Short communication Serum levels of fibroblast growth factor 23 are elevated in patients with active Lupus nephritis Aline L. Resende a , Rosilene M. Elias a , Myles Wolf b , Luciene M. dos Reis a , Fabiana G. Graciolli a , Geuza D. Santos c , Cristiane B. Dias a , Vanda Jorgetti a , Viktoria Woronik a , Rosa M.A. Moysés a,c,⇑ a Department of Medicine, Division of Nephrology, Universidade de São Paulo, Brazil b Division of Nephrology and Hypertension, Department of Medicine, Center for Translational Metabolism and Health, Institute for Public Health and Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL, United States c Universidade Nove de Julho – UNINOVE, São Paulo, Brazil article info Article history: Received 31 October 2016 Received in revised form 21 December 2016 Accepted 25 December 2016 Keywords: Cytokines Inflammation Fibroblast growth factor 23 Lupus nephritis Monocyte chemotactic protein-1 Systemic lupus erythematosus abstract Background: Fibroblast growth factor 23 (FGF23), a phosphate-regulating hormone is an established car- diovascular risk factor. Recently, FGF23 has been related to inflammation. Lupus is an inflammatory dis- ease, and whether FGF23 is associated with Lupus nephritis (LN) activity is unknown. Materials and methods: We studied 15 pre-menopausal patients with recent LN diagnose (62 months) and compared them to 1:1 age-matched healthy control group. We measured serum levels of intact FGF23, interleukin-6 (IL-6), tumor necrosis factor a (TNFa), and urinary levels of monocyte chemotactic protein (MCP1). Results: LN patients (29.5 ± 10 years) presented proteinuria of 4.7 ± 2.9 g/day, and estimated glomerular filtration rate of 37 (31–87) ml/min/1.73 m 2 . They demonstrated higher FGF23 levels when compared to healthy controls [106.7 (80.3–179) vs. 33.6 (25.8–60.9) pg/ml, p < 0.001]. FGF23 levels correlated with urinary MCP1 (r = 0.62, p < 0.001), serum TNFa (r = 0.58, p < 0.001) and serum IL-6 (r = 0.46, p = 0.01). Only the correlation between FGF23 and MCP1 remained significant after adjustments for 25(OH) vita- min D and renal function. Conclusion: Newly diagnosed LN patients demonstrated elevated FGF23 levels that were positively cor- related to urinary MCP1, independently of vitamin D levels and kidney function. If FGF23 may predict clinical outcomes in LN warrants further evaluation. Ó 2016 Elsevier Ltd. All rights reserved. 1. Introduction Systemic Lupus Erythematosus (SLE) is an autoimmune disease that systemically affects several organs. Inflammatory cytokines are thought to contribute to initiation and amplification of end organ damage, although the mechanisms that might influence the loss of self-tolerance are not completely known. Despite con- troversies on their direct pathogenic role in SLE, Interleukin 6 (IL- 6) and Tumor Necrosis Factor a (TNF a), have already been described as biomarkers of SLE activity [1]. Lupus nephritis (LN) occurs in 15% of patients at diagnosis and is characterized by intense inflammation. Urinary levels of monocyte chemoattractant protein-1 (MCP-1) are recognized as a biomarker of LN activity with good sensitivity and specificity [2]. Osteocytes secrete fibroblast growth factor 23 (FGF23), which is a-phosphate-regulating hormone. In early Chronic Kidney Disease (CKD), serum levels of FGF23 increase as a physiologic response to maintain neutral phosphate balance. However, due to the inhi- bition of the 1a-hydroxylase, FGF23 aggravates calcitriol defi- ciency, contributing to the pathogenesis of secondary hyperparathyroidism [3]. Epidemiologic studies have correlated elevated levels of FGF23 with several cardiovascular disease (CVD) manifestations in both general population and CKD patients [4]. Recent studies have demonstrated that higher FGF23 levels are associated with inflammatory markers, in an independent way, raising the possibility that inflammation might influence the corre- lation between FGF23 and CVD [5]. Increased serum levels of FGF23 have already been described in SLE patients, in a study enrolling patients with normal and impaired renal function [6]. However, renal function, a drive for FGF23 elevation, instead of inflammation, could explain this result. Whether FGF23 would be elevated in SLE patients and associated http://dx.doi.org/10.1016/j.cyto.2016.12.022 1043-4666/Ó 2016 Elsevier Ltd. All rights reserved. ⇑ Corresponding author at: Universidade Nove de Julho (UNINOVE), Rua Iperoig, 690 ap 121 – Perdizes, São Paulo, SP 05016-000, Brazil. E-mail address: rosa.moyses@uol.com.br (R.M.A. Moysés). Cytokine 91 (2017) 124–127 Contents lists available at ScienceDirect Cytokine journal homepage: www.journals.elsevier.com/cytokine