KEIO RESEARCHERS INFORMATION SYSTEM

Career 【 Display / hide 】

Career 【 Display / hide 】

• 1995.04

  -

  1997.03

  慶應義塾大学医学部, 病理学教室, 慶應義塾大学医学部助手（病理学）

• 1997.04

  -

  2007.03

  慶應義塾大学医学部, 病理学教室, 慶應義塾大学助手（医学部病理学）

• 2007.04

  -

  2013.11

  慶應義塾大学医学部, 病理学教室, 慶應義塾大学助教（医学部病理学）

• 2013.12

  -

  Present

  慶應義塾大学医学部, 病理学教室, 慶應義塾大学専任講師（医学部病理学）

Academic Background 【 Display / hide 】

Academic Background 【 Display / hide 】

• 1989.04

  -

  1995.03

  Keio University, School of Meicine

  University, Graduated

Academic Degrees 【 Display / hide 】

Academic Degrees 【 Display / hide 】

• 博士（医学）, Keio University, Dissertation, 2010.11

  Using immunofluorescent digital slide technology to quantify protein expression in archival paraffin-embedded tissue sections

Research Areas 【 Display / hide 】

Research Areas 【 Display / hide 】

• Life Science / Human pathology

Research Keywords 【 Display / hide 】

Research Keywords 【 Display / hide 】

• Digital Pathology

• Renal Pathology

Papers 【 Display / hide 】

Papers 【 Display / hide 】

• Hepatitis B Virus-related Membranous Nephropathy with Crescentic Formation in an Inactive Carrier of Positive Hepatitis B Surface Antigen with Undetectable DNA under Anti-viral Treatment: A Case Report.

  Kounoue N, Oguchi H, Mikami T, Yamaguchi Y, Hashiguchi A, Nagai H, Watanabe K, Furukawa S, Hisamatsu K, Sakai K

  Internal medicine (Tokyo, Japan)  2023.05

  Joint Work,  ISSN  0918-2918

  • Access to Document (DOI)

• Immunohistochemistry May Not Replace Immunofluorescence in Paraffin-embedded Tissue for Detecting Masked Monoclonal Immunoglobulin Deposits: A Case Report.

  Oda Y, Ikeda Y, Abe H, Hashiguchi A, Hatanaka K, Sawai T, Ushiku T, Nangaku M

  Internal medicine (Tokyo, Japan)  2023.04

  Joint Work,  ISSN  0918-2918

  • Access to Document (DOI)

• DNA-damaged podocyte-CD8 T cell crosstalk exacerbates kidney injury by altering DNA methylation

  Nakamichi R., Hishikawa A., Chikuma S., Yoshimura A., Sasaki T., Hashiguchi A., Abe T., Tokuhara T., Yoshimoto N., Nishimura E.S., Hama E.Y., Azegami T., Nakayama T., Hayashi K., Itoh H.

  Cell Reports （Cell Reports)  42 （ 4 ） 112302 2023.04

  Joint Work

  　View Summary

  Recent epigenome-wide studies suggest an association between blood DNA methylation and kidney function. However, the pathological importance remains unclear. Here, we show that the homing endonuclease I-PpoI-induced DNA double-strand breaks in kidney glomerular podocytes cause proteinuria, glomerulosclerosis, and tubulointerstitial fibrosis with DNA methylation changes in blood cells as well as in podocytes. Single-cell RNA-sequencing analysis reveals an increase in cytotoxic CD8+ T cells with the activating/costimulatory receptor NKG2D in the kidneys, which exhibit a memory precursor effector cell phenotype, and the CD44high memory CD8+ T cells are also increased in the peripheral circulation. NKG2D blockade attenuates the renal phenotype caused by podocyte DNA damage. Blood methylome shows increased DNA methylation in binding sites for STAT1, a transcription factor contributing to CD8+ T cell homeostasis. Collectively, podocyte DNA damage alters the blood methylome, leading to changes in CD8+ T cells, which contribute to sustained renal injury in chronic kidney disease.

  • Access to Document (DOI)

• Significance of podocyte DNA damage and glomerular DNA methylation in CKD patients with proteinuria

  Yoshimoto N., Hayashi K., Hishikawa A., Hashiguchi A., Nakamichi R., Sugita-Nishimura E., Yoshida-Hama E., Azegami T., Nakayama T., Itoh H.

  Hypertension Research （Hypertension Research)  46 （ 4 ） 1000 - 1008 2023.04

  Joint Work,  ISSN  09169636

  　View Summary

  The number of chronic kidney disease (CKD) patients is increasing worldwide, and it is necessary to diagnose CKD patients in earlier stages to improve their prognosis. Previously, in a study using human samples, we reported that DNA methylation and DNA damage in podocytes are potential markers for kidney function decline in IgA nephropathy; however, these candidate markers have not been adequately investigated in other glomerular diseases. Here, we report that the association of podocyte DNA damage and DNA methylation with eGFR decline and proteinuria differs depending on the type of glomerular disease. Patients diagnosed with minor glomerular abnormality (MGA, n = 33), membranous nephropathy (MN, n = 9) or diabetic nephropathy (DN, n = 10) following kidney biopsy at Keio University Hospital from 2015 to 2017 were included. In MGA patients, both podocyte DNA damage and glomerular DNA methylation were associated with the severity of proteinuria. In DN patients, podocyte DNA double-strand breaks (DSBs) and glomerular DNA methylation were associated with an eGFR decline. When patients with urinary protein levels of more than 1 g/gCr were examined, fewer podocyte DNA DSBs were detected in MN patients than in MGA patients, and the level of glomerular DNA methylation was lower in MN patients than in MGA or DN patients. These results indicate that investigating podocyte DNA DSBs and DNA methylation changes may be useful for understanding the pathogenesis of CKD with proteinuria in humans. [Figure not available: see fulltext.].

  • Access to Document (DOI)

• Case report: Importance of early and continuous tocilizumab therapy in nephrotic syndrome associated with idiopathic multicentric Castleman disease: A case series

  Kojima D., Yamaguchi S., Hashiguchi A., Hayashi K., Uchiyama K., Yoshimoto N., Adachi K., Nakayama T., Nishioka K., Tajima T., Morimoto K., Yoshino J., Yoshida T., Monkawa T., Kanda T., Itoh H.

  Frontiers in Medicine （Frontiers in Medicine)  9   1037032 2023.01

  Joint Work,  ISSN  2296-858X

  　View Summary

  Idiopathic multicentric Castleman disease (iMCD) is a systemic and polyclonal lymphoproliferative disease involving multiple organs, including the kidneys, due to the overproduction of interleukin-6 (IL-6). Recently, several reports have suggested that excessive IL-6 actions in iMCD could have a causal relationship with the development of diverse histopathological renal manifestations that cause nephrotic syndrome. However, the treatment for such cases remains unclear. We report a series of three cases of nephrotic syndrome due to iMCD that helps to delineate the importance of early and continuous therapy with the anti-interleukin-6 receptor antibody tocilizumab. First, treatment was suspended for infectious control, and the patient presented with nephrotic syndrome due to diffuse mesangial and endocapillary hypercellularity without immune deposits complicating acute kidney injury. Second, iMCD was treated with prednisolone alone. The patient suddenly developed nephrotic syndrome due to immune-complex glomerulonephritis, not otherwise specified, complicated with acute kidney injury. In the third case, nephrotic syndrome secondary to membranous glomerulonephritis was diagnosed, with a skin rash and IgE antibodies to tocilizumab, and was therefore treated with prednisolone alone. In contrast to the first two cases, the third progressed to end-stage renal disease on hemodialysis. Taken together, this series suggests that clinicians should maintain clinical vigilance for iMCD as a possible underlying component of nephrotic syndrome, since iMCD presents with a variety of renal pathologies. Prompt initiation and continuous administration of tocilizumab are likely key determinants of renal outcomes in such cases. In particular, when tocilizumab is suspended due to infection or in the perioperative period, consideration of its expeditious resumption should be made, taking into account both the withdrawal period and systemic conditions.

  • Access to Document (DOI)

display all >>

Papers, etc., Registered in KOARA 【 Display / hide 】

Papers, etc., Registered in KOARA 【 Display / hide 】

• The results of renal biopsies performed within the past thirty five years at Keio University Hospital, with an analysis in detail of the cases with membranous nephropathy.

  Hashiguchi, Akinori

  Journal of the Keio Medical Society （慶應医学会)  82 （ 3 ） 143 - 155 2005.09

  ISSN  03685179

Reviews, Commentaries, etc. 【 Display / hide 】

Reviews, Commentaries, etc. 【 Display / hide 】

• Erratum: DNA-damaged podocyte-CD8 T cell crosstalk exacerbates kidney injury by altering DNA methylation (Cell Reports (2023) 42(4), (S2211124723003133), (10.1016/j.celrep.2023.112302))

  Nakamichi R., Hishikawa A., Chikuma S., Yoshimura A., Sasaki T., Hashiguchi A., Abe T., Tokuhara T., Yoshimoto N., Nishimura E.S., Hama E.Y., Azegami T., Nakayama T., Hayashi K., Itoh H.

  Cell Reports (Cell Reports)  42 ( 5 )  2023.05

  Joint Work

  　View Summary

  (Cell Reports 42, 112302; April 25, 2023) In the originally published version of this article, Figure 4 was accidentally constructed with a duplicate of panel (D) in place of the intended panel (E). The figure has been corrected online. The authors regret this error. [Formula presented] [Formula presented]

  • Access to Document (DOI)

• Minimal Change Disease Associated With Durvalumab

  Toda M.G., Fujii K., Kato A., Yoshifuji A., Komatsu M., Amino Y., Kitazono S., Hashiguchi A., Ryuzaki M.

  Kidney International Reports (Kidney International Reports)  6 ( 10 ) 2733 - 2734 2021.10

  Article, review, commentary, editorial, etc. (scientific journal), Joint Work,  ISSN  24680249

  • Access to Document (DOI)

• IgA腎症のOxford分類と日本分類(組織学的重症度分類)の腎機能予後予測に関する比較

  城 謙輔, 中里 毅, 橋口 明典, 清水 章, 久野 敏, 片渕 律子, 川村 哲也

  日本腎臓学会誌 ((一社)日本腎臓学会)  61 ( 3 ) 394 - 394 2019.05

  Other, Joint Work,  ISSN  0385-2385

• IgA腎症の生検時の臨床データと病理所見の関連性

  鎌野 千佐子, 清水 章, 城 謙輔, 橋口 明典, 久野 敏, 片渕 律子, 川村 哲也

  日本腎臓学会誌 ((一社)日本腎臓学会)  61 ( 3 ) 395 - 395 2019.05

  Other, Joint Work,  ISSN  0385-2385

• 前立腺癌の腫瘍局在が診断・治療・予後に及ぼす影響

  松本 一宏, 高松 公晴, 武田 利和, 小坂 威雄, 田中 伸之, 森田 伸也, 水野 隆一, 篠島 利明, 菊地 栄次, 浅沼 宏, 橋口 明典, 陣崎 雅弘, 大家 基嗣

  日本泌尿器科学会総会 ((一社)日本泌尿器科学会総会事務局)  107回   PP1 - 075 2019.04

  Other, Joint Work

display all >>

Presentations 【 Display / hide 】

Presentations 【 Display / hide 】

• 肺炎球菌性菌血症で発見されたC3 nephritic factor陽性のC3腎炎/MPGNの7歳女児

  森下 俊真, 遠藤 翔太, 武政 洋一, 大貫 裕太, 櫻谷 浩志, 村上 仁彦, 藤永 周一郎, 橋口 明典

  日本小児腎臓病学会雑誌, 

  2022.11

  , 

  (一社)日本小児腎臓病学会

• 寛解後もC3低値が持続し追跡腎生検でC3NeF陽性C3腎炎と診断した1例

  荒尾 正人, 飛田和 えりか, 吉村 萌, 秋岡 祐子, 橋口 明典

  日本小児腎臓病学会雑誌, 

  2022.11

  , 

  (一社)日本小児腎臓病学会

• 妊娠末期に発症した膜性腎症の1例

  伊藤 智章, 中村 健吾, 篠塚 圭祐, 二木 功治, 緒方 謙太郎, 橋口 明典

  日本腎臓学会誌, 

  2022.10

  , 

  (一社)日本腎臓学会

• 間質にIgM-λ陽性の沈着物を認めたprimary renal lymphomaの一例

  川口 隆久, 唐澤 隆明, 橋口 明典, 大嶋 洋佑, 渡辺 雄祐, 熊谷 聡佑, 有馬 功一郎, 安藤 孝

  日本腎臓学会誌, 

  2022.10

  , 

  (一社)日本腎臓学会

• 膜性腎症とMPO-ANCA関連血管炎を合併した高齢男性の1例

  野間 悠太朗, 竜崎 正毅, 田島 敬也, 伊藤 亘, 松本 朋美, 坂口 知広, 森田 洋平, 貫井 紀宏, 池上 良, 橋口 明典, 久保田 英司

  日本腎臓学会誌, 

  2022.10

  , 

  (一社)日本腎臓学会

display all >>

Courses Taught 【 Display / hide 】

Courses Taught 【 Display / hide 】

• GENERAL PATHOLOGY

  2023

• DISEASES OF ORGAN SYSTEMS

  2023

• GENERAL PATHOLOGY

  2022

• DISEASES OF ORGAN SYSTEMS

  2022

• GENERAL PATHOLOGY

  2021

display all >>

Courses Previously Taught 【 Display / hide 】

Courses Previously Taught 【 Display / hide 】

• 病理学各論（講義）

  Keio University

  2017.04

  -

  2018.03

  , 

  Lecture

• 臨床実習（病理診断部）

  Keio University

  2017.04

  -

  2018.03

  , 

  Laboratory work/practical work/exercise

• 病理学各論（実習）

  Keio University

  2017.04

  -

  2018.03

  , 

  Laboratory work/practical work/exercise

• 病理学総論（実習）

  Keio University

  2017.04

  -

  2018.03

  , 

  Laboratory work/practical work/exercise

• 病理学各論（講義）

  Keio University

  2016.04

  -

  2017.03

  , 

  Lecture

display all >>

Memberships in Academic Societies 【 Display / hide 】

Memberships in Academic Societies 【 Display / hide 】

• The Japanese Society of Pathology

  　

• Japanese Society of Nephrology

  　

• The Japanese Society of Digital Pathology