Peripheral vascular calcification in long-haemodialysis patients: associated factors and survival consequences

Gadrey, Jean; Bresson, Éric; Terrat, Jean-Claude; Vanel, Thierry; Hurot, Jean-Marc; Lorriaux, Christie; Mayor, Brice; Chazot, Charles

doi:10.1093/ndt/gfn571

Cited by 209 publications

(170 citation statements)

References 43 publications

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“…Furthermore, among the mineral metabolites we tested, FGF23 was most strongly correlated with each inflammatory marker, and FGF23 but not PTH or phosphate was associated with greater odds for severe inflammation in multivariable models. Given the associations between inflammation, atherosclerosis, and vascular calcification (21), and that some studies have shown association between elevated FGF23 and calcification in CKD and ESRD (22,23), these results provide new insight into another potential mechanism underlying the strong associations between elevated FGF23, cardiovascular disease, and mortality. Further studies are needed to determine whether FGF23 might contribute to atherosclerosis and vascular calcification by stimulating inflammation or whether inflammation might contribute to the development of vascular disease through effects on FGF23.…”

Section: Discussionmentioning

confidence: 83%

Fibroblast Growth Factor 23 and Inflammation in CKD

Mendoza

Isakova²,

Ricardo³

et al. 2012

Clinical Journal of the American Society of Nephrology

239

171

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SummaryBackground and objectives Levels of fibroblast growth factor 23 (FGF23) and inflammatory markers are commonly elevated in CKD, and each is associated with adverse clinical outcomes. This study tested the hypothesis that FGF23 is independently associated with inflammation in CKD.Design, setting, participants, & measurements The association between levels of FGF23 and the inflammatory markers IL-6, C-reactive protein (CRP), TNF-a, and fibrinogen was assessed in a cross-sectional analysis of 3879 participants enrolled in the Chronic Renal Insufficiency Cohort (CRIC) study between June 2003 and September 2008.Results FGF23 correlated directly with IL-6 (r=0.4), CRP (r=0.2), TNF-a (r=0.4), and fibrinogen (r=0.3; P,0.001 for each). In univariate and multivariable-adjusted linear regression analyses, natural log (ln) transformed FGF23 was significantly associated with lnIL-6, lnCRP, lnTNF-a, and fibrinogen (P,0.001 for each). Each unit higher lnFGF23 was associated with severe inflammation, defined as levels of all inflammatory markers in the highest 25th percentile, in univariate (odds ratio [OR], 2.4 [95% confidence interval (CI), 2.0-2.9]) and multivariable-adjusted (OR, 2.0 [95% CI, 1.6-2.5]) logistic regression analyses. Ascending FGF23 quartiles were independently associated with severe inflammation (OR, 5.6 for the highest versus lowest FGF23 quartile [95% CI, 2.3-13.9]; P for trend , 0.001).Conclusions Higher FGF23 levels are independently associated with higher levels of inflammatory markers in patients with CKD and with significantly greater odds of severe inflammation. Future studies should evaluate whether inflammation modifies the association between FGF23 and adverse outcomes in CKD.

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Section: Discussionmentioning

confidence: 83%

Fibroblast Growth Factor 23 and Inflammation in CKD

Mendoza

Isakova²,

Ricardo³

et al. 2012

Clinical Journal of the American Society of Nephrology

239

171

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“…In patients with CKD, FGF23 levels are thought to increase as a compensatory response to maintain normal P balance, because the capacity for renal P excretion declines (8). Recent studies indicate that increased levels of FGF23 are associated with mortality, CKD progression, and calcification in CKD patients (9)(10)(11)(12). These evidences suggest that early treatment of calcium-phosphate alterations may lead to improved management of CKD progression and associated CV complications.…”

Section: Introductionmentioning

confidence: 99%

Acute Effects of Very-Low-Protein Diet on FGF23 Levels

Iorio¹,

Micco²,

Torraca³

et al. 2012

Clinical Journal of the American Society of Nephrology

104

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SummaryBackground and objectives High levels of fibroblast growth factor 23 are associated with mortality, CKD progression, and calcification in CKD patients. The aim of this pilot study is to assess whether a very-low-protein diet (0.3 g/kg per day) with a consequent low intake of phosphorus would reduce fibroblast growth factor 23 compared with a low-protein diet (0.6 g/kg per day) in CKD patients not yet on dialysis.Design, setting, participants, & measurements A prospective, randomized, controlled crossover study was performed in which 32 patients were randomized into two groups. Group A (16 patients) received a very-lowprotein diet (0.3 g/kg body wt per day) supplemented with ketoanalogues during the first week and a lowprotein diet during the second week, and group B (16 patients) received a low-protein diet during the first week and a very-low-protein diet during the second week. Fibroblast growth factor 23, seric, and urinary phosphate levels were measured at baseline and the end of each study period.Results After only 1 week of the very-low-protein diet, reductions in fibroblast growth factor 23 levels (33.5%), serum phosphate (12%), and urinary phosphate (34%) with the very-low-protein diet compared with the lowprotein diet were observed. Serum and urinary phosphate levels and protein intake were significant determinants of fibroblast growth factor 23 (95% confidence interval=1.04-1.19, 1.12-1.37, and 1.51-2.23, respectively).Conclusions A very-low-protein diet supplemented with ketoanalogues reduced fibroblast growth factor 23 levels in CKD patients not yet on dialysis.

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“…49 In addition to the possible relations between FGF-23, CKD progression, hyperparathyroidism, ventricular hypertrophy, and mortality, high FGF-23 levels are believed to correlate with vascular calcification. 50,51 Our group studied, for one year, 72 patients undergoing hemodialysis and found a positive correlation between FGF-23 levels and the vascular calcification score assessed by use of coronary tomography in the group of patients treated with sevelamer hydrochloride. 52 dIscussIon An important question that remains unanswered relates to the possible existence of other actions of FGF-23, whether that hormone is only an indirect marker of toxicity of other factors, like P, or whether it has a direct toxic effect on vascular endothelium and renal tissue.…”

Section: Fgf-23 and Clinical And Experimental Studiesmentioning

confidence: 94%

FGF-23: estado da arte

Oliveira

Moysés

2010

J. Bras. Nefrol.

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Approximately 10 years ago, a member of the family of the fibroblast growth factors, the hormone FGF-23 (fibroblast growth factor 23) was discovered. Its currently known functions involve phosphorus (P) metabolism and inhibition of 1α hydroxylase, the enzyme responsible for the synthesis of calcitriol. That discovery led to a better understanding of the mechanisms of P control, an element associated with mortality, especially in chronic kidney disease. This study reviews several aspects of that hormone, such as its discovery, function, production, mechanism of action, and the most recent clinical studies about it. Afterwards, a discussion about the possible effects of those studies on clinical practice will be presented.

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Peripheral vascular calcification in long-haemodialysis patients: associated factors and survival consequences

Cited by 209 publications

References 43 publications

Fibroblast Growth Factor 23 and Inflammation in CKD

Fibroblast Growth Factor 23 and Inflammation in CKD

Acute Effects of Very-Low-Protein Diet on FGF23 Levels

FGF-23: estado da arte

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