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Upregulation of Fractalkine in Human Crescentic GlomerulonephritisFuruichi K.a · Wada T.a · Iwata Y.a · Sakai N.a · Yoshimoto K.a · Shimizu M.a · Kobayashi K.a · Takasawa K.b · Kida H.b · Takeda S.-i.c · Matsushima K.d · Yokoyama H.a
aFirst Department of Internal Medicine and Division of Blood Purification, School of Medicine, Kanazawa University, Kanazawa; bDepartment of Internal Medicine, Kanazawa National Hospital, Kanazawa; cKurobe Municipal Hospital, Kurobe; dDepartment of Molecular Preventive Medicine, School of Medicine, University of Tokyo, Japan
Background/Aim: To evaluate the importance of fractalkine, a novel member of the CX3C chemokine, and natural killer (NK) cells in human crescentic glomerulonephritis, we determined the presence of fractalkine in the diseased kidneys immunohistochemically, and the correlation among fractalkine, NK cells and the degree of renal damage. Methods: Twenty-three patients (13 males and 10 females) with primary or secondary crescentic glomerular disease were evaluated in this study. Fractalkine and CD16-positive cells including NK cells were detected immunohistochemically. Results: Fractalkine-positive cells were detected in the interstitium of 23 patients with crescentic glomerulonephritis, while they were not detected in the glomeruli. In addition, CD16-positive cells were detected in both the glomeruli (1.3 ± 0.2/glomerulus) and interstitium (1.3 ± 0.2/visual field). The number of fractalkine-positive cells in the interstitium correlated with the number of CD16-positive cells before glucocorticoid therapy (r = 0.43, p = 0.047, n = 23). The number of fractalkine-positive cells in the interstitium before glucocorticoid therapy (0.2 ± 0.1/visual field) decreased after therapy (0.1 ± 0.1/visual field, p = 0.050) in 11 cases tested. The number of CD16-positive cells in the diseased kidneys did not change after glucocorticoid therapy. Conclusion: These results suggest that the local production of fractalkine may explain the presence of CD16-positive cells including NK cells, which may participate in the interstitial lesions of human crescentic glomerulonephritis before corticoid therapy.
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