{'fraction_non_alphanumeric': 0.025423728813559324, 'fraction_numerical': 0.021791767554479417, 'mean_word_length': 5.511811023622047, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Association study of Japanese IgA nephropathy with microsatellite markers in 6q22–23, IGAN1

A heretofore undefined genetic component has been implicated in the development of IgA nephropathy (IgAN), although not generally considered a hereditary disease. Previous literatures disclosed that 3.8–14% of IgAN patients had genetic predisposition in their family. In our preliminary study, about 10% of biopsy-proven IgAN patients had a family history of haematuria and/or proteinuria. Recently, a linkage analysis of familial IgAN in Italy and US identified the disease susceptibility locus in 6q22–23, IGAN1. To address whether the disease susceptibility to IgAN are involved in this region also in Japanese patients, we conducted an association study of Japanese patients with IgAN using microsatellite markers in this region.