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2. Transcription factor MafB in podocytes protects against the development of focal segmental glomerulosclerosis

Author

Usui, Toshiaki, Morito, Naoki, Shawki, Hossam H., Sato, Yoshinori, Tsukaguchi, Hiroyasu, Hamada, Michito, Jeon, Hyojung, Yadav, Manoj Kumar, Kuno, Akihiro, Tsunakawa, Yuki, Okada, Risa, Ojima, Takaaki, Kanai, Maho, Asano, Keigo, Imamura, Yuki, Koshida, Ryusuke, Yoh, Keigyou, Usui, Joichi, Yokoi, Hideki, Kasahara, Masato, Yoshimura, Ashio, Muratani, Masafumi, Kudo, Takashi, Oishi, Hisashi, Yamagata, Kunihiro, and Takahashi, Satoru

Published
2020
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10. Plasma Globotriaosylsphingosine and α-Galactosidase A Activity as a Combined Screening Biomarker for Fabry Disease in a Large Japanese Cohort

Author

Maruyama, Hiroki, primary, Taguchi, Atsumi, additional, Mikame, Mariko, additional, Izawa, Atsushi, additional, Morito, Naoki, additional, Izaki, Kazufumi, additional, Seto, Toshiyuki, additional, Onishi, Akifumi, additional, Sugiyama, Hitoshi, additional, Sakai, Norio, additional, Yamabe, Kenji, additional, Yokoyama, Yukio, additional, Yamashita, Satoshi, additional, Satoh, Hiroshi, additional, Toyoda, Shigeru, additional, Hosojima, Michihiro, additional, Ito, Yumi, additional, Tazawa, Ryushi, additional, and Ishii, Satoshi, additional

Published
2021
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11. Cover Image

Author

Watanabe, Megumi, primary, Kaneko, Shuzo, additional, Usui, Joichi, additional, Takahashi, Kazuhiro, additional, Kawanishi, Kunio, additional, Takahashi‐Kobayashi, Mayumi, additional, Shimizu, Tatsuya, additional, Ishii, Ryota, additional, Tawara, Takashi, additional, Tsunoda, Ryoya, additional, Nagai, Kei, additional, Kawamura, Tetsuya, additional, Fujita, Akiko, additional, Kai, Hirayasu, additional, Morito, Naoki, additional, Saito, Chie, additional, Oda, Tatsuya, additional, Nagata, Michio, additional, and Yamagata, Kunihiro, additional

Published
2021
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12. Anti-PM/Scl Antibody-positive Systemic Sclerosis Complicated by Multiple Organ Involvement

Author

Shimizu, Tatsuya, primary, Saito, Chie, additional, Watanabe, Megumi, additional, Ishii, Ryota, additional, Kawamura, Tetsuya, additional, Nagai, Kei, additional, Fujita, Akiko, additional, Kaneko, Shuzo, additional, Kai, Hirayasu, additional, Morito, Naoki, additional, Usui, Joichi, additional, Yokosawa, Masahiro, additional, Kondo, Yuya, additional, Inoue, Sae, additional, Okiyama, Naoko, additional, and Yamagata, Kunihiro, additional

Published
2021
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13. Anti-glomerular Basement Membrane Glomerulonephritis During the First Trimester of Pregnancy

Author

Kai, Hirayasu, primary, Usui, Joichi, additional, Tawara, Takashi, additional, Takahashi-Kobayashi, Mayumi, additional, Ishii, Ryota, additional, Tsunoda, Ryoya, additional, Fujita, Akiko, additional, Nagai, Kei, additional, Kaneko, Shuzo, additional, Morito, Naoki, additional, Saito, Chie, additional, Hamada, Hiromi, additional, and Yamagata, Kunihiro, additional

Published
2021
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18. Literature review of allograft adenovirus nephritis and a case presenting as mass lesions in a transplanted kidney without symptoms of urinary tract infection or acute kidney injury

Author

Watanabe, Megumi, primary, Kaneko, Shuzo, additional, Usui, Joichi, additional, Takahashi, Kazuhiro, additional, Kawanishi, Kunio, additional, Takahashi‐Kobayashi, Mayumi, additional, Shimizu, Tatsuya, additional, Ishii, Ryota, additional, Tawara, Takashi, additional, Tsunoda, Ryoya, additional, Nagai, Kei, additional, Kawamura, Tetsuya, additional, Fujita, Akiko, additional, Kai, Hirayasu, additional, Morito, Naoki, additional, Saito, Chie, additional, Oda, Tatsuya, additional, Nagata, Michio, additional, and Yamagata, Kunihiro, additional

Published
2020
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21. Mice lacking core 1-derived O-glycan in podocytes develop transient proteinuria, resulting in focal segmental glomerulosclerosis

Author

Fuseya, Sayaka, primary, Suzuki, Riku, additional, Okada, Risa, additional, Hagiwara, Kozue, additional, Sato, Takashi, additional, Narimatsu, Hisashi, additional, Yokoi, Hideki, additional, Kasahara, Masato, additional, Usui, Toshiaki, additional, Morito, Naoki, additional, Yamagata, Kunihiro, additional, Kudo, Takashi, additional, and Takahashi, Satoru, additional

Published
2020
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27. Plasma Exchange Is Highly Effective for Anti‐Neutrophil Cytoplasmic Antibody‐Associated Vasculitis Patients With Rapidly Progressive Glomerulonephritis Who Have Advanced to Dialysis Dependence: A Single‐Center Case Series

Author

Nishida, Reimi, primary, Kaneko, Shuzo, additional, Usui, Joichi, additional, Kawamura, Tetsuya, additional, Tsunoda, Ryoya, additional, Tawara, Takashi, additional, Fujita, Akiko, additional, Nagai, Kei, additional, Kai, Hirayasu, additional, Morito, Naoki, additional, Saito, Chie, additional, and Yamagata, Kunihiro, additional

Published
2019
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29. Literature review of allograft adenovirus nephritis and a case presenting as mass lesions in a transplanted kidney without symptoms of urinary tract infection or acute kidney injury.

Author

Watanabe, Megumi, Kaneko, Shuzo, Usui, Joichi, Takahashi, Kazuhiro, Kawanishi, Kunio, Takahashi‐Kobayashi, Mayumi, Shimizu, Tatsuya, Ishii, Ryota, Tawara, Takashi, Tsunoda, Ryoya, Nagai, Kei, Kawamura, Tetsuya, Fujita, Akiko, Kai, Hirayasu, Morito, Naoki, Saito, Chie, Oda, Tatsuya, Nagata, Michio, and Yamagata, Kunihiro

Subjects
ACUTE kidney failure, URINARY tract infections, NEPHRITIS, ADENOVIRUS diseases, HEMATOPOIETIC stem cells, LITERATURE reviews, ADENOVIRUSES
Abstract

Adenovirus (AdV) infection is a common complication in bone marrow/hematopoietic stem cell transplant and solid organ transplant recipients. AdV infection usually presents as hemorrhagic cystitis, but sometimes it can progress to acute kidney injury showing AdV nephritis (AdVN). We present the case of a 52‐year‐old Japanese female who had received a living kidney transplantation (KT) from her husband. At 21 months post‐KT, the patient presented with a fever, but no renal dysfunction and no abnormal urine findings. A contrast‐enhanced computed tomography (CT) scan revealed a few mass lesions with hypoperfusion in the transplanted kidney. An enhanced CT‐guided biopsy targeting one of these lesions revealed a necrotizing tubulointerstitial nephritis suggesting AdVN. The polymerase chain reaction tests for ADV were negative in a urine sample but positive in the sera and the frozen kidney biopsy samples. AdVN can manifest as an unusual pattern of acute lobar nephritis/acute focal bacterial nephritis‐like localization without symptoms of acute kidney injury or urinary tract infection. Enhanced CT can provide clues for clinical diagnosis. [ABSTRACT FROM AUTHOR]

Published
2021
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30. A mutation in transcription factor MAFB causes Focal Segmental Glomerulosclerosis with Duane Retraction Syndrome

Author

Sato, Yoshinori, primary, Tsukaguchi, Hiroyasu, additional, Morita, Hiroyuki, additional, Higasa, Koichiro, additional, Tran, Mai Thi Nhu, additional, Hamada, Michito, additional, Usui, Toshiaki, additional, Morito, Naoki, additional, Horita, Shoichiro, additional, Hayashi, Takao, additional, Takagi, Junko, additional, Yamaguchi, Izumi, additional, Nguyen, Huan Thanh, additional, Harada, Masayo, additional, Inui, Kiyoko, additional, Maruta, Yuichi, additional, Inoue, Yoshihiko, additional, Koiwa, Fumihiko, additional, Sato, Hiroshi, additional, Matsuda, Fumihiko, additional, Ayabe, Shinya, additional, Mizuno, Seiya, additional, Sugiyama, Fumihiro, additional, Takahashi, Satoru, additional, and Yoshimura, Ashio, additional

Published
2018
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34. MafA-deficient and beta cell-specific MafK-overexpressing hybrid transgenic mice develop human-like severe diabetic nephropathy

Author

Shimohata, Homare, Yoh, Keigyou, Fujita, Akiko, Morito, Naoki, Ojima, Masami, Tanaka, Hiromi, Hirayama, Kouichi, Kobayashi, Masaki, Kudo, Takashi, Yamagata, Kunihiro, and Takahashi, Satoru

Subjects
ComputingMethodologies_DOCUMENTANDTEXTPROCESSING
Abstract

application/pdf, Transcription factor MafA is a key molecule in insulin secretion and the development of pancreatic islets. Previously, we demonstrated that some of theMafA-deficient mice develop overt diabetes mellitus, and the phenotype of these mice seems to be mild probably because of redundant functions of other Maf proteins. In this study, we generated hybrid transgenic mice that were MafA-deficient and also over-expressed MafK specifically in beta cells (MafA −/−MafK+). MafA−/−MafK+ mice developed severe overt diabetes mellitus within 5 weeks old, and showed higher levels of proteinuria and serum creatinine. Histological analysis revealed that embryonic development ofbeta cells in the MafA −/−MafK+ mice was significantly suppressed and the reduced number of beta cells was responsible for the early onset of diabetes. Furthermore, after uninephrectomy, these mice demonstrated three characteristics of human diabetic nephropathy: diffuse, nodular, and exudative lesions. MafA−/−MafK+ mice might be a useful model for the analysis of human diabetic nephropathy.

Published
2009

40. Two autosomal dominant polycystic kidney (ADPKD) cases with advanced renal dysfunction, effectively treated with tolvaptan

Author

Kai, Hirayasu, primary, Shinozaki, Yuki, additional, Nishikubo, Airi, additional, Watanabe, Megumi, additional, Tawara, Takashi, additional, Iwase, Mamiko, additional, Tsunoda, Ryouya, additional, Moriyama, Noriaki, additional, Usui, Toshiaki, additional, Kawamura, Tetsuya, additional, Nagai, Kei, additional, Hagiwara, Masahiro, additional, Saito, Chie, additional, Morito, Naoki, additional, Usui, Joichi, additional, and Yamagata, Kunihiro, additional

Published
2015
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41. Role of endogenous retroviruses in murine SLE

Author

Baudino, Lucie Clementine, Yoshinobu, Kumiko, Morito, Naoki, Santiago-Raber, Marie-Laure, and Izui, Shozo

Subjects
Mice, Lupus Erythematosus, Systemic/physiopathology/*virology, immune system diseases, viruses, Animals, Endogenous Retroviruses/immunology/*physiology, Humans, Viral Envelope Proteins/metabolism, Toll-Like Receptor 7/metabolism, ddc:616.07, skin and connective tissue diseases
Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disorder characterized by B cell hyperactivity leading to the production of various autoantibodies and subsequent development of glomerulonephritis, i.e. lupus nephritis. Among the principal targets of the autoantibodies produced in murine SLE are nucleic acid-protein complexes and the envelope glycoprotein gp70 of endogenous retroviruses. Recent studies have revealed that the innate receptor TLR7 plays a pivotal role in the development of a wide variety of autoimmune responses against DNA- and RNA-containing nuclear antigens, while TLR9 rather plays a protective role. In addition, the regulation of autoimmune responses against endogenous retroviral gp70 by TLR7 suggests the implication of endogenous retroviruses in this autoimmune response. Moreover, the demonstration that TLR7 is involved in the acute phase expression of serum gp70 uncovers an additional pathogenic role of TLR7 in murine lupus nephritis by promoting the expression of nephritogenic gp70 autoantigen. Clearly, the eventual identification of endogenous retroviruses implicated in murine SLE and of mouse genes regulating their production could provide a clue for the potential role of endogenous retroviruses in human SLE.

Published
2010

42. Anaemia is an essential complication of ANCA-associated renal vasculitis: a single center cohort study.

Author

Tetsuya Kawamura, Joichi Usui, Shuzo Kaneko, Ryoya Tsunoda, Eri Imai, Hirayasu Kai, Naoki Morito, Chie Saito, Michio Nagata, Kunihiro Yamagata, Kawamura, Tetsuya, Usui, Joichi, Kaneko, Shuzo, Tsunoda, Ryoya, Imai, Eri, Kai, Hirayasu, Morito, Naoki, Saito, Chie, Nagata, Michio, and Yamagata, Kunihiro

Subjects
ANEMIA, ANTINEUTROPHIL cytoplasmic antibodies, VASCULITIS, NEPHROLOGISTS, BLOOD diseases, ANEMIA diagnosis, AUTOIMMUNE disease diagnosis, AUTOANTIBODIES, AUTOIMMUNE diseases, LONGITUDINAL method, RETROSPECTIVE studies, DISEASE complications
Abstract

Background: Anaemia is a common complication of patients with antineutrophil cytoplasmic antibody (ANCA)-associated renal vasculitis. Nevertheless, the cause and degree of such cases of anaemia have not been elucidated in detail. We aimed to investigate the prevalence, cause, pathogenesis of anaemia and the impact of anaemia on prognosis in patients with ANCA-associated renal vasculitis.Methods: We identified 45 patients with ANCA-associated renal vasculitis that were clinically and/or histologically diagnosed and treated from 2003 to 2014 at University of Tsukuba Hospital. The relationships between anaemia and various clinicopathological findings were evaluated.Results: At the time of diagnosis of ANCA-associated renal vasculitis, all patients showed anaemia, with a mean haemoglobin level of 7.5 ± 1.3 g/dL. Renal anaemia was diagnosed in 92% of patients, anaemia of chronic disease (ACD) in 56%, and anaemia due to hemorrhage in 20%. Next, the patients were divided into two groups according to anaemia severity: minimum haemoglobin (min Hb) < 7.5 (n = 24) and min Hb ≥ 7.5 (n = 21). A comparison of baseline characteristics showed that serum albumin, maximum serum creatinine, minimum estimated glomerular filtration rate (eGFR), serum cystatin C, and the area of tubulointerstitial damage were significantly different between the haemoglobin groups (p <  0.05). No significant intergroup differences were observed in iron-related or inflammation-related data. With regard to the relationship between anaemia severity and prognosis, patients in the min Hb < 7.5 group tended to have a lower eGFR. Anaemia severity was associated with markedly lower survival (Log-rank test, p = 0.03).Conclusions: In this cohort of patients with ANCA-associated renal vasculitis, all subjects exhibited anaemia. In regard to the cause and pathogenesis, the most prevalent form of anaemia was renal anaemia, not ACD, and a potential reason for the high prevalence of anaemia in our cohort may have been the interaction between renal anaemia and ACD. Moreover, anaemia severity was significantly associated with the degree of renal dysfunction and life prognosis. [ABSTRACT FROM AUTHOR]

Published
2017
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50. Overexpression of RORγt under control of the CD2 promoter induces polyclonal plasmacytosis and autoantibody production in transgenic mice

Author

Yoh, Keigyou, primary, Morito, Naoki, additional, Ojima, Masami, additional, Shibuya, Kazuko, additional, Yamashita, Yumi, additional, Morishima, Yuko, additional, Ishii, Yukio, additional, Kusakabe, Manabu, additional, Nishikii, Hidekazu, additional, Fujita, Akiko, additional, Matsunaga, Emi, additional, Okamura, Midori, additional, Hamada, Michito, additional, Suto, Akira, additional, Nakajima, Hiroshi, additional, Shibuya, Akira, additional, Yamagata, Kunihiro, additional, and Takahashi, Satoru, additional

Published
2012
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