%0 Journal Article
%T Immunohistochemical Characteristics of IgG4-Related Tubulointerstitial Nephritis: Detailed Analysis of 20 Japanese Cases
%A Mitsuhiro Kawano
%A Ichiro Mizushima
%A Yutaka Yamaguchi
%A Naofumi Imai
%A Hitoshi Nakashima
%A Shinichi Nishi
%A Satoshi Hisano
%A Nobuaki Yamanaka
%A Motohisa Yamamoto
%A Hiroki Takahashi
%A Hisanori Umehara
%A Takao Saito
%A Takako Saeki
%J International Journal of Rheumatology
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/609795
%X Although tubulointerstitial nephritis with IgG4+ plasma cell (PC) infiltration is a hallmark of IgG4-related kidney disease (IgG4-RKD), only a few studies are available about the minimum number of IgG4+£¿PC needed for diagnosis along with IgG4+/IgG+£¿PC ratio in the kidney. In addition, the significance of the deposition of IgG or complement as a reflection of humoral immunity involvement is still uncertain. In this study, we analyzed 20 Japanese patients with IgG4-RKD to evaluate the number of IgG4+£¿PCs along with IgG4+/IgG+£¿PC ratio and involvement of humoral immunity. The average number of IgG4+£¿PCs was 43.8/hpf and the average IgG4+/IgG+ or IgG4+/CD138+ ratio was 53%. IgG and C3 granular deposits on the tubular basement membrane (TBM) were detected by immunofluorescence microscopy in 13% and 47% of patients, respectively. Nine patients had a variety of glomerular lesions, and 7 of them had immunoglobulin or complement deposition in the glomerulus. In conclusion, we confirmed that infiltrating IgG4+£¿PCs > 10/hpf and/or IgG4/IgG (CD138)+£¿PCs > 40% was appropriate as an item of the diagnostic criteria for IgG4-RKD. A relatively high frequency of diverse glomerular lesions with immunoglobulin or complement deposits and deposits in TBM may be evidence of immune complex involvement in IgG4-related disease. 1. Introduction The main histopathological finding in the kidney of IgG4-RD is tubulointerstitial nephritis (TIN) [1¨C3], which may result in renal failure [4]. IgG4-related TIN is composed of dense lymphoplasmacytic infiltrates with fibrosis and copious IgG4+ plasma cell infiltration, which are common features shared by other involved organs [5], and these common pathologic features in the kidney have clearly been described by previous studies [1¨C3]. However, the minimum number of IgG4+ plasma cells needed for diagnosis has been differently reported in each affected organ [6¨C9], and only a few studies are available about the actual number of IgG4+ plasma cells evaluated along with IgG4+/IgG+ plasma cell ratio in IgG4-related kidney disease (IgG4-RKD) [2]. In addition to this issue, case reports or case series of a variety of glomerular disease concurrent with TIN have been accumulated [10¨C26]. These glomerular lesions are frequently accompanied by immunoglobulin or complement deposits suggesting that immune complexes might be involved in the pathogenesis of some cases with IgG4-RKD [2, 3]. However, the significance of these glomerular lesions as a reflection of humoral immunity involvement is still uncertain, and whether these glomerular lesions represent
%U http://www.hindawi.com/journals/ijr/2012/609795/