KEIO RESEARCHERS INFORMATION SYSTEM

Other Affiliation 【 Display / hide 】

Other Affiliation 【 Display / hide 】

• School of Medicine, Vice Dean

• Keio Information Technology Center, Deputy Director

• 教学マネジメント推進センター, Deputy Director

Career 【 Display / hide 】

Career 【 Display / hide 】

• 1991.04

  -

  1992.03

  慶應義塾大学病院内科研修医

• 1996.01

  -

  1998.12

  学術振興会特別研究員(PD)

• 1999.01

  -

  1999.06

  慶應義塾大学医学部助手（医学部）

• 1999.07

  -

  2002.03

  Division of Nephrology, University of Washington Research Fellow

• 2002.04

  -

  2007.03

  慶應義塾大学医学部腎臓内分泌代謝内科助手

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Academic Background 【 Display / hide 】

Academic Background 【 Display / hide 】

• 1991

  Keio University, School of Medicine

  University, Graduated

• 1996.03

  Keio University, Graduate School, Division of Medicine, 内科学

  Graduate School, Completed, Doctoral course

Academic Degrees 【 Display / hide 】

Academic Degrees 【 Display / hide 】

• 博士（医学）, Keio University, Coursework, 1996.03

Licenses and Qualifications 【 Display / hide 】

Licenses and Qualifications 【 Display / hide 】

• 医師免許, 1991.05

• 日本内科学会認定内科医, 1996.09

• 労働衛生コンサルタント（保健衛生）, 1998.06

• 日本腎臓学会腎臓専門医, 2003.04

• 日本透析医学会専門医, 2005.04

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Research Areas 【 Display / hide 】

Research Areas 【 Display / hide 】

• Life Science / Nephrology (Nephrology)

• 医学教育学

Research Keywords 【 Display / hide 】

Research Keywords 【 Display / hide 】

• 医学教育学

• electrolyte, acid-base disorder

Research Themes 【 Display / hide 】

Research Themes 【 Display / hide 】

• Interprofessional education, 

  2011.04

  -

  Present

• 医学教育学, 

  2011.04

  -

  Present

• electrolyte, acid-base disorder, 

  2002.04

  -

  Present

• development and induction of renal tubular cells, 

  2002.04

  -

  Present

Books 【 Display / hide 】

Books 【 Display / hide 】

• ハルペリン 病態から考える電解質異常

  Kamel S. Kamel、Mitchell L. Halperin著、門川俊明 翻訳, メディカルサイエンスインターナショナル, 2018.06

• なぜパターン認識だけで腎病理は読めないのか?

  MONKAWA TOSHIAKI, 医学書院, 2017.05

• 電解質輸液塾

  MONKAWA TOSHIAKI, 中外医学社, 2013.04

• レジデントのための血液透析患者マネジメント

  MONKAWA TOSHIAKI, 医学書院, 2011.06

• 研究留学術

  MONKAWA TOSHIAKI, 医歯薬出版, 2002.07

Papers 【 Display / hide 】

Papers 【 Display / hide 】

• 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 2023.01

  　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)

• Antineutrophil cytoplasmic antibody-associated vasculitis predominantly manifesting tubulointerstitial nephritis: A case report

  Nishioka K., Yamaguchi S., Hashiguchi A., Yoshimoto N., Tajima T., Yasuda I., Uchiyama K., Kaneko K., Aso M., Yoshino J., Monkawa T., Kanda T., Hayashi K., Itoh H.

  SAGE Open Medical Case Reports (SAGE Open Medical Case Reports)  11 2023.01

  　View Summary

  The common histopathology of antineutrophil cytoplasmic antibody-associated vasculitis comprises pauci-immune crescentic glomerulonephritis with concomitant tubulointerstitial nephritis. Tubulointerstitial nephritis in the absence of glomerular involvement in patients with antineutrophil cytoplasmic antibody-associated vasculitis is uncommon. We report a case of antineutrophil cytoplasmic antibody-associated vasculitis-associated acute kidney injury manifesting as tubulointerstitial nephritis without glomerulonephritis. A 75-year-old woman with fever, cough, and myalgia developed kidney dysfunction with inflammatory reactions and tubular-type proteinuria, without glomerular hematuria. A kidney biopsy revealed tubulointerstitial nephritis with arteritis. We ruled out important underlying etiologies of tubulointerstitial nephritis, including infection, drug reactions, and autoimmune diseases. Since chest high-resolution computed tomography demonstrated mild interstitial pneumonia in bilateral lower lung fields, myeloperoxidase antineutrophil cytoplasmic antibody was measured and found to be positive. Therefore, we diagnosed the patient with antineutrophil cytoplasmic antibody-associated vasculitis-associated tubulointerstitial nephritis but not glomerulonephritis, and interstitial pneumonia. The patient’s kidney function and symptoms markedly improved with prednisolone treatment. Clinicians should maintain high-level vigilance for antineutrophil cytoplasmic antibody-associated vasculitis as a possible underlying component of tubulointerstitial nephritis, particularly when kidney function deteriorates with tubulointerstitial injuries without glomerular features.

  • Access to Document (DOI)

• Compared effectiveness of sodium zirconium cyclosilicate and calcium polystyrene sulfonate on hyperkalemia in patients with chronic kidney disease

  Nakayama T., Yamaguchi S., Hayashi K., Uchiyama K., Tajima T., Azegami T., Morimoto K., Yoshida T., Yoshino J., Monkawa T., Kanda T., Itoh H.

  Frontiers in Medicine (Frontiers in Medicine)  10 2023

  　View Summary

  Hyperkalemia is a well-recognized electrolyte abnormality in patients with chronic kidney disease (CKD). Potassium binders are often used to prevent and treat hyperkalemia. However, few studies have evaluated the difference in serum potassium (K+) level-lowering effect during the post-acute phase between the novel potassium binder, sodium zirconium cyclosilicate (ZSC), and conventional agents. This retrospective study included patients who received potassium binders (either ZSC or calcium polystyrene sulfonate [CPS]) in our hospital between May 2020 and July 2022. The patients were divided into the ZSC and CPS groups. After propensity score matching, we compared changes from baseline to the first follow-up point, at least 4 weeks after initiating potassium binders, in electrolytes including K+ level between the two groups. Of the 132 patients, ZSC and CPS were administered in 48 and 84 patients, respectively. After matching, 38 patients were allocated to each group. The ZSC group showed greater reduction in K+ levels than did the CPS group (P < 0.05). Moreover, a significant increase in serum sodium minus chloride levels, a surrogate marker for metabolic acidosis, was observed in the ZSC group (P < 0.05). Our results demonstrated that ZSC could potentially improve hyperkalemia and metabolic acidosis in patients with CKD.

  • Access to Document (DOI)

• DNA repair factor KAT5 prevents ischemic acute kidney injury through glomerular filtration regulation

  Hishikawa A., Hayashi K., Kubo A., Miyashita K., Hashiguchi A., Kinouchi K., Yoshimoto N., Nakamichi R., Akashio R., Sugita E., Azegami T., Monkawa T., Suematsu M., Itoh H.

  iScience (iScience)  24 ( 12 )  2021.12

  　View Summary

  The “preconditioning effect” in AKI is a phenomenon in which an episode of ischemia-reperfusion results in tolerance to subsequent ischemia-reperfusion injury. However, its relationship between DNA damage repair has not been elucidated. Here, we show the role of KAT5 in the preconditioning effect. Preconditioning attenuated DNA damage in proximal tubular cells with elevated KAT5 expression. Ischemia-reperfusion (IR) injuries were exacerbated, and preconditioning effect vanished in proximal tubular-cell-specific KAT5 knockout mice. Investigation of tubuloglomerular feedback (TGF) by MALDI-IMS and urinary adenosine revealed that preconditioning caused attenuated TGF at least in part via KAT5. In addition, K-Cl cotransporter 3 (KCC3) expression decreased in damaged proximal tubular cells, which may be involved in accelerated TGF following IR. Furthermore, KAT5 induced KCC3 expression by maintaining chromatin accessibility and binding to the KCC3 promoter. These results suggest a novel mechanism of the preconditioning effect mediated by the promotion of DNA repair and attenuation of TGF through KAT5.

  • Access to Document (DOI)

• Induction of human pluripotent stem cells into kidney tissues by synthetic mRNAs encoding transcription factors

  Hiratsuka K., Monkawa T., Akiyama T., Nakatake Y., Oda M., Goparaju S., Kimura H., Chikazawa-Nohtomi N., Sato S., Ishiguro K., Yamaguchi S., Suzuki S., Morizane R., Ko S., Itoh H., Ko M.

  Scientific Reports (Scientific Reports)  9 ( 1 )  2019.12

  　View Summary

  © 2019, The Author(s). The derivation of kidney tissues from human pluripotent stem cells (hPSCs) and its application for replacement therapy in end-stage renal disease have been widely discussed. Here we report that consecutive transfections of two sets of synthetic mRNAs encoding transcription factors can induce rapid and efficient differentiation of hPSCs into kidney tissues, termed induced nephron-like organoids (iNephLOs). The first set - FIGLA, PITX2, ASCL1 and TFAP2C, differentiated hPSCs into SIX2+SALL1+ nephron progenitor cells with 92% efficiency within 2 days. Subsequently, the second set - HNF1A, GATA3, GATA1 and EMX2, differentiated these cells into PAX8+LHX1+ pretubular aggregates in another 2 days. Further culture in both 2-dimensional and 3-dimensional conditions produced iNephLOs containing cells characterized as podocytes, proximal tubules, and distal tubules in an additional 10 days. Global gene expression profiles showed similarities between iNephLOs and the human adult kidney, suggesting possible uses of iNephLOs as in vitro models for kidneys.

  • Access to Document (DOI)

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

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

• Master regulatory factors for regeneration and EMT of kidney tubular cells

  Monkawa, Toshiaki

  科学研究費補助金研究成果報告書 2017

• The direct differentiation method of renal tubular cells by master transcription factors identified from TF-inducible human ES bank

  Monkawa, Toshiaki

  科学研究費補助金研究成果報告書 2015

• An investigation of mechanism of progression of kidney disease using renal tubular cells differentiated from ES/iPS cells

  Monkawa, Toshiaki

  科学研究費補助金研究成果報告書 2014

• Mechanism of regeneration of renal tubular cells and differentiation from ES and iPS cells to renal tubular cells

  Monkawa, Toshiaki

  科学研究費補助金研究成果報告書 2011

Presentations 【 Display / hide 】

Presentations 【 Display / hide 】

• 慶應義塾大学における海外施設での臨床実習プログラム

  MONKAWA TOSHIAKI

  第49回日本教育学会大会, 

  2017.08

  , 

  Oral presentation (general)

• もう一度やり直す腎生理

  MONKAWA TOSHIAKI

  第46回日本腎臓学会東部学術大会, 

  2016.10

  , 

  Symposium, workshop panel (public)

• タブレット端末iPad配付と教学システムのデジタル化

  MONKAWA TOSHIAKI

  第48回日本教育学会大会, 

  2016.07

  , 

  Oral presentation (general)

• 腎臓専門医制度 腎臓専門医(内科)のカリキュラム

  MONKAWA TOSHIAKI

  第59回日本腎臓学会学術大会, 

  2016.06

  , 

  Symposium, workshop panel (public)

• K代謝異常

  MONKAWA TOSHIAKI

  第25回臨床内分泌代謝アップデート, 

  2015.11

  , 

  Symposium, workshop panel (nominated)

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Research Projects of Competitive Funds, etc. 【 Display / hide 】

Research Projects of Competitive Funds, etc. 【 Display / hide 】

• Master regulatory factors for regeneration and EMT of kidney tubular cells

  2015.04

  -

  2018.03

  MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (C), Principal investigator

Awards 【 Display / hide 】

Awards 【 Display / hide 】

• Best Teacher

  2015.03, Keio University School of Medicine

• 日本内科学会奨励賞

  MONKAWA TOSHIAKI, 2004.04, 日本内科学会

  Type of Award： Award from Japanese society, conference, symposium, etc.

Courses Taught 【 Display / hide 】

Courses Taught 【 Display / hide 】

• MEDICAL PROFESSIONALISM 4

  2024

• MEDICAL PEDAGOGY: SEMINAR

  2024

• MEDICAL PEDAGOGY: PRACTICE

  2024

• MD-PHD LABORATORY TRAINING

  2024

• INTRODUCTION TO MEDICINE

  2024

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Courses Previously Taught 【 Display / hide 】

Courses Previously Taught 【 Display / hide 】

• 地域基盤型臨床実習

  Keio University

  2017.04

  -

  2018.03

  , 

  Full academic year, Laboratory work/practical work/exercise, Within own ｆaculty, 110people

• 選択臨床実習

  Keio University

  2017.04

  -

  2018.03

  , 

  Full academic year, Laboratory work/practical work/exercise

• 診断学実習

  Keio University

  2017.04

  -

  2018.03

  , 

  Full academic year, Laboratory work/practical work/exercise, Within own ｆaculty

• MEDICAL PROFESSIONALISM 4

  Keio University

  2015.04

  -

  2016.03

  , 

  Full academic year, Laboratory work/practical work/exercise, Within own ｆaculty, 118people

• CLINICAL REASONING

  Keio University

  2015.04

  -

  2016.03

  , 

  Full academic year, Laboratory work/practical work/exercise, Within own ｆaculty, 118people

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Educational Activities and Special Notes 【 Display / hide 】

Educational Activities and Special Notes 【 Display / hide 】

• なぜパターン認識だけで腎病理は読めないのか?

  2017.05

  , Development of Textbook and Teaching Material

• Denkaishitsu-Yueki-Juku

  2013.04

  , Development of Textbook and Teaching Material

• Management of hemodialysis patient for residents

  2011.06

  , Development of Textbook and Teaching Material

• Interprofessional education at Keio University

  2011.04

  -

  Present

  , Special Affairs

Social Activities 【 Display / hide 】

Social Activities 【 Display / hide 】

• 医学中央雑誌

  2010

  -

  Present

• 医学のあゆみ

  2007

  -

  Present

Memberships in Academic Societies 【 Display / hide 】

Memberships in Academic Societies 【 Display / hide 】

• 日本腎臓学会, 

  1995.11

  -

  Present

• 日本透析医学会

  　

• 日本内科学会

  　

• 日本医学教育学会, 

  2008

  -

  Present

Committee Experiences 【 Display / hide 】

Committee Experiences 【 Display / hide 】

• 1995.11

  -

  Present

  評議員, 日本腎臓学会

• 　

  会員, 日本透析医学会

• 　

  Member, 日本内科学会

• 2008

  -

  Present

  representative, 日本医学教育学会

• 2010

  -

  Present

  Editor, 医学中央雑誌

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