scholarly journals The increased risk of cardiovascular events in chronic kidney disease: pathogenetic mechanisms, the possibility of correction

2014 ◽  
Vol 5 (3-4) ◽  
pp. 54-60
Author(s):  
O. Yu Barysheva ◽  
A. A Melentieva ◽  
L. M Kheyfetz ◽  
A. T Balashov
Keyword(s):  
Chronic Kidney Disease ◽  
Cardiovascular Risk ◽  
Growth Factor ◽  
Kidney Disease ◽  
Cardiovascular Events ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Pathogenetic Mechanisms ◽  
Increased Risk

The paper discusses the pathogenetic mechanisms linking cardiovascular risk and chronic kidney disease (CKD). Presents data on the role of hypercalcemia, hyperphosphatemia, secondary hyperparathyroidism, fibroblast growth factor-23, Klotho, an important the components of the pathogenesis of mineral and bone disorders increase the risk cardiovascular events in CKD. Discussed the causes and features dyslipidemia in CKD, particularly correction. Presents data on options calciphylaxis, causes, development, peculiarities of treatment.

Strength of Fibroblast Growth Factor 23 as a Cardiovascular Risk Predictor in Chronic Kidney Disease Weaken by ProBNP Adjustment

2019 ◽  
Vol 49 (3) ◽  
pp. 203-211 ◽  
Author(s):  
Insa E. Emrich ◽  
Vincent Brandenburg ◽  
Alexander B. Sellier ◽  
Johanna Schauerte ◽  
Johanna Wiedenroth ◽  
...  
Keyword(s):  
Risk Factors ◽  
Heart Failure ◽  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Cardiovascular Events ◽  
Fibroblast Growth Factor 23 ◽  
Cardiovascular Effects ◽  
Fibroblast Growth ◽  
Conventional Risk Factors

Background: Various epidemiological studies linked high fibroblast growth factor 23 (FGF23) levels with cardiovascular events in chronic kidney disease (CKD). It remains enigmatic whether high FGF23 exerts adverse cardiovascular effects, or whether it reflects detrimental effects of residual confounders. Earlier studies adjusted for CKD-mineral bone disease (CKD-MBD) regulators of FGF23 rather than for recently discovered non-CKD-MBD regulators, among which iron deficiency and heart failure are of particular importance. Moreover, they used c-terminal FGF23 (cFGF23) assays rather than more specific intact FGF23 (iFGF23) assays. Methods: The CARE FOR HOMe study analyzed plasma ferritin, iFGF23, cFGF23 and N-terminal proBNP (NT-proBNP) along with conventional risk factors, among 575 CKD G2-G4 patients to determine the interaction between FGF23, its non-CKD-MBD regulators, and incident cardiovascular events in CKD patients. The participants were followed up for 5.1 ± 2.1 years for the occurrence of atherosclerotic events and hospitalization for acute decompensated heart failure. Results: cFGF23 correlated strongly with high iFGF23 (r = 0.607), fairly with high NT-proBNP (r = 0.453) and weakly with low ferritin (r = –0.207); correlation coefficients of iFGF23 with NT-proBNP and ferritin were numerically lower. In Kaplan-Meier analyses, both endpoints were predicted by cFGF23 and iFGF23. In Cox regression models, cFGF23 remained an outcome predictor after adjustment for conventional risk factors and ferritin. This prediction was largely eliminated when further adjusting for NT-proBNP. iFGF23 was less consistently associated with adverse outcome in partly adjusted models, and failed to predict outcome in fully adjusted models. Conclusion: In summary, iron deficiency and heart failure affect plasma FGF23. As adjustment for NT-proBNP virtually eliminates the association between plasma FGF23 and predefined outcome, we speculate that high FGF23, rather than exerting detrimental cardiovascular effects, mirrors prevalent heart disease.

scholarly journals Effects of Aldosterone, Osteoprotegerin and Fibroblast Growth Factor-23 and Some Biochemical Markers in Chronic Kidney Disease Patients' (Stage II-IV) among Patients with or without Cardiovascular Events

2018 ◽  
pp. 150-158
Author(s):  
Zeyad Abass Ameen ◽  
Shatha Ali
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Cardiovascular Events ◽  
Fibroblast Growth Factor 23 ◽  
Chronic Kidney Disease Stage ◽  
Stage Ii ◽  
Disease Stage ◽  
Fibroblast Growth ◽  
Fgf 23

Chronic Kidney Disease (CKD) is a public health problem and many studies support the link between kidney dysfunction and cardiovascular events.  Aldosterone has been shown for decades that a plasma aldosterone concentration is elevated in CKD. Whilst, Osteoprotegerin (OPG), after its capacity to protect bone, also osteoprotegerin is elevated in patients with chronic kidney disease (CKD), where it could predict the deterioration of kidney function, cardiovascular, vascular events and all-cause mortality. On the other hand, fibroblast growth factors (FGFs), in patients with CKD, its levels seem to increase progressively as kidney function worsens. The aim of the present study is to assess the correlations between serum osteoprotegerin, aldosterone and fibroblast growth factor-23 levels in patients with chronic kidney disease stage (II-IV) with and without cardiovascular events. The study includes fifty-nine patients with chronic kidney disease(CKD) and according to CKD-EPI /Creatinine/ 2009 equation to be allocated as stage II-IV, patients were divided into three groups: Group1 (29 patients) with chronic kidney disease(CKD) stage (II-IV) with cardiovascular events. Group2 (30 patients) with chronic kidney disease stage (II-IV) without cardiovascular event, to be compared with Group 3(23 apparently healthy subjects), age and sex matched to that of patients. Serum obtained from their blood specimens to measure; glucose, urea, creatinine, calcium, phosphate, sodium, potassium, aldosterone, FGF-23, Osteoprotergen. Data analysis showed that fasting serum glucose levels of CKD patients (with and without CV disorder) had significantly higher values as compared to the controls (76.5% and 29% respectively). Serum Aldosterone, FGF-23, OPG levels were presented with no significant variation among studied groups with CV events or those without CV events.

scholarly journals Role of fibroblast growth factor 23 in patients with chronic kidney disease

2020 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Song-Yan Wang ◽  
Fan Yang ◽  
Shuang Ma ◽  
Li-Juan Cui ◽  
Rui Zhang
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth

scholarly journals Lipocalin 2 stimulates bone fibroblast growth factor 23 production in chronic kidney disease

Bone Research ◽  
2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Guillaume Courbon ◽  
Connor Francis ◽  
Claire Gerber ◽  
Samantha Neuburg ◽  
Xueyan Wang ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Kidney Disease ◽  
Iron Deficiency ◽  
Fibroblast Growth Factor ◽  
Kidney Function ◽  
Fibroblast Growth Factor 23 ◽  
Left Ventricular ◽  
Fibroblast Growth ◽  
Lipocalin 2

AbstractBone-produced fibroblast growth factor 23 (FGF23) increases in response to inflammation and iron deficiency and contributes to cardiovascular mortality in chronic kidney disease (CKD). Neutrophil gelatinase-associated lipocalin (NGAL or lipocalin 2; LCN2 the murine homolog) is a pro-inflammatory and iron-shuttling molecule that is secreted in response to kidney injury and may promote CKD progression. We investigated bone FGF23 regulation by circulating LCN2. At 23 weeks, Col4a3KO mice showed impaired kidney function, increased levels of kidney and serum LCN2, increased bone and serum FGF23, anemia, and left ventricular hypertrophy (LVH). Deletion of Lcn2 in CKD mice did not improve kidney function or anemia but prevented the development of LVH and improved survival in association with marked reductions in serum FGF23. Lcn2 deletion specifically prevented FGF23 elevations in response to inflammation, but not iron deficiency or phosphate, and administration of LCN2 increased serum FGF23 in healthy and CKD mice by stimulating Fgf23 transcription via activation of cAMP-mediated signaling in bone cells. These results show that kidney-produced LCN2 is an important mediator of increased FGF23 production by bone in response to inflammation and in CKD. LCN2 inhibition might represent a potential therapeutic approach to lower FGF23 and improve outcomes in CKD.

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