Glomerular Galactose‐Deficient IgA1 Deposition in 192 Autopsy Cases in Japan

Aim Glomerular IgA deposition is incidentally observed in asymptomatic individuals; however, it remains unclear whether these cases represent a preclinical stage of IgA nephropathy (IgAN). We aimed to address this question by staining kidney samples from autopsy cases with the anti‐galactose‐deficient IgA1 (Gd‐IgA1: the key effector molecule in the pathogenesis of IgAN) antibody, KM55. Methods Kidney samples from 192 autopsy cases in Japan were stained with anti‐IgA antibody and KM55. The deposition of complement C3, IgG and IgM in glomeruli, as well as the histological findings and clinical data were analysed in cases positive for glomerular IgA. Results Glomerular IgA deposition was detected in 13 cases (6.8%), all of which were stained with KM55. Of 10 cases with available urinary data prior to admission, six did not have abnormal urinary findings. 7 of 13 were positive for glomerular Gd‐IgA1 alone without obvious histological changes. Glomerular IgG and IgM were detected in 1 of 13 and 5 of 13 cases, respectively. 2 of 13 were positive for glomerular C3, with one showing mesangial proliferation. Conclusion Our results indicate that asymptomatic cases with glomerular IgA deposition may frequently include subclinical IgAN, characterised by glomerular deposition of Gd‐IgA1 (KM55‐positive) without prominent histopathological changes or obvious clinical symptoms.