Effect of Salt Intervention on Serum Levels of Fibroblast Growth Factor 23 (FGF23) in Chinese Adults: An Intervention Study

Hu, Jiawen; Wang, Yang; Chu, Chao; Mu, Jianjun

doi:10.12659/msm.906489

Cited by 12 publications

(9 citation statements)

References 27 publications

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“…↓1, 25 the expected increase in BP and resulted in a significant decline of FGF23 levels [106], thus supporting the notion that changes in Na intake induce opposing regulatory changes in FGF23.…”

Section: Nonpharmacologic Interventionssupporting

confidence: 60%

Fibroblast growth factor 23—Klotho and hypertension: experimental and clinical mechanisms

2020

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Hypertension (HTN) and chronic kidney disease (CKD) are increasingly recognized in pediatric patients and represent risk factors for cardiovascular morbidity and mortality later in life. In CKD, enhanced tubular sodium reabsorption is a leading cause of HTN due to augmented extracellular fluid volume expansion. The renin-angiotensin-aldosterone system (RAAS) upregulates various tubular sodium cotransporters that are also targets of the hormone fibroblast growth factor 23 (FGF23) and its co-receptor Klotho. FGF23 inhibits the activation of 1,25-dihydroxyvitamin D that is a potent suppressor of renin biosynthesis. Here we review the complex interactions and disturbances of the FGF23-Klotho axis, vitamin D, and the RAAS relevant to blood pressure regulation and discuss the therapeutic strategies aimed at mitigating their pathophysiologic contributions to HTN.

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Section: Nonpharmacologic Interventionssupporting

confidence: 60%

Fibroblast growth factor 23—Klotho and hypertension: experimental and clinical mechanisms

2020

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“…A recent study demonstrated an inverse correlation between 24‐hour urinary sodium levels and serum FGF23 concentrations in healthy adults. 27 As all participants of this study were prescribed a special diet restricting salt consumption during the treatment, we felt it was unlikely that salt intake played a confounding role in the antihypertensive treatment.…”

Section: Discussionmentioning

confidence: 99%

Plasma Fibroblast Growth Factor 23 as a Predictor for Fosinopril Therapeutic Efficacy in Pediatric Primary Hypertension

Lin

Cui

Yuan

et al. 2022

JAHA

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Background Plasma fibroblast growth factor 23 (FGF23) has been reported to be a predictive biomarker for therapeutic effectiveness of angiotensin‐converting enzyme inhibitors in heart failure. Higher plasma FGF23 levels have been shown in pediatric primary hypertension, but the predictive value of FGF23 for angiotensin‐converting enzyme inhibitors’ effectiveness in pediatric primary hypertension has not been documented. Methods and Results This is a prospective study. An exploratory study with 139 patients was first conducted to determine the cutoff value of FGF23 for the prediction of treatment responsiveness. After receiving fosinopril for 4 weeks, of all 139 patients, 91 responded, while 48 did not respond to the treatment, and the responders had a significantly higher baseline plasma FGF23 level than nonresponders ( P <0.01). Multiple regression analysis revealed a significant impact of baseline plasma FGF23 levels on fosinopril responsiveness ( P <0.05). The receiver operating characteristic curve analysis showed that the plasma FGF23 predicted the effectiveness of fosinopril treatment with an area under the curve of 0.784 (95% CI, 0.704–0.863) for a sensitivity and a specificity of 67.0% and 89.6%, respectively, for a cutoff value of 62.08 RU/mL. Subsequently, another group of 40 patients were recruited for validation. The blood pressure control rate in those (n=22) with baseline plasma FGF23 >62.08 RU/mL was significantly higher than that in children (n=18) with FGF23 ≤62.08 RU/mL ( P <0.05). Conclusions Plasma FGF23 might be a valuable biomarker to guide fosinopril therapy for primary hypertension in children.

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“…As described before, this intervention study included three periods, namely, a 3-day normal diet, a 7-day low-Na + diet (51.3 mmol/d sodium or 3.0 g/d NaCl), and a 7-day high-Na + diet (307.7 mmol/d sodium or 18 g/d NaCl) ( Figure 2). 11…”

Section: Dietary Interventionmentioning

confidence: 99%

“…Previously, we, as well as other researchers, found salt intake could influence serum level of FGF23. 11,21,22 As one of the key As mentioned above, the dysregulation of sodium excretion played pivotal role in the development of salt sensitivity. We found the regulation of serum FGF23 by salt intake was more prominent in salt-resistant participants in previous study.…”

Section: F I G U R Ementioning

confidence: 99%

“…Previously, we and other researchers have found salt intake could influence serum level of FGF23, and the response of FGF23 was more significant in salt-resistant participants. 11 Therefore, it is intriguing to figure out the responses of Klotho to dietary salt intake and the influence of salt sensitivity on the responses of Klotho. After that, we would get a better understanding on the regulation of sodium balance and the differences of sodium regulation between salt-sensitive and salt-resistant participants.…”

Section: Introductionmentioning

confidence: 99%

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Effects of salt intervention on serum levels of Klotho influenced by salt sensitivity

Chu

Shi

et al. 2020

J of Clinical Hypertension

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Klotho was involved in sodium reabsorption and the regulation of blood pressure. Animal studies indicated Klotho deficiency could mediate the development of saltsensitive hypertension, indicating its correlation with salt sensitivity. We aimed to explore the responses of Klotho to salt intake through dietary intervention in Chinese adults. Forty-four participants were enrolled from Lantian county of Shaanxi, China. All participants sequentially underwent a 3-day normal diet, a 7-day low-Na + diet, and a 7-day high-Na + diet. The concentrations of serum Klotho were assessed by using ELISA kits. Serum level of Klotho was 360.44 ± 93.89 pg/mL at baseline and increased while changed to low-salt diet (478.65 ± 183.25 vs 360.44 ± 93.89 pg/mL, P < .001). During high-salt diet, serum Klotho decreased to 354.37 ± 98.16 pg/mL (P < .001, compared to low-salt diet). The overall responses of Klotho were more prominent in salt-resistant participants. Serum Klotho of salt-resistant group changed from 353.92 ± 97.65 pg/mL to 496.76 ± 196.21 pg/mL while changed from normal diet to low-salt diet (P < .001) and decreased to 350.37 ± 99.50 pg/mL during high-salt intake (P < .001). Furthermore, the response of serum Klotho to low-salt intervention was much greater in salt-resistant individuals than in salt-sensitive ones. The responses of serum Klotho to dietary salt intervention were influenced by salt sensitivity, which was more prominent in salt-resistant participants.

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Effect of Salt Intervention on Serum Levels of Fibroblast Growth Factor 23 (FGF23) in Chinese Adults: An Intervention Study

Cited by 12 publications

References 27 publications

Fibroblast growth factor 23—Klotho and hypertension: experimental and clinical mechanisms

Fibroblast growth factor 23—Klotho and hypertension: experimental and clinical mechanisms

Plasma Fibroblast Growth Factor 23 as a Predictor for Fosinopril Therapeutic Efficacy in Pediatric Primary Hypertension

Effects of salt intervention on serum levels of Klotho influenced by salt sensitivity

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