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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Facility-based educational systems and peritonitis incidence in peritoneal dialysis: findings from a nationwide survey in Japan. Reviewed International journal

Nagashima A, Kosugi T, Tagami G, Kurahashi S, Ototake S, Nakagaki M, Harada K, Toda N, Kadoya H, Eriguchi M, Sakai Y, Mizuno M, Nakayama M, Ito Y

Clinical and experimental nephrology Vol. 30 ( 5 ) page： 780 - 791 2026.5

Multidisciplinary introduction of peritoneal dialysis enabling ICU liberation and home-based care in Ebstein's anomaly with refractory ascites and CKD: a case report. Reviewed International journal

Funahashi Y, Fukui S, Kato N, Kosugi T, Mizuno M, Maruyama S

CEN case reports Vol. 15 ( 3 ) 2026.4

Survey of exit-site management practices of peritoneal dialysis in Japan. Reviewed International journal

Satoshi Kurahashi, Hiroyuki Kadoya, Satoshi Ototake, Takaaki Kosugi, Masahiro Nakagaki, Ai Nagashima, Kenji Harada, Naohiro Toda, Masahiro Eriguchi, Yukinao Sakai, Masashi Mizuno, Satoshi Suzuki, Keisuke Maruyama, Tomoko Inoue, Nanae Matsuo, Yudo Tanno, Yoshitaka Ishibashi, Takefumi Mori, Masaaki Nakayama, Hideki Kawanishi, Jun Minakuchi, Yasuhiko Ito

Clinical and experimental nephrology Vol. 30 ( 1 ) page： 152 - 161 2026.1

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

BACKGROUND: Catheter exit-site infection is a major cause of withdrawal from peritoneal dialysis (PD). However, methods for caring for the peritoneal catheter and exit sites are not established and vary among facilities. No survey has been conducted on exit-site management in Japan. Here, we aimed to identify successful examples that led to best practices. METHODS: The Japanese Society for Peritoneal Dialysis-led PD-related infection project was launched in 2023, under which a survey was conducted at 14 facilities nationwide that provide PD therapy. The survey content included questions about the timing of the initiation of exit-site care, the materials used in exit-site protection, and the disinfectants used for exit-site care. RESULTS: Seventy-one percent of the exit-site direction was downward. In all facilities, the exit site was dressed immediately after its creation for several days up to a certain period. Many facilities started exit-site care within 1-2 weeks of PD initiation. Notably, 50% of the facilities did not use disinfectants. Twelve facilities used gauze or film dressings to protect the exit site. The catheter was secured in many facilities; however, the distance of fixation varied. The timing for starting a shower after exit-site creation was commonly 1-4 weeks post-surgery. Nine facilities allowed bathing without a cover, typically after > 1 month. Of these, 7 did not use Spa Clean. CONCLUSIONS: These findings provide insights into exit-site care trends across facilities. Further studies and trials are needed to establish the best practice on exit-site care for Japanese patients undergoing PD.

DOI： 10.1007/s10157-025-02776-8

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The Antibiotic effect of Silver CAPD Catheter on Peritoneal Dialysis-related infections (ASCA-PD) study: a multicenter randomized open-label trial protocol. Reviewed International journal Open Access

Masahiro Eriguchi, Yasuhiko Ito, Hisako Yoshida, Masaru Matsui, Takaaki Kosugi, Ai Nagashima, Genri Tagami, Shohei Yamada, Tsutomu Sakurada, Masahiro Nakagaki, Kenji Harada, Satoshi Kurahashi, Naohiro Toda, Satoshi Ototake, Masashi Mizuno, Hiroyuki Kadoya, Seiji Kishi, Shunnosuke Kunoki, Yukinao Sakai, Yuichi Sato, Koji Hashimoto, Masatoshi Matsunami, Tomo Suzuki, Shunsuke Takahashi, Kenji Nakata, Kiyoto Koibuchi, Hideaki Oka, Taro Kamimura, Hidenobu Matsumoto, Takeshi Yoshida, Kazuhiko Tsuruya

Trials Vol. 27 ( 1 ) page： 66 - 66 2025.12

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

BACKGROUND: Peritoneal dialysis (PD) offers greater flexibility than hemodialysis, especially in patients with limited mobility or demanding schedules; however, PD-related infection is a major complication and a cause of withdrawal from peritoneal dialysis. The Antibiotic effect of Silver continuous ambulatory peritoneal dialysis (CAPD) Catheter on Peritoneal Dialysis-related infections (ASCA-PD) study will evaluate the effectiveness of a novel silver CAPD catheter, incorporating silver-based antimicrobial technology, for preventing these infections and improving PD adherence. METHODS/DESIGN: This randomized, open-label, parallel-group, multicenter trial will evaluate the efficacy and safety of a silver CAPD catheter compared with those of a conventional catheter at 14 Japanese facilities. A total of 250 adult patients with newly initiated PD will be enrolled and randomized 1:1 to receive either catheter type. The key exclusion criteria are prior PD, emergency PD initiation, non-abdominal exit-site placement, metal allergy, life expectancy <1 year, severe liver disease, certain dermatologic conditions, and immunosuppression. After providing informed consent, patients will undergo nasal swab screening for methicillin-resistant Staphylococcus aureus. Randomization will be stratified by facility and diabetes status. The primary outcome is the composite endpoint of all exit-site and tunnel infections within 12 months of PD initiation. Secondary outcomes include individual infection events, catheter removal, peritonitis, catheter patency, allergic reactions, technique failure (transition to hemodialysis for ≥30 days or death), and transition to hybrid dialysis. A Poisson regression model will be used to analyze the primary outcome, adjusting for observation time, treatment group, and stratification factors. Time-to-event secondary outcomes will be analyzed by competing risk regression. Subgroup analyses will be carried out to explore the impacts of age, sex, diabetes, insertion method, and body mass index. DISCUSSION: Unlike previous designs, our silver CAPD catheter incorporates AgNPs into silicone, enabling sustained antimicrobial effects both externally and internally, potentially overcoming limitations seen in prior human studies. This study will demonstrate the efficacy of silver CAPD catheters for preventing PD-related infections, especially during the initiation phase of PD, with the aim of providing a new therapeutic option. TRIAL REGISTRATION: Japan Registry of Clinical Trials, jRCTs052250003. Registered on April 4, 2025.

DOI： 10.1186/s13063-025-09250-6

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Absence of complement terminal pathway activity in C6-deficient mice prolongs survival in a mouse model of severe malarial infection. Reviewed International coauthorship International journal Open Access

Tomoaki Kamiya, Yuki Miyasaka, Hangsoo Kim, Sosuke Fukui, Masatoshi Inoue, Masatoshi Ishigami, Yasuhiro Suzuki, Shoichi Maruyama, Tamio Ohno, Timothy R Hughes, B Paul Morgan, Masashi Mizuno

Immunobiology Vol. 230 ( 6 ) page： 153140 - 153140 2025.11

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

BACKGROUND: Malaria is an important and serious parasite-induced disease associated with severe anemia and multiple organ failure (MOF) that can be lethal in humans. We explored the contribution of the terminal pathway of complement in a mouse model of malaria-induced lethal MOF following infection with Plasmodium (P.) bergei. METHODS: We compared organ damage and survival between C57BL/6 J mice deficient in the terminal pathway component C6 (C6def) and wild type C57BL/6 J mice (WT) after intraperitoneal injection of 106P. bergei-parasitized erythrocytes. We measured survival, relevant blood parameters, assessed severity of injury and complement activation in relevant organs. RESULTS: All WT mice died between 7 and 13 days after exposure to the parasite challenge; in contrast, C6def mice showed prolonged survival with 80 % alive at day 20, although all then died by day 26. Parasite load and anemia at day 7 were similar in C6def and WT mice. Liver and lung injuries, fibrosis and organ complement deposition assessed at day 7 post-infection were significantly milder in C6def mice compared to WT. Blood platelet count at day 7 post-infection was markedly reduced in WT but not in C6def mice; in contrast, white cell count was increased and hemoglobin levels decreased to similar degrees in WT and C6def mice post-infection. Albumin levels were reduced, significantly more in WT, while blood markers of liver injury were increased, significantly more in WT. Serum levels of complement activation product, C5a, and IL6 were increased in both groups, the latter significantly higher in WT versus C6def mice. CONCLUSION: We show that complement terminal pathway activation exacerbates organ injuries and thrombocytopenia associated with P. bergei infection, contributing to rapid progression to death in the model. Inhibition of terminal pathway activation in human malarial infections using available drugs might slow progression to organ failure, extending the window of opportunity for the effective use of anti-malarial medicines.

DOI： 10.1016/j.imbio.2025.153140

Transglutaminase 2 in human peritoneal dialysis-related peritoneal injury. Reviewed International journal Open Access

Shunnosuke Kunoki, Masashi Ikeno, Hideki Tatsukawa, Yukinao Sakai, Hiroshi Kinashi, Keisuke Kamiya, Masafumi Suzuki, Masashi Mizuno, Makoto Yamaguchi, Hiroyuki Sasakura, Yuki Morioka, Masataka Banshodani, Mitsuhiro Tawada, Masato Iwabu, Takuji Ishimoto, Kosei Takeuchi, Kiyotaka Hitomi, Hideki Kawanishi, Yasuhiko Ito

Physiological reports Vol. 13 ( 18 ) page： e70567 2025.9

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

Patients undergoing long-term peritoneal dialysis (PD) frequently develop peritoneal fibrosis and angiogenesis, leading to membrane dysfunction. Transglutaminase 2 (TG2) stabilizes the extracellular matrix against proteases. In an animal model, inhibition of TG2 reduced peritoneal fibrosis, angiogenesis, and inflammation. We investigated the expression of TG2 in 163 human peritoneal membrane tissue samples, including controls, tissues exposed to conventional acidic or low-glucose degradation product (GDP) pH-neutral solutions, and those with peritonitis or encapsulating peritoneal sclerosis (EPS), and explored the role of TG2 in high-glucose-induced pathophysiology in mesothelial cells. TG2 expression was upregulated in association with peritoneal membrane injury and was the highest in peritonitis. TG2 expression was correlated with peritoneal membrane thickness, CD68-positive macrophages, and myofibroblast expression. TG2 was expressed in mesothelial cells, α-smooth muscle actin-positive myofibroblast expression, macrophages, and endothelial cells in the diseased state. In cultured mesothelial cells, high-glucose-induced upregulation of collagen 1, TGF-β1, and TG2 was suppressed by a TG2 inhibitor or by TGF-β1 small interfering RNA. TG2 is involved in the development of peritoneal injury during PD. High-glucose dialysate is involved in the induction of peritoneal fibrosis through the interactive regulation of TGF-β and TG2. Targeting TG2 may offer therapeutic potential for managing PD complications and EPS.

DOI： 10.14814/phy2.70567

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特集透析療法の課題,展望総論腹膜透析の現状と残された課題

水野正司, 金恒秀, 福井聡介, 鈴木康弘

腎と透析 Vol. 98 ( 1 ) page： 13 - 17 2025.1

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

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

CEN Case Rep. Vol. 14 page： 188 - 193 2025

特集腎疾患の診断と治療最前線 II.各論1:糸球体疾患(診断と治療) 12.C3腎症 Invited

水野正司

腎と透析 Vol. 97 ( 7 ) page： 130 - 135 2024.12

Delaying treatment for peritonitis could be related to longer hospitalization in patients on peritoneal dialysis Reviewed International journal

Koshitori, Y; Takai, N; Isomura, Y; Hiramatsu, T; Suzuki, Y; Kim, H; Fukui, S; Mizuno, M

RENAL REPLACEMENT THERAPY Vol. 10 ( 1 ) 2024.11

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 Open Access

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 International journal

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 Open Access

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

Role of endothelial hyaluronan in peritoneal membrane transport and disease conditions during peritoneal dialysis. Reviewed Open Access

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.

Sci Rep. Vol. 14 ( 1 ) page： 7412 2024.3

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

Hisashi Kamido, Shinya Yamamoto, Hideki Yokoi, Masashi Mizuno, Motoko Yanagita

Cureus Vol. 16 ( 2 ) page： e55102 2024.2

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

C3 nephropathy is a renal disease caused by the aberrant activation of the alternative complement pathway. The long-term renal prognosis of C3 nephropathy is generally poor, and elucidation of its pathogenesis is clinically important. Genetic abnormalities within complement genes, encompassing autoantibodies targeting complement components and complement factor H-related proteins (CFHRs), can lead to abnormal complement activation. CFHR5 is one of the best-known responsible genes for C3 nephritis. Moreover, the renal prognosis can vary depending on the specific type of genetic mutation. Here, we report the case of a young woman with C3 nephritis and a heterozygous rare variant, P453S, in CFHR5. The P453S variant, characterized by amino acid substitutions with a low allele frequency, was located in the region essential for CFHR5 protein function, and multiple in silico analyses were done suggesting the pathological significance of P453S. The renal function of our patient remains stable. The P453S variant might contribute to the suppression of the CFHR5 protein's function, resulting in gradual complement progression and a favorable renal prognosis.

DOI： 10.7759/cureus.55102

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Papers - MIZUNO, Masashi