NDT Advance Access originally published online on December 21, 2007
Nephrology Dialysis Transplantation 2008 23(4):1452-1455; doi:10.1093/ndt/gfm890
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please e-mail: journals.permissions@oxfordjournals.org
Presence of autoantibodies against tubular and uveal cells in a patient with tubulointerstitial nephritis and uveitis (TINU) syndrome
1 Department of Pathology, CHU Sainte-Justine, University of Montreal, Canada 2 Department of Nephrology, CHU Sainte-Justine, University of Montreal, Canada 3 Department of Pediatric Immunology, CHU Sainte-Justine, University of Montreal, Canada
Hervé Sartelet, Department of pathology, CHU Sainte-Justine, University of Montreal, 3175, Côte Sainte-Catherine Montréal, Québec, H3T 1C5, Canada. Tel: +1-514-345-4649; Fax: +1-514-345-4819; E-mail: herve.sartelet.hsj@ssss.gouv.qc.ca
Keywords: autoantibodies; granulomatous inflammation; TINU syndrome
| The first 10% of the full text of this article appears below. |
| Introduction |
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Tubulointerstitial nephritis and uveitis (TINU) syndrome is characterized by acute tubulointerstitial nephritis with a favourable course and chronic recurrent uveitis. Since the first description in 1975 [1], more than 150 cases have been described in the literature [2]. Most of the patients with TINU syndrome are adolescents and young women, with a median age of onset of 15 (range 9 to 74) years. Renal tubulointerstitial infiltrates are primarily composed of activated lymphocytes, among which the helper/inducer T-cell subset is reported to be predominant [3,4]. In addition, TINU syndrome can be associated with granuloma in kidney or in another localization like bone marrow [1,5–7]. The pathogenesis of TINU syndrome remains unclear, but cell-mediated immunity, in particular delayed-type hypersensitivity, could play a large role in this disorder [8
| Case |
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| Renal biopsy |
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| Indirect immunofluorescence |
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