its co-receptor klotho and well beyond mineral metabolism. This review article will discuss the current experimental and clinical evidence regarding the role of FGF23 in physiology and pathophysiology of CKD and its associated complications with an emphasis on CVD.
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UR - http://www.scopus.com/inward/citedby.url?scp=85020295627&partnerID=8YFLogxK
U2 - 10.1159/000468952
DO - 10.1159/000468952
M3 - Article
C2 - 28535521
AN - SCOPUS:85020295627
VL - 190
SP - 83
EP - 95
JO - Contributions to Nephrology
JF - Contributions to Nephrology
SN - 0302-5144
ER -