FGF23 and inflammation—a vicious coalition in CKD

Czaya, Brian; Faul, Christian

doi:10.1016/j.kint.2019.05.018

Cited by 29 publications

(19 citation statements)

References 9 publications

(17 reference statements)

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“…In addition, one study revealed that PTH had direct and indirect effects through 1,25(OH)2D3 on FGF23 secretion [41]. In the previous studies, the role of Inflammatory Mediators was demonstrated as a potential factor in elevation of FGF23 [19,20]. However, rise of serum ferritin in transfusion dependent thalassemia is related to the repeated transfusions and red blood cells destruction independent of any inflammatory process.…”

Section: Discussionmentioning

confidence: 99%

“…It has been shown that elevations in serum FGF23 concentrations positively correlate with increased serum levels of inflammatory markers in patients with CKD. Many clinical studies have reported the associations between FGF23 and inflammatory markers in disease states [19][20][21][22]. Another effect of FGF23 on the hematopoietic system was proposed in prior investigation that revealed an inhibitory role of FGF23 red blood cell production was reported.…”

Section: Introductionmentioning

confidence: 95%

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Association of vitamin D and FGF23 with serum ferritin in hypoparathyroid thalassemia: a case control study

et al. 2020

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Background FGF23 controls serum l,25(OH)2D3 levels and phosphate homeostasis. This study evaluates the effects of ferritin on intact PTH, FGF23, and l,25(OH)2D3 in patients with major thalassemia. It also evaluates FGF23 changes in patients with hypoparathyroidism to clarify the interaction between FGF23 and PTH in the absence of proper PTH functioning in human. Methods In this case-control study, 25 major-beta thalassemia patients with hypoparathyroidism were age- and gender-matched with major-beta thalassemia patients having normal parathyroid function. Biochemical studies assessed the serum calcium, albumin, phosphorus, alkaline phosphatase, PTH, FGF23, 25(OH) D, 1,25(OH)2D3, ferritin, and the fractional excretion of phosphorous. Results FGF23 was higher in the patients with hypoparathyroidism than the controls (P = 0.002). The fractional excretion of phosphorous was lower in patients with hypoparathyroidism, despite the high level of FGF23 (P = 0.001). There was a correlation between serum 1,25(OH)2D3 and FGF23 with ferritin in the controls (P = < 0.001and P = < 0.001, respectively). Conclusions The present study showed a strong positive correlation between serum ferritin and levels of FGF23 and 1,25(OH)2D3. We hypothesized that ferritin could have a stimulatory effect on the production of 1,25(OH)2D3. Moreover, a rise in FGF23 in patients with thalassemia, might be either associated with the stimulating effect of PTH and 1,25(OH)2D3, or directly related to the stimulating effect of ferritin.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 95%

Association of vitamin D and FGF23 with serum ferritin in hypoparathyroid thalassemia: a case control study

et al. 2020

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“…It has also been proposed that mediators of inflammation (e.g., interleukin 6 and tumor necrosis factor) contribute to fibroblast growth factor (FGF)-23 elevation and that, in turn, FGF-23 increases cytokine production, thus linking systemic inflammation with dysregulated phosphate metabolism in a vicious cycle [165,166]. It has been proposed that inflammatory mediators function as drug targets to decrease the burden of FGF23-associated injury in various tissues, thus offering a novel therapeutic opportunity to decrease the burden of cardiovascular diseases including vascular calcification in kidney disease patients [165,167]. Nevertheless, even in CKD patients within normal range of serum phosphate levels, vascular calcification is often observed.…”

Section: Bone Disease and Vascular Calcificationmentioning

confidence: 99%

Lifestyle, Inflammation, and Vascular Calcification in Kidney Transplant Recipients: Perspectives on Long-Term Outcomes

Sotomayor

Velde-Keyzer

Borst

et al. 2020

JCM

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After decades of pioneering and improvement, kidney transplantation is now the renal replacement therapy of choice for most patients with end-stage kidney disease (ESKD). Where focus has traditionally been on surgical techniques and immunosuppressive treatment with prevention of rejection and infection in relation to short-term outcomes, nowadays, so many people are long-living with a transplanted kidney that lifestyle, including diet and exposure to toxic contaminants, also becomes of importance for the kidney transplantation field. Beyond hazards of immunological nature, a systematic assessment of potentially modifiable—yet rather overlooked—risk factors for late graft failure and excess cardiovascular risk may reveal novel targets for clinical intervention to optimize long-term health and downturn current rates of premature death of kidney transplant recipients (KTR). It should also be realized that while kidney transplantation aims to restore kidney function, it incompletely mitigates mechanisms of disease such as chronic low-grade inflammation with persistent redox imbalance and deregulated mineral and bone metabolism. While the vicious circle between inflammation and oxidative stress as common final pathway of a multitude of insults plays an established pathological role in native chronic kidney disease, its characterization post-kidney transplant remains less than satisfactory. Next to chronic inflammatory status, markedly accelerated vascular calcification persists after kidney transplantation and is likewise suggested a major independent mechanism, whose mitigation may counterbalance the excess risk of cardiovascular disease post-kidney transplant. Hereby, we first discuss modifiable dietary elements and toxic environmental contaminants that may explain increased risk of cardiovascular mortality and late graft failure in KTR. Next, we specify laboratory and clinical readouts, with a postulated role within persisting mechanisms of disease post-kidney transplantation (i.e., inflammation and redox imbalance and vascular calcification), as potential non-traditional risk factors for adverse long-term outcomes in KTR. Reflection on these current research opportunities is warranted among the research and clinical kidney transplantation community.

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“…Although the role of FGF23 in promoting inflammation in diseases such as chronic kidney or lung disease [35][36][37] , might suggest a deleterious role in ALS patients, one report observed that ectopic FGF23 can improve aspects of mitochondrial function in skeletal muscle 31 . Its upregulation in ALS may therefore represent an attempt to compensate for mitochondrial dysfunction in skeletal muscle that starts at the very earliest stages of disease pathology 38 .…”

Section: Discussionmentioning

confidence: 99%

FGF23, A Novel Muscle Biomarker Detected in The Early Stages of ALS

Kazamel

Benatar

et al. 2021

Preprint

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Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease characterized by progressive muscle weakness. Skeletal muscle is a prime source for biomarker discovery since it is one of the earliest sites to manifest disease pathology. From a prior RNA sequencing project, we identified FGF23 as a potential muscle biomarker in ALS. Here, we validate this finding with a large collection of ALS muscle samples and found a 13-fold increase over normal controls. FGF23 was also increased in the SOD1G93A mouse, beginning at a very early stage and well before the onset of clinical symptoms. FGF23 levels progressively increased through end-stage in the mouse. Immunohistochemistry of ALS muscle showed prominent FGF23 immunoreactivity in the endomysial connective tissue and along the muscle membrane. ELISA of plasma samples from the SOD1G93A mouse showed an increase in FGF23 at end-stage whereas no increase was detected in a large cohort of ALS patients. In conclusion, FGF23 is a novel muscle biomarker in ALS and joins a molecular signature that emerges in very early preclinical stages. The early appearance of FGF23 and its progressive increase with disease advancement offers a new direction for exploring the molecular basis or response to the underlying pathology of ALS.

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FGF23 and inflammation—a vicious coalition in CKD

Cited by 29 publications

References 9 publications

Association of vitamin D and FGF23 with serum ferritin in hypoparathyroid thalassemia: a case control study

Association of vitamin D and FGF23 with serum ferritin in hypoparathyroid thalassemia: a case control study

Lifestyle, Inflammation, and Vascular Calcification in Kidney Transplant Recipients: Perspectives on Long-Term Outcomes

FGF23, A Novel Muscle Biomarker Detected in The Early Stages of ALS

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