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Faculty of Medicine School of Medicine Department of community Pediatrics and Support Raising Next-Generation |
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TANAKA Etsuko
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Papers 【 display / non-display 】
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Tanigawa S, Tanaka E, Miike K, Ohmori T, Inoue D, Cai CL, Taguchi A, Kobayashi A, Nishinakamura R
Nature communications 13 ( 1 ) 611 2022.2
Authorship：Lead author Language：English Publishing type：Research paper (scientific journal) Publisher：Nature Communications
Organs consist of the parenchyma and stroma, the latter of which coordinates the generation of organotypic structures. Despite recent advances in organoid technology, induction of organ-specific stroma and recapitulation of complex organ configurations from pluripotent stem cells (PSCs) have remained challenging. By elucidating the in vivo molecular features of the renal stromal lineage at a single-cell resolution level, we herein establish an in vitro induction protocol for stromal progenitors (SPs) from mouse PSCs. When the induced SPs are assembled with two differentially induced parenchymal progenitors (nephron progenitors and ureteric buds), the completely PSC-derived organoids reproduce the complex kidney structure, with multiple types of stromal cells distributed along differentiating nephrons and branching ureteric buds. Thus, integration of PSC-derived lineage-specific stroma into parenchymal organoids will pave the way toward recapitulation of the organotypic architecture and functions.
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Re-evaluating the MYH9 p.I1816V variant in a patient with atypical clinical presentation Reviewed
此元 隆雄, 若松 美仁, 阪口 嘉美, 黒木 純, 田中 悦子, 盛武 浩
Pediatric nephrology 2025.11
Language：English Publishing type：Research paper (scientific journal) Publisher：Springer Science and Business Media LLC
MYH9-related disease (MYH9-RD) is an autosomal dominant disorder typically characterized by macrothrombocytopenia, leukocyte inclusion bodies, and variable non-hematologic manifestations such as hearing loss and nephropathy. We herein describe a 16-year-old boy presenting with persistent proteinuria and biopsy-proven membranous nephropathy with focal segmental sclerosis. Genetic testing identified a rare MYH9 variant (p.I1816V), previously reported in association with Epstein syndrome. However, the patient had normal platelet counts, no leukocyte inclusions, and no abnormalities in non-muscle myosin heavy chain IIA (NMMHC-IIA) expression in neutrophils or podocytes. Although globally rare, the p.I1816V variant is more frequent in East Asian populations and is predicted to be benign by multiple in silico tools. This case illustrates the challenges of interpreting rare variants in the absence of supportive clinical findings and highlights the need for cautious evaluation in the era of next-generation sequencing.
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Re-evaluating the MYH9 p.I1816V variant in a patient with atypical clinical presentation Reviewed
Konomoto T., Wakamatsu F., Sakaguchi H., Kurogi J., Tanaka E., Moritake H.
Pediatric Nephrology 41 ( 4 ) 993 - 997 2025
Language：English Publishing type：Research paper (scientific journal) Publisher：Pediatric Nephrology
MYH9-related disease (MYH9-RD) is an autosomal dominant disorder typically characterized by macrothrombocytopenia, leukocyte inclusion bodies, and variable non-hematologic manifestations such as hearing loss and nephropathy. We herein describe a 16-year-old boy presenting with persistent proteinuria and biopsy-proven membranous nephropathy with focal segmental sclerosis. Genetic testing identified a rare MYH9 variant (p.I1816V), previously reported in association with Epstein syndrome. However, the patient had normal platelet counts, no leukocyte inclusions, and no abnormalities in non-muscle myosin heavy chain IIA (NMMHC-IIA) expression in neutrophils or podocytes. Although globally rare, the p.I1816V variant is more frequent in East Asian populations and is predicted to be benign by multiple in silico tools. This case illustrates the challenges of interpreting rare variants in the absence of supportive clinical findings and highlights the need for cautious evaluation in the era of next-generation sequencing.
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長期不登校となっていた腎不全患児への社会生活スキルトレーニングの実施
長尾 愛美、田中 悦子、黒木 純、阪口 嘉美、此元 隆雄、盛武 浩
日本小児PD・HD研究会雑誌 36 44 - 46 2025
Language：Japanese Publishing type：Case report
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Wakamatsu Fumito, Kurogi Jun, Ebihara Shusei, Sakaguchi Hiromi, Nagasawa Shun, Nakagawa Midori, Yamada Ai, Tanaka Etsuko, Kinoshita Mariko, Konomoto Takao, Moritake Hiroshi
Japanese journal of pediatric nephrology 38 ( 0 ) n/a 2025
Language：Japanese Publishing type：Research paper (scientific journal) Publisher：The Japanese Society for Pediatric Nephrology
Sinusoidal obstruction syndrome (SOS) is a serious complication of hematopoietic stem cell transplantation, characterized by diuretic-resistant edema and weight gain. Severe cases can progress to multiple organ failure due to abdominal compartment syndrome, and the mortality rate remains high even with defibrotide, a known effective treatment for SOS.We present a case of severe SOS in a patient who was treated with extracorporeal ultrafiltration (ECUM) as part of continuous renal replacement therapy (CRRT). The patient received defibrotide immediately upon diagnosis of SOS following peripheral hematopoietic stem cell transplantation; however, he subsequently developed severe ascites and respiratory distress. Initiation of ECUM led to rapid improvement in fluid overload, including ascites, along with increased urine output. The patient was successfully weaned off ECUM within a short period, and his SOS symptoms improved. This case suggests that ECUM may effectively alleviate ascites related to SOS.Effective management of fluid overload is critical in the treatment of SOS. Regardless of renal function, close monitoring of fluid volume using percentage fluid overload (%FO) is essential, and CRRT should be initiated promptly based on the patient’s clinical status. ECUM may serve as an effective treatment option for managing SOS-related fluid overload.
Books 【 display / non-display 】
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領域横断的視点による腎・泌尿器疾患の診療
田中悦子（ Role： Sole author , ネイルパテラ症候群）
中山書店 2025
Language：Japanese Book type：Textbook, survey, introduction
MISC 【 display / non-display 】
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腎臓の発生機構とその再構成 Invited
田中悦子、西中村隆一
細胞 57 ( 12 ) 5 - 9 2025
Authorship：Lead author Language：Japanese Publishing type：Article, review, commentary, editorial, etc. (scientific journal)
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Tanigawa S., Tanaka E., Miike K., Ohmori T., Inoue D., Cai C.L., Taguchi A., Kobayashi A., Nishinakamura R.
Nature Communications 14 ( 1 ) 2023.12
Publishing type：Rapid communication, short report, research note, etc. (scientific journal) Publisher：Nature Communications
The original version of the Supplementary Information associatedwith this Article contained an error in the legend of Supplementary Fig. 1d, which stated ‘Tamoxifen was injected at E9.5 and the mice were analyzed at E15.5’. The correct version of the legend now states ‘Tamoxifen was injected at E11.5 and the mice were analyzed at E15.5’ The HTML has been updated to include a corrected version of the Supplementary Information.
Presentations 【 display / non-display 】
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In vitro reconstitution of higher order kidney structure solely from pluripotent stem cells by establishing stromal progenitor induction protocol Invited International coauthorship International conference
Etsuko Tanaka
The 18th Congress of Asian Society for Pediatric Research (ASPR) 2023.11.11
Event date： 2023.11.11 - 2023.11.12
Language：English Presentation type：Symposium, workshop panel (nominated)
Awards 【 display / non-display 】
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森田賞
2023.6 日本小児腎臓病学会 Generation of the organotypic kidney structure by integrating pluripotent stem cell-derived renal stroma
田中悦子
Award type：Award from Japanese society, conference, symposium, etc.
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優秀演題奨励賞
2023.6 日本小児腎臓病学会 NPHS1にp.Val822Metを伴い自然寛解を反復した小児ネフローゼ症候群
田中悦子
Award type：International academic award (Japan or overseas)
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優秀演題奨励賞
2022.5 日本小児腎臓病学会 間質前駆細胞の誘導法開発に基づく多能性幹細胞からの腎臓高次構造の再構築
田中 悦子
Award type：Award from Japanese society, conference, symposium, etc.
Grant-in-Aid for Scientific Research 【 display / non-display 】
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NPHS1にp.V822M変異を有する患者由来腎臓オルガノイドを用いた蛋白尿の病態解明
Grant number：25K19496 2025.04 - 2028.03
独立行政法人日本学術振興会 科学研究費基金 若手研究
Authorship：Principal investigator
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Development of an in vitro reconstitution method for reproducing human kidney glomerular structure and function by vascularization and perfusion of organoid
Grant number：24K22384 2024.04 - 2027.03
Japan Society for the Promotion of Science Grants-in-Aid for Scientific Research Grant-in-Aid for Challenging Research (Exploratory)
Authorship：Coinvestigator(s)
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ヒトiPS細胞由来腎臓オルガノイドを用いたLMX1B変異に伴う腎症の病態解明
Grant number：22K16246 2022.04 - 2026.03
独立行政法人日本学術振興会 科学研究費基金 若手研究
田中 悦子
Authorship：Principal investigator
Available Technology 【 display / non-display 】
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遺伝性腎疾患の病態モデルを作製し、機序解明と治療法開発をする
生体外で血流をもつ腎臓オルガノイドを作製する＜共同研究＞
誘導腎臓上皮細胞（ポドサイト）を用いて、ポドサイト障害の機序を検討するRelated fields where technical consultation is available：ヒトiPS細胞から腎臓オルガノイドの作製
Message：ヒトiPS細胞由来腎臓オルガノイドを用いた研究に興味のある方と、臨床に生かせるような共同研究ができたらいいなと思っています。よろしくお願いいたします。