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Abstract Number: 2127

A Role of Vascular Cell Adhesion Molecule 1 and Activated Leukocyte Cell Adhesion Molecule in Lupus Nephritis

Ioannis Parodis1,2, Sirisha Gokaraju3, Agneta Zickert1,2, Ting Zhang3, Deena Habazi3, Anders Larsson4, Elisabet Svenungsson1,2, Chandra Mohan3 and Iva Gunnarsson1,2, 1Division of Rheumatology, Department of Medicine, Karolinska Institutet, Stockholm, Sweden, Stockholm, Sweden, 2Rheumatology, Karolinska University Hospital, Stockholm, Sweden, Stockholm, Sweden, 3Department of Biomedical Engineering, University of Houston, Houston, Texas, USA, Houston, TX, 4Department of Medical Sciences/Clinical Chemistry, Uppsala University, Uppsala, Sweden, Uppsala, Sweden

Meeting: 2018 ACR/ARHP Annual Meeting

Keywords: Adhesion molecules, Biomarkers, lupus nephritis and systemic lupus erythematosus (SLE), Urinary Biomarkers

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Session Information

Date: Tuesday, October 23, 2018

Title: Systemic Lupus Erythematosus – Etiology and Pathogenesis Poster III

Session Type: ACR Poster Session C

Session Time: 9:00AM-11:00AM

Background/Purpose: Reliable non-invasive biomarkers for lupus nephritis (LN) are lacking. We investigated two adhesion molecules as urinary biomarkers in LN, i.e. vascular cell adhesion molecule 1 (VCAM-1) and activated leukocyte cell adhesion molecule (ALCAM), the latter also known as cluster of differentiation 166 (CD166).

Methods: Patients with systemic lupus erythematosus (SLE) (n=111, all female) and non-SLE population based controls (n=99, all female) were included. At inclusion, we assessed renal activity using the renal descriptors of the SLE disease activity index 2000 (SLEDAI-2K) and the renal domain of the British Isles Lupus Assessment Group (BILAG) index. Renal BILAG was not assessed in patients with end-stage renal disease (n=2). Urine and plasma VCAM-1 and urine ALCAM levels in samples obtained from patients and controls at the time of inclusion were estimated using enzyme-linked immunosorbent assay. Urine VCAM-1 and ALCAM levels were next adjusted by urine creatinine. For comparisons, we used the Mann-Whitney U test.

Results: In comparative analysis between SLE patients and controls, we observed higher urine VCAM-1 levels (P=0.001) and a trend towards higher plasma VCAM-1 concentrations (P=0.051) in SLE patients, but urine levels of ALCAM did not differ between the two groups. Furthermore, urinary VCAM-1/creatinine and ALCAM/creatinine ratio levels were higher in SLE patients (P<0.001 for both). We next conducted comparative analysis between SLE patients with current renal activity (renal BILAG A–C; n=10) and SLE patients with no current renal activity or no history of renal involvement (renal BILAG D–E; n=98). In this analysis, plasma VCAM-1 and urine ALCAM levels were higher in patients with active renal SLE (P=0.007 and P=0.009, respectively), but urine VCAM-1 levels were not found to differ. Urinary VCAM-1/creatinine and ALCAM/creatinine ratio levels were higher in SLE patients with renal activity (P=0.029 and P=0.001, respectively). Finally, we compared SLE patients with a renal SLEDAI-2K>0 (n=31) with SLE patients with renal SLEDAI-2K=0 (n=80). Here, plasma VCAM-1 concentrations were higher in patients with renal SLEDAI-2K>0 (P=0.018), but urine levels of VCAM-1 and ALCAM did not differ. However, both urinary VCAM-1/creatinine and urinary ALCAM/creatinine ratio levels were higher in SLE patients with renal SLEDAI-2K>0 (P=0.023 and P=0.006, respectively).

Conclusion: A role of VCAM-1 in SLE and LN is implicated. While VCAM-1 appears to reflect SLE disease state, ALCAM might have particular importance in renal SLE. After correction for creatinine, urine levels of both VCAM-1 and ALCAM showed ability to distinguish between SLE patients with active renal involvement compared to SLE patients with quiescent nephritis or no nephritis history.


Disclosure: I. Parodis, None; S. Gokaraju, None; A. Zickert, None; T. Zhang, None; D. Habazi, None; A. Larsson, None; E. Svenungsson, None; C. Mohan, None; I. Gunnarsson, None.

To cite this abstract in AMA style:

Parodis I, Gokaraju S, Zickert A, Zhang T, Habazi D, Larsson A, Svenungsson E, Mohan C, Gunnarsson I. A Role of Vascular Cell Adhesion Molecule 1 and Activated Leukocyte Cell Adhesion Molecule in Lupus Nephritis [abstract]. Arthritis Rheumatol. 2018; 70 (suppl 9). https://acrabstracts.org/abstract/a-role-of-vascular-cell-adhesion-molecule-1-and-activated-leukocyte-cell-adhesion-molecule-in-lupus-nephritis/. Accessed .
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