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Impaired Urinary Excretion of Soluble IL-2 Receptors in Patients with Systemic Lupus Erythematosus and Rheumatoid Arthritis

Laboratory of Clinical Immunology, Section of Rheumatology, Department of Internal Medicine, Medical School, University of Ioannina, Ioannina 451 10, Greece

G.S. Germanidis

Laboratory of Clinical Immunology, Section of Rheumatology, Department of Internal Medicine, Medical School, University of Ioannina, Ioannina 451 10, Greece

A.A. Drosos

Laboratory of Clinical Immunology, Section of Rheumatology, Department of Internal Medicine, Medical School, University of Ioannina, Ioannina 451 10, Greece

H.M. Moutsopoulos

Laboratory of Clinical Immunology, Section of Rheumatology, Department of Internal Medicine, Medical School, University of Ioannina, Ioannina 451 10, Greece

Several previous studies have demonstrated increased in vivo release of soluble interleukin-2 receptors (sIL-2R) in patients with disorders associated with cellular activation. In this study attempting to understand better the role of sIL-2R released in vivo, we investigated the sIL-2R levels in paired serum and urine samples from 25 patients with systemic lupus erythematosus (SLE), 41 patients with rheumatoid arthritis (RA) and 20 healthy subjects. Using an ELISA for sIL-2R, we detected significantly increased urinary sIL-2R levels in normal individuals (868 ±114 units/ml) compared to the corresponding serum samples (209 ± 25, P < 0.001, mean urine/serum sIL-2R ratio: 4.5 ± 0.6), which suggests that the clearance of sIL-2R from circulation is largely kidney-dependent.

The patients with SLE and RA exhibited significantly increased serum sIL-2R levels compared to normals (682 ± 115 and 734 ± 101 units/ml, respectively, P < 0.001) and these levels correlated with disease activity. However, urinary excretion of sIL-2R in these patients (SLE: 620 ±154 units/ml; RA: 1084 ± 148 units/ml) was found to be significantly decreased (mean urine/serum sIL-2R ratio in SLE: 0.9 ± 0.2; in RA: 1.9 ± 0.2; P < 0.001) compared to normals, possibly contributing to the accumulation of these soluble receptors in the serum of autoimmune patients after their release from cells. Our findings can be attributed either to the binding of the sIL-2R to serum protein(s) or to distinct structural features of serum sIL-2R in SLE and RA patients, interfering with the urinary excretion of these molecules.

Key Words: Soluble interleukin-2 receptors • Urinary excretion • Cytokines • Systemic lupus erythematosus • Rheumatoid arthritis

Lupus, Vol. 1, No. 2, 105-109 (1992)
DOI: 10.1177/096120339200100208


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