Faculty Profiles - UCHIDA Haruhito

Papers - UCHIDA Haruhito

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Low-dose rituximab induction therapy is effective in immunological high-risk renal transplantation without increasing cytomegalovirus infection. Reviewed International journal

Kasumi Yoshinaga, Motoo Araki, Koichiro Wada, Yuki Maruyama, Yosuke Mitsui, Takuya Sadahira, Risa Kubota, Shingo Nishimura, Yasuyuki Kobayashi, Hidemi Takeuchi, Katsuyuki Tanabe, Masashi Kitagawa, Hiroshi Morinaga, Haruhito Adam Uchida, Shinji Kitamura, Hitoshi Sugiyama, Jun Wada, Masami Watanabe, Toyohiko Watanabe, Yasutomo Nasu

International journal of urology : official journal of the Japanese Urological Association 27 ( 12 ) 1136 - 1142 2020.10

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

OBJECTIVES: To analyze the effect and impact of low-dose rituximab induction therapy on cytomegalovirus infection in living-donor renal transplantation. METHODS: A total of 92 recipients undergoing living-donor renal transplantation at Okayama University Hospital from May 2009 to August 2018 were evaluated retrospectively. Indications for preoperative rituximab (200 mg/body) were the following: (i) ABO major mismatch; (ii) ABO minor mismatch; (iii) donor-specific anti-human leukocyte antigen antibody-positive; and (iv) focal segmental glomerulosclerosis. We excluded four recipients who were followed <3 months, five who received >200 mg/body rituximab and seven who received prophylactic therapy for cytomegalovirus. RESULTS: There were 59 patients in the rituximab group and 17 in the non-rituximab group. Groups differed significantly in age (median age 53 vs 37 years, respectively; P = 0.04), but not in sex (male 64% vs 65%, P = 1.00), focal segmental glomerulosclerosis (3% vs 0%, P = 1.00) or percentage of cytomegalovirus-seronegative recipients of renal allografts from cytomegalovirus-seropositive donors (12% vs 18%, P = 0.68). The estimated glomerular filtration rate did not differ significantly between groups until 24 months after transplantation. Cytomegalovirus clinical symptoms (10% vs 24%, P = 0.22), including fever ≥38°C (5% vs 12%, P = 0.31) and gastrointestinal symptoms (5% vs 12%, P = 0.31), and the 5-year survival rates of death-censored graft loss (90% vs 83%, P = 0.43) did not differ significantly between groups. CONCLUSIONS: Low-dose rituximab induction therapy is effective in immunological high-risk recipients without increasing cytomegalovirus infection in the absence of valganciclovir prophylaxis.

DOI： 10.1111/iju.14382

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PAD合併により著明に増悪したフレイルな透析患者の予後

竹内英実, 内田治仁, 大高望, 梅林亮子, 杉山斉, 和田淳

日本透析医学会雑誌 53 ( Suppl.1 ) 736 - 736 2020.10

内シャント再設置術の成績・術式・リスク因子の検討

藤井泰宏, 大澤晋, 内田治仁, 竹内英実, 大高望, 笠原真悟

脈管学 60 ( Suppl. ) S161 - S161 2020.10

腎不全療法選択説明が緊急透析導入と療法選択に与える影響

森永裕士, 笠原由美子, 井本紀子, 角川紫野, 矢田光子, 大高望, 辻憲二, 北川正史, 田邊克幸, 木野村賢, 喜多村真治, 内田治仁, 杉山斉, 和田淳

日本透析医学会雑誌 53 ( Suppl.1 ) 496 - 496 2020.10

末梢動脈疾患が動脈スティフネスパラメータに与える影響の検討

武本梨佳, 内田治仁, 戸田洋伸, 大塚文男, 伊藤浩, 和田淳

脈管学 60 ( Suppl. ) S172 - S172 2020.10

Dysfunction of CD8 + PD-1 + T cells in type 2 diabetes caused by the impairment of metabolism-immune axis. Reviewed International journal

Ichiro Nojima, Shingo Eikawa, Nahoko Tomonobu, Yoshiko Hada, Nobuo Kajitani, Sanae Teshigawara, Satoshi Miyamoto, Atsuhito Tone, Haruhito A Uchida, Atsuko Nakatsuka, Jun Eguchi, Kenichi Shikata, Heiichiro Udono, Jun Wada

Scientific reports 10 ( 1 ) 14928 - 14928 2020.9

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

The metabolic changes and dysfunction in CD8 + T cells may be involved in tumor progression and susceptibility to virus infection in type 2 diabetes (T2D). In C57BL/6JJcl mice fed with high fat-high sucrose chow (HFS), multifunctionality of CD8 + splenic and tumor-infiltrating lymphocytes (TILs) was impaired and associated with enhanced tumor growth, which were inhibited by metformin. In CD8 + splenic T cells from the HFS mice, glycolysis/basal respiration ratio was significantly reduced and reversed by metformin. In the patients with T2D (DM), multifunctionality of circulating CD8 + PD-1 + T cells stimulated with PMA/ionomycin as well as with HLA-A*24:02 CMV peptide was dampened, while metformin recovered multifunctionality. Both glycolysis and basal respiration were reduced in DM, and glycolysis was increased by metformin. The disturbance of the link between metabolism and immune function in CD8 + PD-1 + T cells in T2D was proved by recovery of antigen-specific and non-specific cytokine production via metformin-mediated increase in glycolytic activity.

DOI： 10.1038/s41598-020-71946-3

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Tubulointerstitial Nephritis Cases With IgM-Positive Plasma Cells. Reviewed International journal

Natsumi Matsuoka-Uchiyama, Kenji Tsuji, Kazuhiko Fukushima, Shinji Kitamura, Haruhito A Uchida, Hitoshi Sugiyama, Naoki Takahashi, Masayuki Iwano, Jun Wada

Kidney international reports 5 ( 9 ) 1576 - 1580 2020.9

2型糖尿病に対するメトホルミンの抗腫瘍効果

野島一郎, 榮川伸吾, 梶谷展生, 勅使川原早苗, 宮本聡, 利根淳仁, 内田治仁, 中司敦子, 江口潤, 四方賢一, 鵜殿平一郎, 和田淳

糖尿病 63 ( Suppl.1 ) S - 111 2020.8

中四国地域におけるCKDおよびCVDの関連に関するコホート研究Kakusyo 3C Study:登録3年後のCKD管理状況

西脇麻里子, 内田治仁, 大高望, 辻憲二, 北川正史, 田邊克幸, 木野村賢, 吉田賢司, 前島洋平, 杉山斉, 伊藤浩, 和田淳

日本腎臓学会誌 62 ( 4 ) 378 - 378 2020.7

慢性腎臓病における貧血管理〜Kakusyo 3C Studyからの検討

内山奈津実, 内田治仁, 西脇麻里子, 大高望, 辻憲二, 北川正史, 田邊克幸, 木野村賢, 吉田賢司, 前島洋平, 杉山斉, 伊藤浩, 和田淳

日本腎臓学会誌 62 ( 4 ) 378 - 378 2020.7

岡山市CKDネットワーク(OCKD-NET)におけるCKD病診連携9年後の追跡調査

大西康博, 内田治仁, 大高望, 辻憲二, 田邊克幸, 森永裕士, 木野村賢, 喜多村真治, 前島洋平, 杉山斉, 太田康介, 丸山啓輔, 大城義之, 森岡茂, 大森一慶, 瀧上慶一, 蒲生直幸, 和田淳

日本腎臓学会誌 62 ( 4 ) 307 - 307 2020.7

The Protective Effect of Chlorogenic Acid on Vascular Senescence via the Nrf2/HO-1 Pathway. Reviewed International journal

Yoshiko Hada, Haruhito A Uchida, Nozomu Otaka, Yasuhiro Onishi, Shugo Okamoto, Mariko Nishiwaki, Rika Takemoto, Hidemi Takeuchi, Jun Wada

International journal of molecular sciences 21 ( 12 ) 2020.6

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

The world faces the serious problem of aging. In this study, we aimed to investigate the effect of chlorogenic acid (CGA) on vascular senescence. C57/BL6 female mice that were 14 ± 3 months old were infused with either Angiotensin II (AngII) or saline subcutaneously for two weeks. These mice were administered CGA of 20 or 40 mg/kg/day, or saline via oral gavage. AngII infusion developed vascular senescence, which was confirmed by senescence associated-β-galactosidase (SA-β-gal) staining. CGA administration attenuated vascular senescence in a dose-dependent manner, in association with the increase of Sirtuin 1 (Sirt1) and endothelial nitric oxide synthase (eNOS), and with the decrease of p-Akt, PAI-1, p53, and p21. In an in vitro study, with or without pre-treatment of CGA, Human Umbilical Vein Endothelial Cells (HUVECs) were stimulated with H2O2 for an hour, then cultured in the absence or presence of 0.5-5.0 μM CGA for the indicated time. Endothelial cell senescence was induced by H2O2, which was attenuated by CGA treatment. Pre-treatment of CGA increased Nrf2 in HUVECs. After H2O2 treatment, translocation of Nrf2 into the nucleus and the subsequent increase of Heme Oxygenase-1 (HO-1) were observed earlier in CGA-treated cells. Furthermore, the HO-1 inhibitor canceled the beneficial effect of CGA on vascular senescence in mice. In conclusion, CGA exerts a beneficial effect on vascular senescence, which is at least partly dependent on the Nuclear factor erythroid 2-factor 2 (Nrf2)/HO-1 pathway.

DOI： 10.3390/ijms21124527

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Effect of Angiotensin II on Bone Erosion and Systemic Bone Loss in Mice with Tumor Necrosis Factor-Mediated Arthritis. Reviewed International journal

Takahiko Akagi, Tomoyuki Mukai, Takafumi Mito, Kyoko Kawahara, Shoko Tsuji, Shunichi Fujita, Haruhito A Uchida, Yoshitaka Morita

International journal of molecular sciences 21 ( 11 ) 2020.6

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

Angiotensin II (Ang II) is the main effector peptide of the renin-angiotensin system (RAS), which regulates the cardiovascular system. The RAS is reportedly also involved in bone metabolism. The upregulation of RAS components has been shown in arthritic synovial tissues, suggesting the potential involvement of Ang II in arthritis. Accordingly, in the present study, we investigated the role of Ang II in bone erosion and systemic bone loss in arthritis. Ang II was infused by osmotic pumps in tumor necrosis factor-transgenic (TNFtg) mice. Ang II infusion did not significantly affect the severity of clinical and histological inflammation, whereas bone erosion in the inflamed joints was significantly augmented. Ang II administration did not affect the bone mass of the tibia or vertebra. To suppress endogenous Ang II, Ang II type 1 receptor (AT1R)-deficient mice were crossed with TNFtg mice. Genetic deletion of AT1R did not significantly affect inflammation, bone erosion, or systemic bone loss. These results suggest that excessive systemic activation of the RAS can be a risk factor for progressive joint destruction. Our findings indicate an important implication for the pathogenesis of inflammatory bone destruction and for the clinical use of RAS inhibitors in patients with rheumatoid arthritis.

DOI： 10.3390/ijms21114145

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Frailty Raises as a New Target in Patients with Chronic Hemodialysis in any Country and the Problem we Should Solve Reviewed

Hidemi Takeuchi, Haruhito A Uchida, Jun Wada

Journal of Clinical Trials 10 ( 3 ) 2020.6

Targeting Mitochondrial Fission as a Potential Therapeutic for Abdominal Aortic Aneurysm. Reviewed International journal

Hannah A Cooper, Stephanie Cicalese, Kyle J Preston, Tatsuo Kawai, Keisuke Okuno, Eric T Choi, Shingo Kasahara, Haruhito A Uchida, Nozomu Otaka, Rosario Scalia, Victor Rizzo, Satoru Eguchi

Cardiovascular research 117 ( 3 ) 971 - 982 2020.5

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

AIMS: Angiotensin II is a potential contributor to the development of abdominal aortic aneurysm (AAA). In aortic vascular smooth muscle cells, exposure to angiotensin II induces mitochondrial fission via dynamin-related protein 1 (Drp1). However, pathophysiological relevance of mitochondrial morphology in angiotensin II-associated AAA remains unexplored. Here, we tested the hypothesis that mitochondrial fission is involved in the development of AAA. METHODS AND RESULTS: Immunohistochemistry was performed on human AAA samples and revealed enhanced expression of Drp1. In C57BL6 mice treated with angiotensin II plus β-aminopropionitrile, AAA tissue also showed an increase in Drp1 expression. A mitochondrial fission inhibitor, mdivi1, attenuated AAA size, associated aortic pathology, Drp1 protein induction and mitochondrial fission but not hypertension in these mice. Moreover, Western blot analysis showed that induction of matrix metalloproteinase-2, which precedes the development of AAA, was blocked by mdivi1. Mdivi1 also reduced the development of AAA in apolipoprotein E deficient mice infused with angiotensin II. As with mdivi1, Drp1+/- mice treated with angiotensin II plus β-aminopropionitrile showed a decrease in AAA compared to control Drp1+/+ mice. In abdominal aortic vascular smooth muscle cells, angiotensin II induced phosphorylation of Drp1 and mitochondrial fission, the latter of which was attenuated with Drp1 silencing as well as mdivi1. Angiotensin II also induced vascular cell adhesion molecule-1 expression and enhanced leukocyte adhesion and mitochondrial oxygen consumption in smooth muscle cells, which were attenuated with mdivi1. CONCLUSION: These data indicate that Drp1 and mitochondrial fission play salient roles in AAA development, which likely involves mitochondrial dysfunction and inflammatory activation of vascular smooth muscle cells. TRANSLATIONAL PERSPECTIVES: Mitochondrial fission/fusion regulation is critical to maintain mitochondrial homeostasis. A shift toward mitochondrial fission is associated with a variety of cardiovascular diseases. A GTPase, Drp1 is known to mediate mitochondrial fission and we found evidence of Drp1 dysregulation in human and mouse abdominal aortic aneurysms (AAA). The results from the present study demonstrate that pharmacological as well as genetic inhibition of mitochondrial fission via Drp1 prevents AAA formation and vascular smooth muscle aneurysmal phenotype in mouse models of the disease. These data indicate that intervening in this pathway may have therapeutic potential for treating AAA.

DOI： 10.1093/cvr/cvaa133

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Associated factors of poor treatment outcomes in patients with giant cell arteritis: clinical implication of large vessel lesions. Reviewed International journal

Takahiko Sugihara, Hitoshi Hasegawa, Haruhito A Uchida, Hajime Yoshifuji, Yoshiko Watanabe, Eisuke Amiya, Yasuhiro Maejima, Masanori Konishi, Yohko Murakawa, Noriyoshi Ogawa, Shunsuke Furuta, Yasuhiro Katsumata, Yoshinori Komagata, Taio Naniwa, Takahiro Okazaki, Yoshiya Tanaka, Tsutomu Takeuchi, Yoshikazu Nakaoka, Yoshihiro Arimura, Masayoshi Harigai, Mitsuaki Isobe

Arthritis research & therapy 22 ( 1 ) 72 - 72 2020.4

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

BACKGROUND: Relapses frequently occur in giant cell arteritis (GCA), and long-term glucocorticoid therapy is required. The identification of associated factors with poor treatment outcomes is important to decide the treatment algorithm of GCA. METHODS: We enrolled 139 newly diagnosed GCA patients treated with glucocorticoids between 2007 and 2014 in a retrospective, multi-center registry. Patients were diagnosed with temporal artery biopsy, 1990 American College of Rheumatology classification criteria, or large vessel lesions (LVLs) detected by imaging based on the modified classification criteria. Poor treatment outcomes (non-achievement of clinical remission by week 24 or relapse during 52 weeks) were evaluated. Clinical remission was defined as the absence of clinical signs and symptoms in cranial and large vessel areas, polymyalgia rheumatica (PMR), and elevation of C-reactive protein (CRP) levels. A patient was determined to have a relapse if he/she had either one of the signs and symptoms that newly appeared or worsened after achieving clinical remission. Re-elevation of CRP without clinical manifestations was considered as a relapse if other causes such as infection were excluded and the treatment was intensified. Associated factors with poor treatment outcomes were analyzed by using the Cox proportional hazard model. RESULTS: Cranial lesions, PMR, and LVLs were detected in 77.7%, 41.7%, and 52.5% of the enrolled patients, respectively. Treatment outcomes were evaluated in 119 newly diagnosed patients who were observed for 24 weeks or longer. The mean initial dose of prednisolone was 0.76 mg/kg/day, and 29.4% received any concomitant immunosuppressive drugs at baseline. Overall, 41 (34.5%) of the 119 patients had poor treatment outcomes; 13 did not achieve clinical remission by week 24, and 28 had a relapse after achieving clinical remission. Cumulative rates of the events of poor treatment outcomes in patients with and without LVLs were 47.5% and 17.7%, respectively. A multivariable model showed the presence of LVLs at baseline was significantly associated with poor treatment outcomes (adjusted hazard ratio [HR] 3.54, 95% CI 1.52-8.24, p = 0.003). Cranial lesions and PMR did not increase the risk of poor treatment outcomes. CONCLUSION: The initial treatment intensity in the treatment algorithm of GCA could be determined based upon the presence or absence of LVLs detected by imaging at baseline.

DOI： 10.1186/s13075-020-02171-6

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JCS 2017 Guideline on Management of Vasculitis Syndrome - Digest Version. Reviewed

Mitsuaki Isobe, Koichi Amano, Yoshihiro Arimura, Akihiro Ishizu, Shuichi Ito, Shinya Kaname, Shigeto Kobayashi, Yoshinori Komagata, Issei Komuro, Kimihiro Komori, Kei Takahashi, Kazuo Tanemoto, Hitoshi Hasegawa, Masayoshi Harigai, Shouichi Fujimoto, Tatsuhiko Miyazaki, Tetsuro Miyata, Hidehiro Yamada, Akitoshi Yoshida, Takashi Wada, Yoshinori Inoue, Haruhito A Uchida, Hideki Ota, Takahiro Okazaki, Mitsuho Onimaru, Tamihiro Kawakami, Reiko Kinouchi, Atsushi Kurata, Hisanori Kosuge, Ken-Ei Sada, Kunihiro Shigematsu, Eiichi Suematsu, Eijun Sueyoshi, Takahiko Sugihara, Hitoshi Sugiyama, Mitsuhiro Takeno, Naoto Tamura, Michi Tsutsumino, Hiroaki Dobashi, Yoshikazu Nakaoka, Kenji Nagasaka, Yasuhiro Maejima, Hajime Yoshifuji, Yoshiko Watanabe, Shoichi Ozaki, Takeshi Kimura, Hiroshi Shigematsu, Keiko Yamauchi-Takihara, Toyoaki Murohara, Shin-Ichi Momomura

Circulation journal : official journal of the Japanese Circulation Society 84 ( 2 ) 299 - 359 2020.1

Polypharmacy and frailty in chronic kidney disease

Hidemi Takeuchi, Haruhito Adam Uchida, Jun Wada

Recent Advances of Sarcopenia and Frailty in CKD 223 - 237 2020.1

Language：English Publishing type：Part of collection (book) Publisher：Springer Singapore

The prognoses of various diseases have improved because of progress in the field of medicine and clinical practice guidelines developed in countries around the world. However, polypharmacy and frailty have become a global public health concern because of the increase in longevity. Although polypharmacy and frailty are associated with a broad range of negative outcomes, they occur concurrently in patients with chronic kidney disease (CKD) at a higher rate. Elderly patients with CKD usually require multiple medications to prevent CKD progression and complications, and their conditions are generally complicated. In this article, we outline polypharmacy and frailty, which frequently occur in patients with CKD and introduce notes and approaches to overcome these issues.

DOI： 10.1007/978-981-15-2365-6_14

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Podocyte autophagy is associated with foot process effacement and proteinuria in patients with minimal change nephrotic syndrome. Reviewed International journal

Ayu Ogawa-Akiyama, Hitoshi Sugiyama, Masashi Kitagawa, Keiko Tanaka, Yuzuki Kano, Koki Mise, Nozomu Otaka, Katsuyuki Tanabe, Hiroshi Morinaga, Masaru Kinomura, Haruhito A Uchida, Jun Wada

PloS one 15 ( 1 ) e0228337 2020

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

Autophagy is a cellular mechanism involved in the bulk degradation of proteins and turnover of organelle. Several studies have shown the significance of autophagy of the renal tubular epithelium in rodent models of tubulointerstitial disorder. However, the role of autophagy in the regulation of human glomerular diseases is largely unknown. The current study aimed to demonstrate morphological evidence of autophagy and its association with the ultrastructural changes of podocytes and clinical data in patients with idiopathic nephrotic syndrome, a disease in which patients exhibit podocyte injury. The study population included 95 patients, including patients with glomerular disease (minimal change nephrotic syndrome [MCNS], n = 41; idiopathic membranous nephropathy [IMN], n = 37) and 17 control subjects who underwent percutaneous renal biopsy. The number of autophagic vacuoles and the grade of foot process effacement (FPE) in podocytes were examined by electron microscopy (EM). The relationships among the expression of autophagic vacuoles, the grade of FPE, and the clinical data were determined. Autophagic vacuoles were mainly detected in podocytes by EM. The microtubule-associated protein 1 light chain 3 (LC3)-positive area was co-localized with the Wilms tumor 1 (WT1)-positive area on immunofluorescence microscopy, which suggested that autophagy occurred in the podocytes of patients with MCNS. The number of autophagic vacuoles in the podocytes was significantly correlated with the podocyte FPE score (r = -0.443, p = 0.004), the amount of proteinuria (r = 0.334, p = 0.033), and the level of serum albumin (r = -0.317, p = 0.043) in patients with MCNS. The FPE score was a significant determinant for autophagy after adjusting for the age in a multiple regression analysis in MCNS patients (p = 0.0456). However, such correlations were not observed in patients with IMN or in control subjects. In conclusion, the results indicated that the autophagy of podocytes is associated with FPE and severe proteinuria in patients with MCNS. The mechanisms underlying the activation of autophagy in association with FPE in podocytes should be further investigated in order to elucidate the pathophysiology of MCNS.

DOI： 10.1371/journal.pone.0228337

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The Aging Population and Research into Treatments for Abdominal Aortic Aneurysms. Reviewed

Ryoko Umebayashi, Haruhito Adam Uchida, Jun Wada

Acta medica Okayama 73 ( 6 ) 475 - 477 2019.12

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

Abdominal aortic aneurysms (AAAs) usually expand asymptomatically until the occurrence of a life-threatening event such as aortic rupture, which is closely associated with high mortality. AAA and aortic dissection are ranked among the top 10 causes of death in Japan. The major risk factors for AAA are age over 65 years, male gender, family history, and smoking. Thus, for prevention, smoking cessation is the most important lifestyle-intervention. For treatment, since AAA generally affects elderly people, less invasive treatment is preferable. However, the only established treatment for AAA is open repair and endovascular repair. This review describes potential medical treatments to slow aneurysm growth or prevent AAA rupture.

DOI： 10.18926/AMO/57710

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Papers - UCHIDA Haruhito