Faculty Profiles - MIZUNO, Masashi

Papers - MIZUNO, Masashi

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The effects of functional suppression of a membrane-bound complement regulatory protein, CD59, in the synovial tissue in rats Reviewed International coauthorship International journal

M Mizuno, K Nishikawa, RM Goodfellow, SJ Piddlesden, BP Morgan, S Matsuo

ARTHRITIS AND RHEUMATISM Vol. 40 ( 3 ) page： 527 - 533 1997.3

Authorship：Lead author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：LIPPINCOTT-RAVEN PUBL

Objective. To investigate the roles of CD59 in the synovial tissue by functional suppression of CD59.
Methods. Rats treated with cobra venom factor to deplete complement or untreated rats were injected intraarticularly with 0.3 mg of the F(ab')(2) fraction of a monoclonal antibody, 6D1, that inhibits the function of rat CD59, The circumference of knee joints was measured, and histologic changes in the synovium were studied.
Results. Joint swelling, thickening of the synovial tissues, infiltration of inflammatory cells into the synovium, and deposition of membrane attack complex (MAC) on the synovial surface were observed after intraarticular injection of 6D1, The inflammatory reaction reached its peak at 24 hours after injection, and finally subsided to normal within 3 days, It was suggested that functional suppression of CD59 in the synovium induced MAC formation followed by synovitis, Serum complement depletion did not completely sup press this reaction, This indicates that complement existing in the joint space is important for the formation of MAC on the synovial surface and for induction of synovitis.
Conclusion. The membrane-bound complement regulatory protein, CD59, plays a key role in the protection of joints against MAC-mediated synovial injury and in maintaining the normal integrity of the joint.

DOI： 10.1002/art.1780400319

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Successfully treated C3 glomerulopathy in which protein and genetic analyses were useful for diagnosis. Reviewed International journal

Kanzaki M, Kurahashi M, Watanabe K, Nishikawa M, Fukuoka K, Shimada N, Mizuno M, Asano K

CEN case reports 2024.9

Pathophysiological Mechanisms of Peritoneal Fibrosis and Peritoneal Membrane Dysfunction in Peritoneal Dialysis. Reviewed International journal

Yasuhiko Ito, Ting Sun, Mitsuhiro Tawada, Hiroshi Kinashi, Makoto Yamaguchi, Takayuki Katsuno, Hangsoo Kim, Masashi Mizuno, Takuji Ishimoto

International journal of molecular sciences Vol. 25 ( 16 ) 2024.8

Language：English Publishing type：Research paper (scientific journal)

The characteristic feature of chronic peritoneal damage in peritoneal dialysis (PD) is a decline in ultrafiltration capacity associated with pathological fibrosis and angiogenesis. The pathogenesis of peritoneal fibrosis is attributed to bioincompatible factors of PD fluid and peritonitis. Uremia is associated with peritoneal membrane inflammation that affects fibrosis, neoangiogenesis, and baseline peritoneal membrane function. Net ultrafiltration volume is affected by capillary surface area, vasculopathy, peritoneal fibrosis, and lymphangiogenesis. Many inflammatory cytokines induce fibrogenic growth factors, with crosstalk between macrophages and fibroblasts. Transforming growth factor (TGF)-β and vascular endothelial growth factor (VEGF)-A are the key mediators of fibrosis and angiogenesis, respectively. Bioincompatible factors of PD fluid upregulate TGF-β expression by mesothelial cells that contributes to the development of fibrosis. Angiogenesis and lymphangiogenesis can progress during fibrosis via TGF-β-VEGF-A/C pathways. Complement activation occurs in fungal peritonitis and progresses insidiously during PD. Analyses of the human peritoneal membrane have clarified the mechanisms by which encapsulating peritoneal sclerosis develops. Different effects of dialysates on the peritoneal membrane were also recognized, particularly in terms of vascular damage. Understanding the pathophysiologies of the peritoneal membrane will lead to preservation of peritoneal membrane function and improvements in technical survival, mortality, and quality of life for PD patients.

DOI： 10.3390/ijms25168607

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特集補体と腎疾患:温故知新腎疾患における補体と病態生理膜性増殖性糸球体腎炎/C3腎症 Invited

水野正司

腎と透析 Vol. 97 ( 1 ) page： 82 - 87 2024.7

Effectiveness of additional topical antibiotics for recurrent or refractory exit-site infection: a case series Reviewed International journal

Asai, N; Suzuki, Y; Asai, A; Kinashi, H; Kamiya, K; Hagita, J; Matsuoka, N; Kawamura, S; Fukui, S; Kim, H; Yamaguchi, M; Katsuno, T; Mizuno, M; Ishimoto, T; Ito, Y

RENAL REPLACEMENT THERAPY Vol. 10 ( 1 ) 2024.6

Rationale and design of the Japanese Biomarkers in Nephrotic Syndrome (J-MARINE) study Reviewed International journal

Kurasawa, S; Kato, S; Ozeki, T; Akiyama, S; Ishimoto, T; Mizuno, M; Tsuboi, N; Kato, N; Kosugi, T; Maruyama, S

CLINICAL AND EXPERIMENTAL NEPHROLOGY Vol. 28 ( 5 ) page： 431 - 439 2024.5

Durvalumab plus carboplatin-etoposide treatment in a patient with small-cell lung cancer on hemodialysis: a case report and literature review. Reviewed International journal

Ushijima F, Hase T, Yamashita Y, Kim H, Shimokata T, Kondo C, Sato T, Baba T, Watanabe S, Futamura K, Ando Y, Mizuno M, Ishii M

International cancer conference journal Vol. 13 ( 2 ) page： 88 - 92 2024.4

Role of endothelial hyaluronan in peritoneal membrane transport and disease conditions during peritoneal dialysis Reviewed International coauthorship International journal

Kamiya, K; Hatayama, N; Tawada, M; Asai, A; Yamauchi, M; Kinashi, H; Kunoki, S; Yamaguchi, M; Mizuno, M; Suzuki, Y; Banshodani, M; Ishimoto, T; Naito, M; Kawanishi, H; Ito, Y

SCIENTIFIC REPORTS Vol. 14 ( 1 ) page： 7412 2024.3

A Case of C3 Nephritis With a Rare Variant of the CFHR5 Gene Reviewed International journal

Kamido, H; Yamamoto, S; Yokoi, H; Mizuno, M; Yanagita, M

CUREUS JOURNAL OF MEDICAL SCIENCE Vol. 16 ( 2 ) page： e55102 2024.2

今月の特集2 補体をめぐる話題注目の補体異常症 C3腎症

金恒秀, 水野正司

臨床検査 Vol. 68 ( 1 ) page： 88 - 92 2024.1

特集補体revisited--抗補体療法はどこまで進んだか? 非典型溶血性尿毒症症候群 Invited

水野正司

医学のあゆみ Vol. 287 ( 10 ) page： 757 - 761 2023.12

遺伝性血管性浮腫(Hereditary angioedema:HAE)診療ガイドライン改訂2023年版

堀内孝彦, 大澤勲, 宮田敏行, 赤津裕康, 今井優樹, 大谷克城, 奥健志, 関根英治, 塚本浩, 中尾実樹, 西村純一, 水野正司, 村上良子, 井上徳光, 一般社団法人日本補体学会HAEガイドライン作成委員会

補体 Vol. 60 ( 1 ) page： 23 - 23 2023.8

学校検尿でみつかった、電顕像にて電子密度の異なる沈着物を認めるDense Deposit Diseaseの13歳女児例

手塚優子, 新野亮治, 木内拓海, 岡本健太郎, 村上至孝, 松田修, 澤井俊宏, 水野正司, 清水章

日本小児腎臓病学会雑誌 Vol. 36 ( Suppl. ) page： 179 - 179 2023.5

Inhibition of Transglutaminase 2 Reduces Peritoneal Injury in a Chlorhexidine-Induced Peritoneal Fibrosis Model. Reviewed International journal

Shunnosuke Kunoki, Hideki Tatsukawa, Yukinao Sakai, Hiroshi Kinashi, Tetsuyoshi Kariya, Yasuhiro Suzuki, Masashi Mizuno, Makoto Yamaguchi, Hiroyuki Sasakura, Masashi Ikeno, Kosei Takeuchi, Takuji Ishimoto, Kiyotaka Hitomi, Yasuhiko Ito

Laboratory investigation; a journal of technical methods and pathology Vol. 103 ( 4 ) page： 100050 - 100050 2023.4

Language：English Publishing type：Research paper (scientific journal)

Long-term peritoneal dialysis (PD) is often associated with peritoneal dysfunction leading to withdrawal from PD. The characteristic pathologic features of peritoneal dysfunction are widely attributed to peritoneal fibrosis and angiogenesis. The detailed mechanisms remain unclear, and treatment targets in clinical settings have yet to be identified. We investigated transglutaminase 2 (TG2) as a possible novel therapeutic target for peritoneal injury. TG2 and fibrosis, inflammation, and angiogenesis were investigated in a chlorhexidine gluconate (CG)-induced model of peritoneal inflammation and fibrosis, representing a noninfectious model of PD-related peritonitis. Transforming growth factor (TGF)-β type I receptor (TGFβR-I) inhibitor and TG2-knockout mice were used for TGF-β and TG2 inhibition studies, respectively. Double immunostaining was performed to identify cells expressing TG2 and endothelial-mesenchymal transition (EndMT). In the rat CG model of peritoneal fibrosis, in situ TG2 activity and protein expression increased during the development of peritoneal fibrosis, as well as increases in peritoneal thickness and numbers of blood vessels and macrophages. TGFβR-I inhibitor suppressed TG2 activity and protein expression, as well as peritoneal fibrosis and angiogenesis. TGF-β1 expression, peritoneal fibrosis, and angiogenesis were suppressed in TG2-knockout mice. TG2 activity was detected by α-smooth muscle actin-positive myofibroblasts, CD31-positive endothelial cells, and ED-1-positive macrophages. CD31-positive endothelial cells in the CG model were α-smooth muscle actin-positive, vimentin-positive, and vascular endothelial-cadherin-negative, suggesting EndMT. In the CG model, EndMT was suppressed in TG2-knockout mice. TG2 was involved in the interactive regulation of TGF-β. As inhibition of TG2 reduced peritoneal fibrosis, angiogenesis, and inflammation associated with TGF-β and vascular endothelial growth factor-A suppression, TG2 may provide a new therapeutic target for ameliorating peritoneal injuries in PD.

DOI： 10.1016/j.labinv.2022.100050

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Video-assisted thoracoscopic surgery for pleuroperitoneal communication International journal

Tsubouchi, H; Nakamura, S; Fukui, T; Kadomatsu, Y; Ueno, H; Ozeki, N; Fukumoto, K; Mizuno, M; Chen-Yoshikawa, TF

ASIAN JOURNAL OF ENDOSCOPIC SURGERY Vol. 16 ( 2 ) page： 262 - 265 2023.4

Nutritional Assessment and Nutrient Supplement in Patients with Chronic Kidney Disease

Mizuno, M

NUTRIENTS Vol. 15 ( 8 ) 2023.4

特集 Genetics in CKD 疾患編補体関連遺伝子の異常と腎疾患

金恒秀, 水野正司

腎と透析 Vol. 94 ( 3 ) page： 405 - 410 2023.3

Case report: Thrombotic microangiopathy concomitant with macrophage activation syndrome in systemic lupus erythematosus refractory to conventional treatment successfully treated with eculizumab Reviewed International journal

Makoto Yamaguchi, Masashi Mizuno, Fumiya Kitamura, Shiho Iwagaitsu, Hironobu Nobata, Hiroshi Kinashi, Shogo Banno, Akimasa Asai, Takuji Ishimoto, Takayuki Katsuno, Yasuhiko Ito

Frontiers in Medicine Vol. 9 page： 1097528 2023.1

Language：English Publishing type：Research paper (scientific journal) Publisher：Frontiers Media SA

Thrombotic microangiopathy (TMA) is a rare but life-threatening complication of systemic lupus erythematosus (SLE). Macrophage activation syndrome (MAS) is also a rare, life-threatening hyperinflammatory condition that is comorbid with SLE. However, the association between TMA and MAS in patients with SLE has rarely been assessed, and the difficulty of diagnosing these conditions remains prevalent. The efficacy of eculizumab has been reported for SLE patients whose conditions are complicated with TMA. However, no study has investigated the therapeutic efficacy of eculizumab for TMA concomitant with SLE-associated MAS. Herein, we report the first case of TMA concomitant with SLE-associated MAS that was initially refractory to conventional immunosuppressive therapy but showed remarkable recovery after eculizumab treatment. Furthermore, we evaluated serum syndecan-1 and hyaluronan levels, which are biomarkers of endothelial damage. We found that these levels decreased after the administration of eculizumab, suggesting that TMA was the main pathology of the patient. This case illustrates that it is important to appropriately assess the possibility of TMA during the course of SLE-associated MAS and consider the use of eculizumab as necessary.

DOI： 10.3389/fmed.2022.1097528

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Recurrent Cerebrovascular Complications under Enzyme Replacement Therapy in a Patient with Fabry Disease on Peritoneal Dialysis Reviewed International journal

Muto Reiko, Suzuki Yasuhiro, Shimizu Hideaki, Yasuda Kaoru, Ishimoto Takuji, Maruyama Shoichi, Ito Yasuhiko, Mizuno Masashi

Internal Medicine Vol. 62 ( 3 ) page： 565 - 569 2023

Authorship：Last author,　Corresponding author Language：English Publishing type：Research paper (scientific journal) Publisher：The Japanese Society of Internal Medicine

<p>Fabry disease is an X-linked lysosomal storage disorder due to mutations in the alpha-galactosidase A gene, which leads to the accumulation of globotriaosylceramide in various organs. In Fabry disease with end-stage renal disease (ESRD), cerebrovascular events are lethal, even with enzyme replacement therapy (ERT). However, the utility of biomarkers to evaluate the ERT response is unclear. We herein report a case of recurrent cerebrovascular complications under ERT in a Fabry disease patient, progressing to ESRD on peritoneal dialysis. Further studies are warranted, but Fabry disease patients with ESRD receiving ERT might need careful long-term follow-up in cases with cerebrovascular manifestations. </p>

DOI： 10.2169/internalmedicine.0185-22

ASSISTED PD：Problems and Countermeasures Based on Home-Visit Nursing Station Surveys Reviewed

Takai Nami, Nakabayashi Kichio, Kawashima Shoichi, Mizuno Masashi, Koide Shigehisa, Kasuga Hirotake, Saka Yosuke, Sakai Emiko, Inaguma Daijo, Ito Yasuhiko

Nihon Toseki Igakkai Zasshi Vol. 56 ( 11 ) page： 401 - 409 2023

Language：Japanese Publishing type：Research paper (scientific journal) Publisher：The Japanese Society for Dialysis Therapy

<p>[Objective] To investigate factors hindering the spread of assisted peritoneal dialysis (PD) to support elderly patients in Japan, a survey of PD acceptance at home nursing stations was administered. [Method] A questionnaire survey was conducted involving 616 home-visit nursing stations in Aichi Prefecture, 368 of which were registered with the Aichi Medical Association or Aichi Council of Home-Visit Nursing Stations. [Results] A total of 132 facilities were surveyed, for a collection rate of 35％. The breakdown was as follows：37 home nursing stations were accepting PD patients, 59 were considering accepting PD patients, and 20 were not considering accepting PD patients. A total of 20％ of the facilities were always involved in PD patient visits. Other facilities had only a few opportunities to see PD patients per year. The most common conditions for acceptance by visiting nurses were："medication management" and "emotional support," followed by "PD-bag exchange" and "exit site care". The most common considerations for acceptance were："preparation of APD cycler" and "monitoring the operation of APD equipment," such as preparation of APD equipment. [Conclusion] In order for home health care nurses, who are key personnel in ASSISTED PD, to be able to accept PD patients without anxiety, collaboration and multidisciplinary cooperation, such as joint visits and sharing of care methods with medical staff at PD treatment facilities, are required.</p>

DOI： 10.4009/jsdt.56.401

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Papers - MIZUNO, Masashi