Serum levels of fibroblast growth factor 23 are elevated in patients with active Lupus nephritis

Resende, Aline Lázara; Elias, Rosilene M.; Wolf, Myles; Reis, Luciene M. dos; Graciolli, Fabiana G.; Santos, Geuza Dutra dos; Dias, Cristiane Bitencourt; Jorgetti, Vanda; Woronik, Viktoria; Moysés, Rosa M.A.

doi:10.1016/j.cyto.2016.12.022

Cited by 13 publications

(11 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…This study confirms previous reports that serum FGF23 is elevated in SLE patients (more so in LN), 32 , 33 and generates a conceptual framework for its atherogenic role in these patients. We excluded subjects with exaggerated ACVD risk profile because of diabetes mellitus, obesity, advanced renal disease or age.…”

Section: Discussionsupporting

confidence: 91%

“…Serum iFGF23 varied the same way as CC-IMT and ICRI (LN > SLE > Controls), with significant differences between the 3 study groups, also in line with the few previous reports. 32 , 33 …”

Section: Discussionmentioning

confidence: 99%

“… 38 Therefore, LN patients typically have in parallel significantly higher level of FGF23 and higher burden of ACVD, compared with SLE patients without nephritis. 33 FGF23 may thus prove to be an important mediator of accelerated ACVD in SLE patients, with a particularly more prominent role in patients with LN. Controlling the circulating level of this key molecule may then become a novel therapeutic approach to reduce cardiovascular morbimortality in SLE patients.…”

Section: Introductionmentioning

confidence: 99%

“…Two small studies reported significantly higher serum FGF23 in SLE patients compared with controls, with a still higher level in patients with lupus nephritis (LN). 32 , 33 The inflammatory reaction of active lupus upregulates FGF23 production by osteocytes. 34 The development of LN is conductive for a further rise of circulating FGF23, possibly induced by hyperparathyroidism, 35 hyperphosphataemia, 36 impaired renal clearance, 37 and klotho deficiency.…”

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Accelerated Atherosclerosis in Systemic Lupus Erythematosus: Role of Fibroblast Growth Factor 23- Phosphate Axis

Ammar¹,

Mohamed²,

Khalil³

et al. 2021

IJNRD

View full text Add to dashboard Cite

Section: Discussionsupporting

confidence: 91%

“…Serum iFGF23 varied the same way as CC-IMT and ICRI (LN > SLE > Controls), with significant differences between the 3 study groups, also in line with the few previous reports. 32 , 33 …”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Accelerated Atherosclerosis in Systemic Lupus Erythematosus: Role of Fibroblast Growth Factor 23- Phosphate Axis

Ammar¹,

Mohamed²,

Khalil³

et al. 2021

IJNRD

View full text Add to dashboard Cite

“…The association between FGF23 and inflammation has been reported in many diseases (Munoz Mendoza et al, 2012; Hanks et al, 2015; Holecki et al, 2015; Dounousi et al, 2016; Francis and David, 2016; Okan et al, 2016; Sato et al, 2016; Resende et al, 2017; Krick et al, 2018). Multiple inflammatory signaling pathways seem to interact closely to regulate FGF23 production and cleavage during acute or chronic inflammation.…”

Section: Epo Iron Ckd and Inflammation Are Important Regulators Ofmentioning

confidence: 91%

The EPO-FGF23 Signaling Pathway in Erythroid Progenitor Cells: Opening a New Area of Research

et al. 2019

View full text Add to dashboard Cite

We provide an overview of the evidence for an erythropoietin-fibroblast growth factor 23 (FGF23) signaling pathway directly influencing erythroid cells in the bone marrow. We outline its importance for red blood cell production, which might add, among others, to the understanding of bone marrow responses to endogenous erythropoietin in rare hereditary anemias. FGF23 is a hormone that is mainly known as the core regulator of phosphate and vitamin D metabolism and it has been recognized as an important regulator of bone mineralization. Osseous tissue has been regarded as the major source of FGF23. Interestingly, erythroid progenitor cells highly express FGF23 protein and carry the FGF receptor. This implies that erythroid progenitor cells could be a prime target in FGF23 biology. FGF23 is formed as an intact, biologically active protein (iFGF23) and proteolytic cleavage results in the formation of the presumed inactive C-terminal tail of FGF23 (cFGF23). FGF23-knockout or injection of an iFGF23 blocking peptide in mice results in increased erythropoiesis, reduced erythroid cell apoptosis and elevated renal and bone marrow erythropoietin mRNA expression with increased levels of circulating erythropoietin. By competitive inhibition, a relative increase in cFGF23 compared to iFGF23 results in reduced FGF23 receptor signaling and mimics the positive effects of FGF23-knockout or iFGF23 blocking peptide. Injection of recombinant erythropoietin increases FGF23 mRNA expression in the bone marrow with a concomitant increase in circulating FGF23 protein. However, erythropoietin also augments iFGF23 cleavage, thereby decreasing the iFGF23 to cFGF23 ratio. Therefore, the net result of erythropoietin is a reduction of iFGF23 to cFGF23 ratio, which inhibits the effects of iFGF23 on erythropoiesis and erythropoietin production. Elucidation of the EPO-FGF23 signaling pathway and its downstream signaling in hereditary anemias with chronic hemolysis or ineffective erythropoiesis adds to the understanding of the pathophysiology of these diseases and its complications; in addition, it provides promising new targets for treatment downstream of erythropoietin in the signaling cascade.

show abstract

FGF23‐related hypophosphatemic rickets preceding the onset of systemic lupus erythematosus: A juvenile case

tabei,

Ohtsu,

Shimada

et al. 2024

Clinical Case Reports

View full text Add to dashboard Cite

Key Clinical MessageThis case report describes the clinical course of a juvenile female with FGF23‐related hypophosphatemic rickets preceding the onset of SLE. Our study demonstrates the possibility of hypophosphatemic rickets as an early symptom of SLE.AbstractFibroblast growth factor 23 (FGF23)‐related hypophosphatemic rickets is observed in both genetic and acquired disorders. Various reports describe FGF23‐related hypophosphatemia with systemic lupus erythematosus (SLE), although FGF23‐related hypophosphatemia preceding the onset of SLE has never been described. Here, we report the case of a 9‐year‐old female with FGF23‐related hypophosphatemic rickets preceding the onset of SLE. The patient presented to us with arthralgia in the lower extremities and abnormality of gait lasting for 8 months. She was diagnosed with FGF23 hypophosphatemic rickets due to the presence of hypophosphatemic rickets symptoms and high serum levels of FGF23. Additional examination excluded hereditary diseases and tumor‐induced osteomalacia. Three months after diagnosis of FGF23‐related hypophosphatemic rickets, she developed nephritis and was diagnosed with SLE. She was treated with prednisolone, hemodialysis, and disease‐modifying drugs, as well as oral sodium phosphate to improve hypophosphatemia. Serum anti‐double‐stranded DNA antibody (dsDNAab) and plasma tumor necrosis factor‐α (TNF‐α) were elevated at FGF23‐related hypophosphatemic rickets diagnosis. During the clinical course, serum FGF23 correlated with dsDNAab and TNF‐α serum levels, which are involved in SLE disease activity. In this case, FGF23‐related hypophosphatemic rickets without hereditary diseases or tumor‐induced osteomalacia occurred before the appearance of juvenile SLE symptoms, and serum FGF23 represented disease activity in SLE.

show abstract

Serum levels of fibroblast growth factor 23 are elevated in patients with active Lupus nephritis

Cited by 13 publications

References 13 publications

Accelerated Atherosclerosis in Systemic Lupus Erythematosus: Role of Fibroblast Growth Factor 23- Phosphate Axis

Accelerated Atherosclerosis in Systemic Lupus Erythematosus: Role of Fibroblast Growth Factor 23- Phosphate Axis

The EPO-FGF23 Signaling Pathway in Erythroid Progenitor Cells: Opening a New Area of Research

FGF23‐related hypophosphatemic rickets preceding the onset of systemic lupus erythematosus: A juvenile case

Contact Info

Product

Resources

About