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Elevated Urinary VCAM-1, P-Selectin, Soluble TNF Receptor-1, and CXC Chemokine Ligand 16 in Multiple Murine Lupus Strains and Human Lupus Nephritis¹

Tianfu Wu^*, Chun Xie^*, Hong W. Wang, Xin J. Zhou, Noa Schwartz, Sergio Calixto^*, Meggan Mackay, Cynthia Aranow, Chaim Putterman and Chandra Mohan^2,*

^* Department of Internal Medicine (Rheumatology) and Center for Immunology, and Department of Pathology, University of Texas Southwestern Medical School, Dallas, TX 75235; Albert Einstein College of Medicine, Bronx, NY 10461; and Division of Rheumatology, Columbia University, NY 10027

In an effort to identify potential biomarkers in lupus nephritis, urine from mice with spontaneous lupus nephritis was screened for the presence of VCAM-1, P-selectin, TNFR-1, and CXCL16, four molecules that had previously been shown to be elevated in experimental immune nephritis, particularly at the peak of disease. Interestingly, all four molecules were elevated 2- to 4-fold in the urine of several strains of mice with spontaneous lupus nephritis, including the MRL/lpr, NZM2410, and B6.Sle1.lpr strains, correlating well with proteinuria. VCAM-1, P-selectin, TNFR-1, and CXCL16 were enriched in the urine compared with the serum particularly in active disease, and were shown to be expressed within the diseased kidneys. Finally, all four molecules were also elevated in the urine of patients with lupus nephritis, correlating well with urine protein levels and systemic lupus erythematosus disease activity index scores. In particular, urinary VCAM-1 and CXCL16 showed superior specificity and sensitivity in distinguishing subjects with active renal disease from the other systemic lupus erythematosus patients. These studies uncover VCAM-1, P-selectin, TNFR-1, and CXCL16 as a quartet of molecules that may have potential diagnostic significance in lupus nephritis. Longitudinal studies are warranted to establish the clinical use of these potential biomarkers.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported in part by National Institutes of Health Grants AR44894, AR50812, AR48692, and AI51392, The Alliance for Lupus Research, a Medical Student Research Preceptorship Award from the American College of Rheumatology Research and Education Foundation, a grant from the New York Chapter of the Arthritis Foundation, and the Gina Finzi Memorial Student Summer Fellowship (to N.S.) from the Lupus Foundation of America.

² Address correspondence and reprint requests to Dr. Chandra Mohan, Department of Internal Medicine/Rheumatology, University of Texas Southwestern Medical Center, Mail Code 8884, Y8.204, 5323 Harry Hines Boulevard, Dallas, TX 75390-8884. E-mail address: Chandra.mohan{at}utsouthwestern.edu

³ Abbreviations used in this paper: SLE, systemic lupus erythematosus; SLEDAI, SLE disease activity index; RA, rheumatoid arthritis; ROC, receiver operating characteristic; AUC, area under the curve; DC, dendritic cell; uPAR, urokinase-type plasminogen activator; GBM, glomerular basement membrane; sTNFR-1, soluble TNFR-1.

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