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Biomarker studies
Analysis of urinary macrophage migration inhibitory factor in systemic lupus erythematosus
  1. Fabien B Vincent1,
  2. Laura Slavin1,
  3. Alberta Y Hoi1,
  4. Arthur Richard Kitching1,
  5. Fabienne Mackay2,3,
  6. James Harris1,
  7. Rangi Kandane-Rathnayake1 and
  8. Eric F Morand1
  1. 1 Centre for Inflammatory Diseases, School of Clinical Sciences at Monash Health, Monash University, Clayton, Victoria, Australia
  2. 2 Department of Microbiology and Immunology, School of Biomedical Sciences, Faculty of Medicine, Dentistry and Health Sciences, The University of Melbourne, Melbourne, Victoria, Australia
  3. 3 Department of Immunology and Pathology, Central Clinical School, Monash University, Melbourne, Victoria, Australia
  1. Correspondence to Dr Fabien B Vincent; fabien.vincent{at}monash.edu

Abstract

Objective To characterise the clinical relevance of urinary macrophage migration inhibitory factor (uMIF) concentrations in patients with systemic lupus erythematosus (SLE).

Methods MIF, adjusted for urine creatinine, was quantified by ELISA in urine samples from 64 prospectively recruited patients with SLE. Serum MIF and urinary monocyte chemoattractant protein 1 (uMCP-1) were quantified by ELISA in a subset of patients (n = 39). Disease activity was assessed using the SLE Disease Activity Index-2000 (SLEDAI-2K) score.

Results uMIF was detectable in all patients with SLE. uMIF was positively correlated with overall SLEDAI-2K, was significantly higher in patients with SLE with high disease activity (SLEDAI-2K≥10) compared with those with inactive disease (SLEDAI-2K<4), and this association remained significant after adjusting for ethnicity, flare and use of immunosuppressants. uMIF was also significantly higher in SLE patients with flare of disease, although not confirmed in multivariable analysis. No significant differences in uMIF levels were observed according to the presence of renal disease activity, as assessed by renal SLEDAI-2K or biopsy-confirmed lupus nephritis. In contrast, uMCP-1 was significantly higher in SLE patients with active renal disease. uMIF expression was not associated with irreversible organ damage accrual or glucocorticoid use.

Conclusions These data suggest uMIF as a potential overall but not renal-specific SLE biomarker, whereas uMCP-1 is a renal-specific SLE biomarker.

  • biomarker
  • lupus nephritis
  • macrophage migration inhibitory factor
  • monocyte chemoattractant protein 1
  • systemic lupus erythematosus

This is an open access article distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited, appropriate credit is given, any changes made indicated, and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/

https://doi.org/10.1136/lupus-2018-000277

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    Footnotes

    • RK-R and EFM contributed equally.

    • Contributors LS collected urine samples and both LS and FBV analysed them. FBV drafted the manuscript. All authors contributed to experimental design, analysis and drafting of the paper. All authors read and gave final approval of the version to be published.

    • Funding FM is recipient of fellowships from the NHMRC of Australia. EFM was supported by the Kim Jolly Lupus Research Trust, and the Monash lupus database has received support from Arthritis and Osteoporosis Victoria and unrestricted educational grants from Glaxosmithkline, UCB and Eli Lilly Australia.

    • Competing interests EFM has been consultants to GSK and Eli Lilly. The other authors have no conflict of interest to declare. This study had no external funding source.

    • Patient consent Obtained.

    • Ethics approval Human Research Ethics Committee, Monash Health.

    • Provenance and peer review Not commissioned; externally peer reviewed.

    • Data sharing statement Requests for non-identifiable data can be made to Dr Fabien B Vincent.