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Defective Fc Receptor-Mediated Function of the Mononuclear Phagocyte System in Lupus Nephritis

TED M. PARRIS, M.D.; ROBERT P. KIMBERLY, M.D.; ROBERT D. INMAN, M.D.; J. STEVEN McDOUGAL, M.D.; ALLAN GIBOFSKY, M.D.; and CHARLES L. CHRISTIAN, M.D.
[+] Article and Author Information

▸From the Department of Medicine, The Hospital for Special Surgery and The New York Hospital, Cornell University Medical College, New York, New York; and The Laboratory of Immunology, Center for Infectious Diseases, Centers for Disease Control, Atlanta, Georgia.

Grant support: in part by grant RR-47, General Clinical Research Center. During this study Dr. Parris was a Fellow of the Arthritis Foundation, New York Chapter; Dr. Kimberly was an Andrew W. Mellon Teacher-Scientist; and Dr. Inman was a Postdoctoral Fellow of the Arthritis Foundation. Dr. Gibofsky was supported by an NIH Clinical Investigator Award AM 00615, National Institutes of Health.

Presented in part in abstract form June 1981 at The 45th Annual Scientific Meeting of the American Rheumatism Association, Boston, Massachusetts.

▸Requests for reprints should be addressed to Robert P. Kimberly, M.D.; The Hospital for Special Surgery, 535 East 70th Street; New York, NY 10021.


© 1982 American College of PhysiciansAmerican College of Physicians


Ann Intern Med. 1982;97(4):526-532. doi:10.7326/0003-4819-97-4-526
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To determine whether patients with systemic lupus erythematosus and nephritis have more profound defects in mononuclear phagocyte system clearance than their counterparts without renal disease, we studied Fc receptor-mediated splenic clearance function in 32 patients. Clearance half-times were prolonged in patients with lupus erythematosus compared with those in normal controls (p < 0.0001) and longer in patients with renal disease than in those without (p < 0.025). Both renal (tau = 0.45, p < 0.0002) and nonrenal (tau = 0.35, p < 0.003) disease activity were significantly but independently associated with clearance half-times. When matched for nonrenal activity, patients with nephritis had greater clearance dysfunction than their counterparts without renal disease. Circulating immune complexes did not correlate with clearance for all patients. Neither B8 nor DR3 histocompatibility antigen markers differentiated the renal and nonrenal disease subgroups. The greater Fc receptor-mediated clearance dysfunction, which occurs in patients with lupus erythematosus and nephritis, could lead to enhanced glomerular deposition of immune complexes as a primary event, or as a secondary event amplifying previously established lesions.

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