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 ]. In addition, some studies suggest that uveitis and tubulointerstitial nephritis have a common immunological pathogenesis and so it was postulated that there may be a common antigenicity between renal and ocular tissues [ 3 , 9 ].
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Abed et al. (2007) studied this question.
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