Background: Fibroblast growth factor (FGF) 23 is a well-known phosphaturic hormone produced mainly by bone cells to maintain phosphate and mineral homeostasis. Serum FGF23 levels are elevated in patients with chronic kidney disease (CKD), and elevated FGF23 might increase the risk of cardiovascular disease (CVD). Several reports have documented an increased incidence of risk factors for osteopenia, CKD, and CVD in people living with HIV (PLWH). However, few reports related to FGF23 in PLWH have been published.
Methods: Male HIV patients who presented to the outpatient clinic of Teikyo University Hospital, Tokyo, Japan, in 2015 and were treated with antiretroviral therapy (ART) for > 6 months were enrolled in the study. In addition to serum FGF23 measurements, the clinical factors assessed included age, ART regimens, and laboratory data. Spearman correlation and multiple regression analysis were performed to determine factors significantly associated with FGF23.
Results: In total, 67 patients were enrolled in the present study. The median age was 43.7 years, the median CD4 count was 529 cells/μL, and the median serum FGF23 level was 36.0 pg/mL. Based on correlation and multiple regression analyses, serum FGF23 levels were significantly correlated with HIV RNA > 50 copies (correlation analysis: t = 3.4259, P = 0.0011 / multiple regression analysis: P = 0.00106) or abacavir (ABC)/lamivudine (3TC) use (t = 2.8618, P = 0.0057 / P = 0.02704).
Conclusion: Factors significantly associated with elevated serum FGF23 levels included poor virologic control and ABC/3TC use.
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http://dx.doi.org/10.2174/1570162X17666190903231203 | DOI Listing |
J Clin Endocrinol Metab
January 2025
Kidney Research Institute, Department of Medicine, University of Washington, Seattle, WA.
Context: The response to treatment with vitamin D varies between patients.
Objective: To identify genetic variants associated with the biochemical response to vitamin D3 supplementation.
Design: Randomized placebo-controlled trial conducted between 2017 and 2019.
Int J Cardiol Heart Vasc
February 2025
Department of Nephropathy, the First Affiliated Hospital of Anhui Medical University, Hefei, Anhui, People's Republic of China.
Background: Heart failure (HF) is a significant cause of death among patients with chronic kidney disease (CKD). Emerging data suggest a crucial role of fibroblast growth factor 23 (FGF23) in the pathogenesis of HF in CKD patients. The present study aimed to investigate whether the serum intact FGF23 (iFGF23) level is elevated when ejection fraction (EF) is preserved and to evaluate its predictive value for incident HF and cardiac mortality in CKD patients with preserved EF.
View Article and Find Full Text PDFBMC Nephrol
January 2025
Department of Nephrology, Southern University of Science and Technology Hospital, Shenzhen, China.
Background: Calcification of the radial artery is one of the main causes of anastomotic stenosis in autogenous arteriovenous fistulas in uremic patients. However, the pathogenesis of calcification is still unknown. This study attempted to screen and validate the risk factors for vascular calcification in patients with uremia.
View Article and Find Full Text PDFClin Kidney J
January 2025
MP3CV Laboratory, Jules Verne University of Picardie, Amiens, France.
Background: The serum calcification propensity test (or T50 test) might become a standard tool for the assessment of vascular calcification risk and T50 might be a valuable biomarker in clinical trials of treatments intended to slow the progression of vascular calcification. Literature data suggest that non-calcium-containing phosphate binders can influence T50 in chronic dialysed patients. However, it is not clear whether similar interventions are effective in patients at earlier stages of chronic kidney disease (CKD).
View Article and Find Full Text PDFHepatol Commun
January 2025
Department of Veterinary Medical Science, Veterinary Pharmacology, Graduate School of Agriculture and Life Sciences, The University of Tokyo, Tokyo, Japan.
Background: Liver fibrosis could lead to serious secondary diseases, including osteodystrophy. The interaction between liver and bone has not been fully elucidated, thus existing therapies for osteodystrophy secondary to liver fibrosis are often ineffective. FGF23 was initially found as an endocrine regulator of phosphate homeostasis, but recently, its involvement in fibrosis has been suggested.
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