Linkage of Fibroblast Growth Factor 23 and Phosphate in Serum: Phosphate and Fibroblast Growth Factor 23 Reduction by Increasing Dose of Sevelamer

Ghorbanihaghjo, Amir; Argani, Hassan; Golmohamadi, Zahra; Rashtchizadeh, Nadereh; Abbasi, Mehran Mesgari; Bargahi, Nasrin; Vatankhah, Amir Mansour; Sanajou, Davoud

doi:10.11005/jbm.2018.25.3.153

Cited by 6 publications

(5 citation statements)

References 28 publications

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“…Another argument to be looked at with caution is that, although not statistically significant, in our study we observed in the group with VC a higher calcium-based phosphate binders intake and lower non-calcium-based phosphate binders intake, resulting in better phosphorous control in that group. In clinical trials for the pharmacological management of phosphate imbalance, phosphate binders, especially non-calcium-based phosphate binders, were reported to low serum phosphorous levels by decreasing fibroblast growth factor-23 (FGF-23), which has been shown to stimulate phosphorous excretion and reduce VC [ 68 ] with protective effects on VC [ 72 ].…”

Section: Discussionmentioning

confidence: 99%

Vascular Calcification and the Gut and Blood Microbiome in Chronic Kidney Disease Patients on Peritoneal Dialysis: A Pilot Study

et al. 2022

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Vascular calcification (VC) is a frequent condition in chronic kidney disease (CKD) and a well-established risk factor for the development of cardiovascular disease (CVD). Gut dysbiosis may contribute to CVD and inflammation in CKD patients. Nonetheless, the role of gut and blood microbiomes in CKD-associated VC remains unknown. Therefore, this pilot study aimed to explore the link between gut and blood microbiomes and VC in CKD patients on peritoneal dialysis (CKD-PD). Our results showed relative changes in specific taxa between CKD-PD patients with and without VC, namely Coprobacter, Coprococcus 3, Lactobacillus, and Eubacterium eligens group in the gut, and Cutibacterium, Pajaroellobacter, Devosia, Hyphomicrobium, and Pelomonas in the blood. An association between VC and all-cause mortality risk in CKD-PD patients was also observed, and patients with higher mortality risk corroborate the changes of Eubacterium eligens in the gut and Devosia genus in the blood. Although we did not find differences in uremic toxins, intestinal translocation markers, and inflammatory parameters among CKD-PD patients with and without VC, soluble CD14 (sCD14), a nonspecific marker of monocyte activation, positively correlated with VC severity. Therefore, gut Eubacterium eligens group, blood Devosia, and circulating sCD14 should be further explored as biomarkers for VC, CVD, and mortality risk in CKD.

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Section: Discussionmentioning

confidence: 99%

Vascular Calcification and the Gut and Blood Microbiome in Chronic Kidney Disease Patients on Peritoneal Dialysis: A Pilot Study

et al. 2022

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“…At all phases of CKD, hyperphosphataemia is a generally acknowledged risk factor for mortality and cardiovascular disease [ 85 ]. It was also reported that the blood P levels increased in adenine-induced CKD rats [ 86 ]. Bifidobacteria produce SCFA and makes the intestinal lumen more acidic and, therefore, enhances Ca ionisation.…”

Section: Discussionmentioning

confidence: 99%

Ameliorating effect of probiotics in a rat model of chronic kidney disease

Inatomi

Honma²

2023

PLoS ONE

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Chronic kidney disease is a prevalent and significant disease worldwide. This study investigated the effects of a medicinal probiotic (BIO-THREE, TOA Biopharma Co., Ltd, Tokyo, Japan) with safety assurance that contained Bacillus subtilis TO-A, Enterococcus faecium T-110, and Clostridium butyricum TO-A in chronic kidney disease. BIO-THREE was approved as a medical drug by the Japanese Ministry of Health, Labour and Welfare and is widely used in the human medical field to improve various symptoms caused by abnormal intestinal microflora. Sixty male rats were randomly assigned to three groups: (1) normal group (n = 20, group 1), rats were given a normal diet for 3 weeks, followed by phosphate-buffered solution (once daily, orally) and a normal diet for 4 weeks; (2) control group (n = 20, Group 2), rats were given a normal diet including 0.75% adenine for 3 weeks, followed by phosphate-buffered saline (once daily, orally) and a normal diet for 4 weeks; and (3) probiotic group (n = 20, Group 3), rats were given a normal diet including 0.75% adenine for 3 weeks, followed by probiotics (once daily, orally) and a normal diet for 4 weeks. Probiotic administration resulted in a decrease in intestinal pH by increasing short-chain fatty acid (SCFA) production, and consequently suppressed the production of urea toxin production, thus, protecting renal function. The lower intestinal pH also promoted a reduction in the blood phosphorus levels by promoting ionisation of calcium and its binding to free phosphorus. This probiotic-induced increase in SCFA production reduced intestinal permeability, inhibited blood lipopolysaccharide and urea toxin production, and prevented the weakening of muscle function and strength. Moreover, it improved dysbiosis in the gut. This study shows the potential of this probiotics approved as medicinal drug to reduce chronic kidney disease progression, especially where safety is required. Further studies are warranted to validate these findings in humans.

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“…Phosphate binders have been shown to reduce serum phosphorus levels by decreasing FGF23, which accelerates phosphorus excretion and prevents vascular calcification. Compared to calcium phosphate binders, a recent randomized study showed that the phosphate binder sevelamer reduced mortality more in elderly hemodialysis patients [ 210 , 211 ].…”

Section: Translational Opportunitiesmentioning

confidence: 99%

Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities

Ortega,

De Leon-Oliva,

Gimeno-Longas

et al. 2024

Biomolecules

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Calcification is a process of accumulation of calcium in tissues and deposition of calcium salts by the crystallization of PO43− and ionized calcium (Ca2+). It is a crucial process in the development of bones and teeth. However, pathological calcification can occur in almost any soft tissue of the organism. The better studied is vascular calcification, where calcium salts can accumulate in the intima or medial layer or in aortic valves, and it is associated with higher mortality and cardiovascular events, including myocardial infarction, stroke, aortic and peripheral artery disease (PAD), and diabetes or chronic kidney disease (CKD), among others. The process involves an intricate interplay of different cellular components, endothelial cells (ECs), vascular smooth muscle cells (VSMCs), fibroblasts, and pericytes, concurrent with the activation of several signaling pathways, calcium, Wnt, BMP/Smad, and Notch, and the regulation by different molecular mediators, growth factors (GFs), osteogenic factors and matrix vesicles (MVs). In the present review, we aim to explore the cellular players, molecular pathways, biomarkers, and clinical treatment strategies associated with vascular calcification to provide a current and comprehensive overview of the topic.

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Linkage of Fibroblast Growth Factor 23 and Phosphate in Serum: Phosphate and Fibroblast Growth Factor 23 Reduction by Increasing Dose of Sevelamer

Cited by 6 publications

References 28 publications

Vascular Calcification and the Gut and Blood Microbiome in Chronic Kidney Disease Patients on Peritoneal Dialysis: A Pilot Study

Vascular Calcification and the Gut and Blood Microbiome in Chronic Kidney Disease Patients on Peritoneal Dialysis: A Pilot Study

Ameliorating effect of probiotics in a rat model of chronic kidney disease

Vascular Calcification: Molecular Networking, Pathological Implications and Translational Opportunities

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