Fibroblast growth factor 23 is associated with carotid artery calcification in chronic kidney disease patients not undergoing dialysis: a cross-sectional study

Nakayama, Masaru; Kaizu, Yoshiki; Nagata, Michio; Ura, Yoriko; Ikeda, Hirofumi; Shimamoto, Sho; Kuma, Kazuyoshi

doi:10.1186/1471-2369-14-22

Cited by 38 publications

(31 citation statements)

References 42 publications

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“…37 An inverse relationship between CAC prevalence and BMD by DXA has also been shown in patients who are osteoporotic with normal kidney function and patients with HIV or metabolic syndrome. [38][39][40][41] In this study, a positive correlation was found between CAC SQRVand FGF23, which is in agreement with several published reports on vascular calcifications [42][43][44][45][46] but not in keeping with another report on patients with CKD not on dialysis. 29 Baseline FGF23 remained an independent predictor for baseline CAC after multivariable adjustment for age, CAD, diabetes, dialysis vintage, and BMD.…”

Section: Discussionsupporting

confidence: 92%

High Parathyroid Hormone Level and Osteoporosis Predict Progression of Coronary Artery Calcification in Patients on Dialysis

Malluche¹,

Blomquist²,

Monier‐Faugere³

et al. 2015

Journal of the American Society of Nephrology

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Coronary artery calcifications (CACs) are observed in most patients with CKD on dialysis (CKD-5D). CACs frequently progress and are associated with increased risk for cardiovascular events, the major cause of death in these patients. A link between bone and vascular calcification has been shown. This prospective study was designed to identify noninvasive tests for predicting CAC progression, including measurements of bone mineral density (BMD) and novel bone markers in adult patients with CKD-5D. At baseline and after 1 year, patients underwent routine blood tests and measurement of CAC, BMD, and novel serum bone markers. A total of 213 patients received baseline measurements, of whom about 80% had measurable CAC and almost 50% had CAC Agatston scores.400, conferring high risk for cardiovascular events. Independent positive predictors of baseline CAC included coronary artery disease, diabetes, dialysis vintage, fibroblast growth factor-23 concentration, and age, whereas BMD of the spine measured by quantitative computed tomography was an inverse predictor. Hypertension, HDL level, and smoking were not baseline predictors in these patients. Three quarters of 122 patients completing the study had CAC increases at 1 year. Independent risk factors for CAC progression were age, baseline total or whole parathyroid hormone level greater than nine times the normal value, and osteoporosis by t scores. Our results confirm a role for bone in CKD-associated CAC prevalence and progression.

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Section: Discussionsupporting

confidence: 92%

High Parathyroid Hormone Level and Osteoporosis Predict Progression of Coronary Artery Calcification in Patients on Dialysis

Malluche¹,

Blomquist²,

Monier‐Faugere³

et al. 2015

Journal of the American Society of Nephrology

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“…Treatment with vitamin D analogues of calcitriol, frequently used in CKD patients, also contributes to increased FGF23 concentrations [88,89]. Elevated FGF23 levels have been associated with increased mortality in patients with end stage renal disease [90] and direct detrimental effects on the cardiovascular system [91], endothelial dysfunction, arterial stiffness [92] and left ventricular hypertrophy [93] have been implicated.…”

Section: The Skeleton and Mineral Homeostasismentioning

confidence: 98%

The dynamic skeleton

Gonciulea

Beur

2015

Rev Endocr Metab Disord

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Adding to its well-known roles in locomotion and calcium balance, the skeleton has recently been appreciated as a true endocrine organ. Bone remodeling, a highly dynamic process, requires synchronized activities and crosstalk between bone cells. Discovery and characterization of the Wnt/β catenin pathway in bone formation, FGF23 regulation of phosphate homeostasis and osteocalcin in energy and glucose homeostasis have reframed our view of the skeleton from simply a target tissue of the endocrine system to an endocrine tissue itself. This comprehensive review provides an overview of these complex pathways, their application to human bone disorders and implications for developing diagnostic and therapeutic targets.

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“…Unlike phosphate, however, the effect of FGF23 on arterial calcification is associated with the degree of kidney function. FGF23 is not associated with coronary artery calcification in individuals with normal renal function (94), and there are conflicting reports of the association in patients with CKD predialysis (62,95). However, FGF23 does correlate with peripheral and aortic calcification in patients on hemodialysis (96,97).…”

Section: Fgf23 and Klotho In Cardiovascular Diseasementioning

confidence: 99%

Phosphate Toxicity in CKD: The Killer among Us

Ritter¹,

Slatopolsky²

2016

CJASN

121

113

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Maintenance of a normal serum phosphate level depends on absorption in the gut, reabsorption and excretion by the kidney, and the flux between the extracellular and skeletal pools. Phosphate homeostasis is a coordinated, complex system of crosstalk between the bone, intestine, kidney, and parathyroid gland. Dysfunction of this system has serious clinical consequences in healthy individuals and those with conditions, such as CKD, in which hyperphosphatemia is associated with increased risks of cardiovascular morbidity and mortality. The last halfcentury of renal research has helped define the contribution of the parathyroid hormone, calcitriol, fibroblast growth factor 23, and Klotho in the regulation of phosphate. However, despite new discoveries and insights gained during this time, what remains unchanged is the recognition that phosphate retention is the initiating factor for the development of many of the complications observed in CKD, namely secondary hyperparathyroidism and bone and cardiovascular diseases. Controlling phosphate load remains the primary goal in the treatment of CKD. This review discusses the clinical effects of dysregulated phosphate metabolism, particularly in CKD, and its association with cardiovascular disease. The importance of early control of phosphate load in the treatment of CKD is emphasized, and the latest research in the treatment of phosphate retention is discussed.

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Fibroblast growth factor 23 is associated with carotid artery calcification in chronic kidney disease patients not undergoing dialysis: a cross-sectional study

Cited by 38 publications

References 42 publications

High Parathyroid Hormone Level and Osteoporosis Predict Progression of Coronary Artery Calcification in Patients on Dialysis

High Parathyroid Hormone Level and Osteoporosis Predict Progression of Coronary Artery Calcification in Patients on Dialysis

The dynamic skeleton

Phosphate Toxicity in CKD: The Killer among Us

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