scholarly journals Calciprotein particles and fibroblast growth factor 23 contribute to the pathophysiology of hypercalcemia in a patient with renal sarcoidosis

2019 ◽  
Author(s):  
Yoshitaka Iwazu ◽  
Makoto Kuro-o ◽  
Yutaka Miura ◽  
Shin-ichi Takeda ◽  
Toshiyuki Yamada ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Oral Prednisone ◽  
Laboratory Data ◽  
High Serum ◽  
Serum Phosphate Level ◽  
Phosphate Metabolism ◽  
Fibroblast Growth ◽  
Calciprotein Particles

Abstract In patients with sarcoidosis, dysregulated calcium metabolism is one of the frequently observed complications. However, little attention has been paid to abnormal phosphate metabolism. Herein we present the case of a 42-year-old Japanese man with renal sarcoidosis who developed acute kidney injury due to hypercalcemia and nephrolithiasis. Laboratory data showed hypercalcemia with a normal serum phosphate level and high serum 1,25-hydroxyvitamin D3, fibroblast growth factor 23 (FGF23) and calciprotein particle (CPP) levels. After treatment with oral prednisone and bisphosphonate, the laboratory abnormalities and renal dysfunction were resolved. Thus increases in FGF23 and CPP may indicate disturbed phosphate metabolism in renal sarcoidosis.

scholarly journals Minireview: Fibroblast Growth Factor 23 in Phosphate Homeostasis and Bone Metabolism

Endocrinology ◽  
2011 ◽  
Vol 152 (1) ◽  
pp. 4-10 ◽  
Author(s):  
Michiko Hori ◽  
Yuichiro Shimizu ◽  
Seiji Fukumoto
Keyword(s):  
Chronic Kidney Disease ◽  
Growth Factor ◽  
Bone Metabolism ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Phosphate Metabolism ◽  
Fibroblast Growth ◽  
Phosphate Homeostasis ◽  
Mineral And Bone Disorder ◽  
Bone Disorder

Abstract Fibroblast growth factor 23 (FGF23) was identified in 2000. Since then, FGF23 has been found to physiologically regulate phosphate metabolism and aberrant actions of FGF23 results in several disorders of phosphate and bone metabolism. In addition, FGF23 plays an important role in the development of chronic kidney disease–mineral and bone disorder. However, further investigations are necessary, especially with regard to the regulation of FGF23 expression. In this minireview, we focus on the physiological and pathophysiological significance of FGF23 in phosphate and bone metabolism.

scholarly journals Calciprotein particles regulate fibroblast growth factor-23 expression in osteoblasts

2020 ◽  
Vol 97 (4) ◽  
pp. 702-712 ◽  
Author(s):  
Ken-ichi Akiyama ◽  
Yutaka Miura ◽  
Hirosaka Hayashi ◽  
Asuka Sakata ◽  
Yoshitaka Matsumura ◽  
...  
Keyword(s):  
Growth Factor ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
Fibroblast Growth ◽  
Calciprotein Particles

scholarly journals The Role of Mutant UDP-N-Acetyl-α-d-Galactosamine-Polypeptide N-Acetylgalactosaminyltransferase 3 in Regulating Serum Intact Fibroblast Growth Factor 23 and Matrix Extracellular Phosphoglycoprotein in Heritable Tumoral Calcinosis

2006 ◽  
Vol 91 (10) ◽  
pp. 4037-4042 ◽  
Author(s):  
Holly J. Garringer ◽  
Corinne Fisher ◽  
Tobias E. Larsson ◽  
Siobhan I. Davis ◽  
Daniel L. Koller ◽  
...  
Keyword(s):  
Growth Factor ◽  
Combination Therapy ◽  
Fibroblast Growth Factor ◽  
Fibroblast Growth Factor 23 ◽  
High Serum ◽  
Biologically Active ◽  
Tumoral Calcinosis ◽  
Fibroblast Growth ◽  
Loss Of Function ◽  
Matrix Extracellular Phosphoglycoprotein

Abstract Context: Familial tumoral calcinosis (TC) results from disruptions in phosphate metabolism and is characterized by high serum phosphate with normal or elevated 1,25 dihydroxyvitamin vitamin D concentrations and ectopic and vascular calcifications. Recessive loss-of-function mutations in UDP-N-acetyl-α-d-galactosamine-polypeptide N-acetylgalactosaminyltransferase 3 (GALNT3) and fibroblast growth factor-23 (FGF23) result in TC. Objective: The objective of the study was to determine the relationship between GALNT3 and FGF23 in familial TC. Design, Setting, and Patients: We assessed the major biochemical defects and potential genes involved in patients with TC. Intervention: Combination therapy consisted of the phosphate binder Sevelamer and the carbonic anhydrase inhibitor acetazolamide. Results: We report a patient homozygous for a GALNT3 exon 1 deletion, which is predicted to truncate the encoded protein. This patient had high serum FGF23 concentrations when assessed with a C-terminal FGF23 ELISA but low-normal FGF23 levels when tested with an ELISA for intact FGF23 concentrations. Matrix extracellular phosphoglycoprotein has been identified as a possible regulator of phosphate homeostasis. Serum matrix extracellular phosphoglycoprotein levels, however, were normal in the family with GALNT3-TC and a kindred with TC carrying the FGF23 S71G mutation. The tumoral masses of the patient with GALNT3-TC completely resolved after combination therapy. Conclusions: Our findings demonstrate that GALNT3 inactivation in patients with TC leads to inadequate production of biologically active FGF23 as the most likely cause of the hyperphosphatemic phenotype. Furthermore, combination therapy may be effective for reducing the tumoral burden associated with familial TC.

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