2022/04/06 更新

写真a

タナベ カツユキ
田邊 克幸
TANABE Katsuyuki
所属
岡山大学病院 講師(特任)
職名
講師(特任)
外部リンク

学位

  • 医学博士 ( 岡山大学 )

研究キーワード

  • 急性腎障害

  • 糖尿病性腎臓病

  • 腎代替療法

  • 慢性腎臓病

研究分野

  • ライフサイエンス / 腎臓内科学

学歴

  • 岡山大学    

    2002年4月 - 2007年6月

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  • 鳥取大学   Faculty of Medicine   School of Medicine

    1996年4月 - 2002年3月

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経歴

  • 岡山大学病院   血液浄化療法部   助教

    2012年9月 - 現在

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  • コロラド大学デンバー校   腎臓病高血圧科   博士研究員

    2009年9月 - 2012年8月

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  • 岡山大学   Graduate School of Medicine , Dentistry and Pharmaceutical Sciences   客員研究員

    2008年10月 - 2009年8月

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  • 岡山大学   腎臓・糖尿病・内分泌内科   医員

    2007年10月 - 2008年9月

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所属学協会

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論文

  • Silica-associated systemic lupus erythematosus with lupus nephritis and lupus pneumonitis: A case report and a systematic review of the literature. 査読 国際誌

    Kazuhiko Fukushima, Haruhito A Uchida, Yasuko Fuchimoto, Tomoyo Mifune, Mayu Watanabe, Kenji Tsuji, Katsuyuki Tanabe, Masaru Kinomura, Shinji Kitamura, Yosuke Miyamoto, Sae Wada, Taisaku Koyanagi, Hitoshi Sugiyama, Takumi Kishimoto, Jun Wada

    Medicine   101 ( 7 )   e28872   2022年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    INTRODUCTION: Several epidemiological studies have shown that silica exposure triggers the onset of systemic lupus erythematosus (SLE); however, the clinical characteristics of silica-associated SLE have not been well studied. PATIENT CONCERNS: A 67-year-old man with silicosis visited a primary hospital because of a fever and cough. His respiratory condition worsened, regardless of antibiotic medication, and he was referred to our hospital. DIAGNOSIS: The patient showed leukopenia, lymphopenia, serum creatinine elevation with proteinuria and hematuria, decreased serum C3 level, and was positive for anti-double stranded DNA antibody, anti-nuclear antibody, and direct Coombs test. He was diagnosed with SLE. Renal biopsy was performed, and the patient was diagnosed with lupus nephritis (class IV-G(A/C) + V defined by the International Society of Nephrology/Renal Pathology Society classification). Computed tomography revealed acute interstitial pneumonitis, bronchoalveolar lavage fluid showed elevation of the lymphocyte fraction, and he was diagnosed with lupus pneumonitis. INTERVENTIONS: Prednisolone (50 mg/day) with intravenous cyclophosphamide (500 mg/body) were initiated. OUTCOMES: The patient showed a favorable response to these therapies. He was discharged from our hospital and received outpatient care with prednisolone slowly tapered off. He had cytomegalovirus and herpes zoster virus infections during treatment, which healed with antiviral therapy. REVIEW: We searched for the literature on sSLE, and selected 11 case reports and 2 population-based studies. The prevalence of SLE manifestations in sSLE patients were comparative to that of general SLE, particularly that of elderly-onset SLE. Our renal biopsy report and previous reports indicate that lupus nephritis of sSLE patients show as various histological patterns as those of general SLE patients. Among the twenty sSLE patients reported in the case articles, three patients developed lupus pneumonitis and two of them died of it. Moreover, two patients died of bacterial pneumonia, one developed aspergillus abscesses, one got pulmonary tuberculosis, and one developed lung cancer. CONCLUSION: Close attention is needed, particularly for respiratory system events and infectious diseases, when treating patients with silica-associated SLE using immunosuppressive therapies.

    DOI: 10.1097/MD.0000000000028872

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  • Vasohibin-1 has α-tubulin detyrosinating activity in glomerular podocytes. 査読 国際誌

    Tomoyo Mifune, Katsuyuki Tanabe, Yuri Nakashima, Satoshi Tanimura, Hitoshi Sugiyama, Yasufumi Sato, Jun Wada

    Biochemical and biophysical research communications   599   93 - 99   2022年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Podocytes are highly specialized epithelial cells in glomeruli, with a complex morphology composed of a cell body, primary processes, and foot processes, which maintain barrier function in glomerular filtration. The microtubule-based cytoskeleton is necessary for podocyte morphology. Microtubule structure and function can be affected by post-translational modification of tubulin, including detyrosination. Recent studies have shown that vasohibin-1 (VASH1), an antiangiogenic factor, has tubulin carboxypeptidase activity that causes detyrosination of α-tubulin. We aimed to examine the role of VASH1 in regulating α-tubulin detyrosination in podocytes and the potential involvement of VASH1 deficiency in renal morphology. In normal mouse kidneys, detyrosinated α-tubulin was mainly identified in glomeruli, especially in podocytes; meanwhile, in cultured immortalized podocytes, α-tubulin detyrosination was promoted with cell differentiation. Notably, α-tubulin detyrosination in glomeruli was diminished in Vash1 homozygous knockout (Vash1-/-) mice, and knockdown of VASH1 in cultured podocytes prevented α-tubulin detyrosination. Although VASH1 deficiency-induced downregulation of detyrosination caused no remarkable glomerular lesions, urinary albuminuria excretion and glomerular volume were significantly higher in Vash1-/- mice than in wild-type mice. Furthermore, decreased glomerular nephrin expression and narrower slit diaphragms width were observed in Vash1-/- mice. Taken together, we demonstrated that α-tubulin detyrosination in podocytes was mainly regulated by VASH1 and that VASH1 deficiency-mediated decreases in α-tubulin detyrosination led to minor alterations in podocyte morphology and predisposition to albuminuria. VASH1 expression and α-tubulin detyrosination may be novel targets for maintaining glomerular filtration barrier integrity.

    DOI: 10.1016/j.bbrc.2022.02.047

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  • Management of corticosteroid-dependent eosinophilic interstitial nephritis: A case report. 査読 国際誌

    Katsuyuki Tanabe, Natsumi Matsuoka-Uchiyama, Tomoyo Mifune, Chieko Kawakita, Hitoshi Sugiyama, Jun Wada

    Medicine   100 ( 50 )   e28252   2021年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    INTRODUCTION: Drug-induced acute interstitial nephritis (DI-AIN) is an important cause of acute kidney injury. In renal biopsy specimens, tubulitis with eosinophilic infiltration is suggestive of DI-AIN. Although corticosteroid therapy and discontinuation of the offending drug can improve renal dysfunction in most cases of DI-AIN, some patients experience AIN recurrence, leading to corticosteroid dependency. Corticosteroid-dependent eosinophilic interstitial nephritis presents a difficult dilemma in diagnosis and information regarding optimum management is limited. PATIENT CONCERNS: A 25-year-old man, who received treatment with carbamazepine, zonisamide, valproate, and lacosamide for temporal lobe epilepsy, showed an increase in serum creatinine level from 0.98 to 1.29 mg/dL over a period of 6 months. Although he exhibited no symptoms, his serum creatinine level continued to increase to 1.74 mg/dL. DIAGNOSIS: Renal biopsy revealed tubulitis and interstitial inflammatory infiltrates with eosinophils. Immunological and ophthalmological examinations showed no abnormal findings, and thus, his renal dysfunction was presumed to be caused by DI-AIN. Although oral prednisolone (PSL) administration (40 mg/d) and discontinuation of zonisamide immediately improved his renal function, AIN recurred 10 months later. The increase in PSL dose along with discontinuation of valproate and lacosamide improved renal function. However, 10 months later, recurrent AIN with eosinophilic infiltration was confirmed by further biopsy. The patient was therefore diagnosed with corticosteroid-dependent eosinophilic interstitial nephritis. INTERVENTIONS: To prevent life-threatening epilepsy, carbamazepine could not be discontinued; hence, he was treated with an increased dose of PSL (60 mg/d) and 1500 mg/d of mycophenolate mofetil (MMF). OUTCOMES: MMF was well tolerated and PSL was successfully tapered to 5 mg/d; renal function stabilized over a 20-month period. LESSONS: The presence of underdetermined autoimmune processes and difficulties in discontinuing the putative offending drug discontinuation are contributing factors to corticosteroid dependency in patients with eosinophilic interstitial nephritis. MMF may be beneficial in the management of corticosteroid-dependent eosinophilic interstitial nephritis by reducing the adverse effects related to high-dose and long-term corticosteroid use.

    DOI: 10.1097/MD.0000000000028252

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  • Presence of decoy cells for 6 months on urine cytology efficiently predicts BK virus nephropathy in renal transplant recipients. 査読 国際誌

    Takanori Sekito, Motoo Araki, Kasumi Yoshinaga, Yuki Maruyama, Takuya Sadahira, Shingo Nishimura, Koichiro Wada, Masami Watanabe, Toyohiko Watanabe, Katsuyuki Tanabe, Hidemi Takeuchi, Hiroshi Morinaga, Masashi Kitagawa, Shinji Kitamura, Hitoshi Sugiyama, Jun Wada, Hiroyuki Yanai, Yasutomo Nasu

    International journal of urology : official journal of the Japanese Urological Association   28 ( 12 )   1240 - 1246   2021年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    OBJECTIVES: To investigate the association between duration of consecutive presence of decoy cells on urine cytology and BK virus nephropathy after kidney transplantation. METHODS: In total, 121 kidney transplant recipients were retrospectively evaluated. The best duration of consecutive presence of decoy cells that could be used to predict BK virus nephropathy was analyzed using the area under the curve for each duration, and recipients were divided into two groups based on the best predictive performance. The effectiveness of SV40 immunostaining on urinary cytology was also analyzed. RESULTS: In total, 2534 urine specimens as well as SV40 immunostaining in 2241 urine specimens were analyzed. Six consecutive months of decoy cell positivity had the best predictive performance for BK virus nephropathy (area under the curve = 0.832). The incidence of BK virus nephropathy in recipients with positive decoy cells for 6 months or more consecutive months (5/44) was significantly higher than in those who had positive decoy cells for less than 6 months (0/77; P = 0.005). Decoy cell positivity had a sensitivity, specificity, positive predictive value, and negative predictive value for BK virus nephropathy of 100%, 66%, 11%, and 100% respectively. SV40 immunostaining provided slightly better specificity (68%) and positive predictive value (12%). CONCLUSIONS: The detection of decoy cells at 6 months or more on urine cytology had high predictive value for BK virus nephropathy in kidney transplant recipients. SV40 immunostaining on urine cytology added minimal diagnostic accuracy.

    DOI: 10.1111/iju.14679

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  • Feasible kidney donation with living marginal donors, including diabetes mellitus. 査読 国際誌

    Kasumi Yoshinaga, Motoo Araki, Koichiro Wada, Takanori Sekito, Shogo Watari, Yuki Maruyama, Yosuke Mitsui, Takuya Sadahira, Risa Kubota, Shingo Nishimura, Kohei Edamura, Yasuyuki Kobayashi, Katsuyuki Tanabe, Hidemi Takeuchi, Masashi Kitagawa, Shinji Kitamura, Jun Wada, Masami Watanabe, Toyohiko Watanabe, Yasutomo Nasu

    Immunity, inflammation and disease   9 ( 3 )   1061 - 1068   2021年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    OBJECTIVES: To compare the donor outcomes of living donor kidney transplantation between standard donors (SDs) and marginal donors (MDs) including diabetic patients (MD + DM). METHODS: MDs were defined according to Japanese guideline criteria: (a) age >70-years, (b) blood pressure ≤130/80 mmHg on hypertension medicine, (c) body mass index >25 to ≤32 kg/m2 , (d) 24-h creatinine clearance ≥70 to <80 ml/min/1.73 m2 , and (e) hemoglobin A1c > 6.2 or ≤6.5 with oral diabetic medicine. Fifty-three of 114 donors were MDs. We compared donor kidney functions until 60 months postoperatively. RESULTS: No kidney function parameters were different between SDs and MDs. When comparing SD and MD + DM, MD + DM had a lower postoperative eGFR (48 vs. 41 (1 (month), p = .02), 49 vs. 40 (12, p < .01), 48 vs. 42 (24, p = .04), 47 vs. 38 (36, p = .01)) and the percentage of residual eGFR (SD vs. MD + DM: 63 vs. 57 (1 (month), p < .01), 63 vs. 57 (2, p < .01), 64 vs. 56 (12, p < .01), 63 vs. 57 (24, p < .01), 63 vs. 52 (36, p = .02)). However, when MD with a single risk factor of DM was compared to SD, the difference disappeared. Nine out of 12 (75%) MD + DM had ≥2 risk factors. CONCLUSIONS: Although long-term observation of donor kidney function is necessary, careful MD + DM selection had the potential to expand the donor pool.

    DOI: 10.1002/iid3.470

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  • Blood concentrations of tacrolimus upon conversion from rabeprazole to vonoprazan in renal transplant recipients: Correlation with cytochrome P450 gene polymorphisms. 査読 国際誌

    Shogo Watari, Motoo Araki, Jun Matsumoto, Kasumi Yoshinaga, Takanori Sekito, Yuki Maruyama, Yosuke Mitsui, Takuya Sadahira, Risa Kubota, Shingo Nishimura, Koichiro Wada, Yasuyuki Kobayashi, Hidemi Takeuchi, Katsuyuki Tanabe, Masashi Kitagawa, Hiroshi Morinaga, Shinji Kitamura, Hitoshi Sugiyama, Noritaka Ariyoshi, Jun Wada, Masami Watanabe, Toyohiko Watanabe, Yasutomo Nasu

    Drug metabolism and pharmacokinetics   40   100407   2021年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    We evaluated the impact of vonoprazan on blood concentrations of tacrolimus via a retrospective analysis of 52 renal transplant recipients who took tacrolimus and converted from rabeprazole to vonoprazan between August 2018 and September 2019. We compared tacrolimus trough levels upon conversion among groups that were classified based on cytochrome P450 (CYP) gene polymorphisms. CYP3A5 groups were heterozygous or homozygous for CYP3A5∗1 and CYP3A5∗3 alleles. CYP2C19 genotypes were classified as extensive (∗1/∗1), intermediate (∗1/∗2 and ∗1/∗3) or poor metabolizers (∗2/∗2, ∗2/∗3 and ∗3/∗3). Tacrolimus trough levels increased only 0.3 ng/mL upon conversion in the CYP3A5∗3/∗3 group: 5.8 [3.4-7.2] vs 6.1 [3.8-7.9]; p = 0.06. No statistically significance changes in tacrolimus levels also occurred in the CYP3A5∗1/∗1 or CYP3A5∗1/∗3 groups. Subgroup analyses of CYP3A5∗3/∗3 demonstrated low changes for all three CYP2C19 subgroups: 5.2 [4.3-6.5] vs 6.2 [4.3-7.9]; p = 0.07, 6.1 [3.4-7.2] vs 6.7 [4.6-7.9]; p = 0.12 and 5.4 [3.6-6.5] vs 4.7 [3.8-6.3]; p = 1.00, respectively. Conversion to vonoprazan thus resulted in little increase of tacrolimus trough levels, even in the group predicted to be most susceptible (CYP3A5∗3/∗3 and 2C19∗1/∗1), thus supporting the safety of concomitant use of vonoprazan with tacrolimus.

    DOI: 10.1016/j.dmpk.2021.100407

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  • ABO Blood Incompatibility Positively Affects Early Graft Function: Single-Center Retrospective Cohort Study. 査読 国際誌

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

    Transplantation proceedings   53 ( 5 )   1494 - 1500   2021年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: We investigated the association between ABO-incompatible (ABO-I) kidney transplantation and early graft function. METHODS: We retrospectively analyzed 95 patients who underwent living donor kidney transplantation between May 2009 and July 2019. It included 61 ABO-compatible (ABO-C) and 34 ABO-I transplantations. We extracted data on immunologic profile, sex, age, cold ischemic time, type of immunosuppression, and graft function. Two definitions were used for slow graft function (SGF) as follows: postoperative day (POD) 3 serum creatinine level >3 mg/dL and estimated glomerular filtration rate (eGFR) <20 mL/min/1.73 m2. Logistic regression analysis was performed to analyze the effect of ABO-I on the incidence of SGF. RESULTS: The characteristics between the ABO-C and ABO-I were not different. ABO-I received rituximab and plasma exchange. Patients also received tacrolimus and mycophenolate mofetil for 2 weeks and prednisolone for 1 week before transplantation as preconditioning. Of the 95 study patients, 19 (20%) and 21 (22%) were identified with SGF according to POD 3 serum creatinine level or eGFR, respectively. Multivariable analysis revealed that ABO-I significantly reduced the incidence of SGF (odds ratio, 0.15; 95% confidence interval, 0.03-0.7; P = .02), and cold ischemic time >150 min increased the incidence of SGF (odds ratio, 6.5; 95% confidence interval, 1.7-25; P = .006). Similar results were identified in POD 3 eGFR. Inferior graft function in patients with SGF was identified up to 6 months after transplantation. CONCLUSION: ABO-I reduces the incidence of SGF, which is associated with an inferior graft function up to 6 months.

    DOI: 10.1016/j.transproceed.2021.03.043

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  • Successful deceased donor kidney transplantation to a recipient with a history of COVID-19 treatment. 査読 国際誌

    Kasumi Yoshinaga, Motoo Araki, Koichiro Wada, Kou Hasegawa, Takanori Sekito, Shuji Miyake, Shogo Watari, Yuki Maruyama, Takuya Sadahira, Shingo Nishimura, Katsuyuki Tanabe, Hidemi Takeuchi, Yuri Nakashima, Masaru Kinomura, Herik Acosta, Yosuke Mitsui, Risa Kubota, Hirochika Nakajima, Kohei Edamura, Yasuyuki Kobayashi, Masami Watanabe, Toyohiko Watanabe, Fumio Otsuka, Jun Wada, Yasutomo Nasu

    Journal of infection and chemotherapy : official journal of the Japan Society of Chemotherapy   27 ( 7 )   1097 - 1101   2021年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    CASE PRESENTATION: A 49-year-old Asian male, who had undergone hemodialysis for >16 years, complained of a fever, dysgeusia and dysosmia, and was diagnosed with COVID-19 pneumonia based on severe acute respiratory syndrome coronavirus 2 polymerase chain reaction (SARS-CoV-2 PCR) and computed tomography (CT). Treatment was started with oral favipiravir and ciclesonide inhalation. On the 10th day of treatment, the patient had a persistent high fever and a chest CT showed exacerbation of pneumonia, so dexamethasone was intravenously started. He was discharged after confirming two consecutive negative SARS-CoV-2 PCR tests. Three months after COVID-19 treatment, a SARS-CoV-2 PCR test was negative and he underwent a deceased donor kidney transplantation. Basiliximab induction with triple drug immunosuppression consisting of extended-release tacrolimus, mycophenolate mofetil and prednisolone, which is our regular immunosuppression protocol, was used. He was discharged on postoperative day 18 without the need for postoperative hemodialysis or any complications. The serum creatinine level was 1.72 mg/dL 95 days postoperatively and he had a favorable clinical course that was similar to deceased donor kidney recipients without a history of SARS-CoV-2 infection. CONCLUSION: We report the first case of a kidney transplantation after COVID-19 treatment in Japan and the fourth case globally. We would like to provide information about our successful case due to the anticipated increase in similar candidates in the near future.

    DOI: 10.1016/j.jiac.2021.03.018

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  • Renal capsular vein thrombosis. 査読

    Katsuyuki Tanabe, Jota Maki, Hikari Nakatou

    Clinical and experimental nephrology   25 ( 4 )   439 - 440   2021年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    A 30-year-old pregnant woman developed postpartum HELLP syndrome. Abdominal computed tomography revealed a high-density vessel structure in contact with the right kidney and connected to the right ovarian vein, suggesting thrombosis in the right inferior renal capsular vein (RCV). RCV thrombosis is a rare thrombotic disorder in postpartum women, and hypercoagulability related to the pregnancy complications may be the predisposing factor. The potential risk for pulmonary embolism in the rare pregnancy-related thrombosis should be recognized.

    DOI: 10.1007/s10157-020-01998-2

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  • Vasohibin-2 Aggravates Development of Ascending Aortic Aneurysms But Not Abdominal Aortic Aneurysms Nor Atherosclerosis in ApoE Deficient Mice. 査読 国際誌

    Nozomu Otaka, Haruhito A Uchida, Michihiro Okuyama, Yoshiko Hada, Yasuhiro Onishi, Yuki Kakio, Hidemi Takeuchi, Ryoko Umebayashi, Katsuyuki Tanabe, Venkateswaran Subramanian, Alan Daugherty, Yasufumi Sato, Jun Wada

    American journal of hypertension   34 ( 5 )   467 - 475   2020年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Vasohibin-2 (VASH2) has been isolated as a homologue of vasohibin-1 (VASH1) that promote angiogenesis counteracting with VASH1. Chronic angiotensin II (AngII) infusion promotes both ascending and abdominal aortic aneurysms (AAs) in mice. The present study aimed to investigate whether exogenous VASH2 influenced AngII-induced vascular pathology in apolipoprotein E deficient (ApoE  -/-) mice. METHODS: Male, ApoE  -/- mice (9 to 14 weeks old) were injected with Ad LacZ or Ad VASH2. After a week, saline or AngII (1,000 ng/kg/min) was infused into the mice subcutaneously via mini-osmotic pumps for 3 weeks. Consequently, all these mice were divided into 4 groups: saline + LacZ (n=5), saline + VASH2 (n=5), AngII + LacZ (n=18), and AngII + VASH2 (n=17). RESULTS: Exogenous VASH2 had no significant effect on ex vivo maximal diameters of abdominal aortas (AngII + LacZ; 1.67±0.17 mm, AngII + VASH2; 1.52±0.16 mm, n.s.) or elastin fragmentation and accumulation of inflammatory cells. Conversely, exogenous VASH2 significantly increased intima areas of aortic arches (AngII + LacZ; 16.6±0.27 mm 2, AngII + VASH2; 18.6±0.64 mm 2, p=0.006). VASH2 effect of AngII-induced ascending AAs was associated with increased cleaved caspase-3 abundance. AngII-induced atherosclerosis was not altered by VASH2. CONCLUSION: The present study demonstrated that augmented VASH2 expression had no effect of AngII-induced abdominal AAs or atherosclerosis, while increasing dilation in the ascending aorta.

    DOI: 10.1093/ajh/hpaa181

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  • Acute Kidney Injury Caused by Evans Syndrome with Systemic Lupus Erythematosus and Systemic Sclerosis. 査読

    Natsumi Matsuoka, Haruki Watanabe, Naoko Kurooka, Sumari Kato, Chika Higashi, Katsuyuki Tanabe, Masaru Kinomura, Nobuharu Fujii, Ken-Ei Sada, Hitoshi Sugiyama, Jun Wada

    Internal medicine (Tokyo, Japan)   60 ( 7 )   1055 - 1060   2020年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    A 65-year-old woman with systemic sclerosis and systemic lupus erythematosus developed acute kidney injury (AKI), Coombs-positive autoimmune hemolytic anemia and autoimmune thrombocytopenia; therefore, she was diagnosed with Evans syndrome (ES). Intravascular hemolysis was suggested as the cause of AKI based on the presence of acute tubular injury and trace hemosiderin deposits on the renal biopsy. The renal function, hemolytic anemia and thrombocytopenia were restored by an increased dose of glucocorticoids, hemodialysis, and plasma exchange. Although ES with severe hemolytic anemia is very rare, it is important to detect possible renal dysfunction when encountering patients with severe hemolysis.

    DOI: 10.2169/internalmedicine.5976-20

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  • Low-dose rituximab induction therapy is effective in immunological high-risk renal transplantation without increasing cytomegalovirus infection. 査読 国際誌

    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年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    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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  • Effects of LDL apheresis on proteinuria in patients with diabetes mellitus, severe proteinuria, and dyslipidemia. 査読

    Takashi Wada, Akinori Hara, Eri Muso, Shoichi Maruyama, Sawako Kato, Kengo Furuichi, Kenichi Yoshimura, Tadashi Toyama, Norihiko Sakai, Hiroyuki Suzuki, Tatsuo Tsukamoto, Mariko Miyazaki, Eiichi Sato, Masanori Abe, Yugo Shibagaki, Ichiei Narita, Shin Goto, Yuichi Sakamaki, Hitoshi Yokoyama, Noriko Mori, Satoshi Tanaka, Yukio Yuzawa, Midori Hasegawa, Takeshi Matsubara, Jun Wada, Katsuyuki Tanabe, Kosuke Masutani, Yasuhiro Abe, Kazuhiko Tsuruya, Shouichi Fujimoto, Shuji Iwatsubo, Akihiro Tsuda, Hitoshi Suzuki, Kenji Kasuno, Yoshio Terada, Takeshi Nakata, Noriaki Iino, Tadashi Sofue, Hitomi Miyata, Toshiaki Nakano, Takayasu Ohtake, Shuzo Kobayashi

    Clinical and experimental nephrology   25 ( 1 )   1 - 8   2020年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND: Patients with diabetes mellitus and severe proteinuria present with poor renal prognoses, despite improvements in diabetes and kidney disease therapies. In this study, we designed a low-density lipoprotein (LDL)-cholesterol apheresis treatment for patients with diabetic nephropathy (DN)/diabetic kidney disease and severe proteinuria. This was a multicenter prospective LICENSE study to confirm the impact of LDL apheresis on proteinuria that exhibited hyporesponsiveness to treatment. In addition, we sought to determine the efficacy and safety of LDL apheresis by comparing the outcomes to those of historical controls in patients with diabetes, refractory hypercholesterolemia, and severe proteinuria. METHODS: This was a prospective, multicenter study, including 40 patients with diabetes, severe proteinuria, and dyslipidemia. LDL apheresis was performed 6-12 times over a 12-week period. The primary endpoint was the proportion of patients with a decrease in proteinuria excretion of at least 30% in the 6 months after starting therapy. The secondary endpoints included serum creatinine levels and laboratory variables, which were evaluated 4, 6, 12, 18, and 24 months after therapy initiation. RESULTS: LDL apheresis was performed on 40 registered patients with diabetes. The proportion of cases in which proteinuria decreased by 30% or more after 6 months of LDL apheresis was 25%, which was similar to that of historical controls. The overall survival and end-stage kidney disease-free survival rates were significantly higher in the LICENSE group compared to those in historical controls. CONCLUSION: Our results suggest that LDL apheresis may be effective and safe for patients with diabetes, proteinuria, and dyslipidemia. TRIAL REGISTRATION: Trial registration number: jRCTs042180076.

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  • Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury. 査読 国際誌

    Hiromasa Miyake, Katsuyuki Tanabe, Satoshi Tanimura, Yuri Nakashima, Tomoyo Morioka, Kana Masuda, Hitoshi Sugiyama, Yasufumi Sato, Jun Wada

    International journal of molecular sciences   21 ( 12 )   4545   2020年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Acute kidney injury (AKI) has been increasingly recognized as a risk factor for transition to chronic kidney disease. Recent evidence suggests that endothelial damage in peritubular capillaries can accelerate the progression of renal injury. Vasohibin-2 (VASH2) is a novel proangiogenic factor that promotes tumor angiogenesis. However, the pathophysiological roles of VASH2 in kidney diseases remain unknown. In the present study, we examined the effects of VASH2 deficiency on the progression of ischemia-reperfusion (I/R) injury-induced AKI. I/R injury was induced by bilaterally clamping renal pedicles for 25 min in male wild-type (WT) and Vash2 homozygous knockout mice. Twenty-four hours later, I/R injury-induced renal dysfunction and tubular damage were more severe in VASH2-deficient mice than in WT mice, with more prominent neutrophil infiltration and peritubular capillary loss. After induction of I/R injury, VASH2 expression was markedly increased in injured renal tubules. These results suggest that VASH2 expression in renal tubular epithelial cells might be essential for alleviating I/R injury-induced AKI, probably through protecting peritubular capillaries and preventing inflammatory infiltration.

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  • Nivolumab-induced IgA nephropathy in a patient with advanced gastric cancer: A case report. 査読 国際誌

    Katsuyuki Tanabe, Hiromitsu Kanzaki, Takahira Wada, Yuri Nakashima, Hitoshi Sugiyama, Hiroyuki Okada, Jun Wada

    Medicine   99 ( 21 )   e20464   2020年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    INTRODUCTION: Immune checkpoint inhibitors including nivolumab, an antibody against programmed death-1, have been increasingly introduced in various cancer treatment regimens, and are reported to be associated with immune-related adverse events. Nivolumab-induced renal injury is generally caused by acute interstitial nephritis and is managed by drug discontinuation and steroid therapy. Although this agent can infrequently induce glomerulonephritis, the pathogenesis and therapeutic strategy remain undetermined. PATIENT CONCERNS: A 78-year-old man was diagnosed with advanced gastric cancer with portal thrombosis. First- and second-line chemotherapies were ineffective; thus, nivolumab monotherapy was initiated. Although it effectively prevented tumor growth, proteinuria and microhematuria appeared 2 months later. Despite drug discontinuation, serum creatinine progressively increased from 0.72 to 1.45 mg/dL. Renal biopsy revealed mesangial IgA and C3 deposition in immunofluorescence analysis and mesangial proliferation with crescent formation in light microscopy. DIAGNOSIS: The patient was diagnosed with IgA nephropathy. Based on the temporal relationship between the nivolumab therapy and abnormal urinalysis, IgA nephropathy was considered to have been induced by nivolumab. INTERVENTIONS: A moderate dose (0.6 mg/kg/day) of prednisolone was orally administrated, with tapering biweekly. OUTCOMES: Steroid therapy stabilized his serum creatinine levels and markedly reduced proteinuria. However, bacterial pneumonia substantially impaired his performance status; thus, nivolumab could not be restarted despite tumor regrowth. LESSONS: IgA nephropathy should be recognized as an uncommon renal adverse event during nivolumab therapy. After drug discontinuation, nivolumab-induced IgA nephropathy is likely to respond to moderate doses of steroid therapy with early tapering. However, more evidence is needed to determine whether nivolumab can be safely restarted during or after steroid therapy.

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  • Targeting angiogenesis and lymphangiogenesis in kidney disease. 査読 国際誌

    Katsuyuki Tanabe, Jun Wada, Yasufumi Sato

    Nature reviews. Nephrology   16 ( 5 )   289 - 303   2020年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    The kidney is permeated by a highly complex vascular system with glomerular and peritubular capillary networks that are essential for maintaining the normal functions of glomerular and tubular epithelial cells. The integrity of the renal vascular network depends on a balance of proangiogenic and antiangiogenic factors, and disruption of this balance has been identified in various kidney diseases. Decreased levels of the predominant proangiogenic factor, vascular endothelial growth factor A (VEGFA), can result in glomerular microangiopathy and contribute to the onset of preeclampsia, whereas upregulation of VEGFA has roles in diabetic kidney disease (DKD) and polycystic kidney disease (PKD). Other factors that regulate angiogenesis, such as angiopoietin 1 and vasohibin 1, have been shown to be protective in animal models of DKD and renal fibrosis. The renal lymphatic system is important for fluid homeostasis in the kidney, as well as the transport of immune cells and antigens. Experimental studies suggest that the lymphangiogenic factor VEGFC might have protective effects in PKD, DKD and renal fibrosis. Understanding the physiological and pathological roles of factors that regulate angiogenesis and lymphangiogenesis in the kidney has led to the development of novel therapeutic strategies for kidney diseases.

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  • Quality of Life and Mental Satisfaction Improve Slowly in Preemptive Kidney Transplantation Compared With Nonpreemptive Kidney Transplantation. 査読 国際誌

    Yosuke Mitsui, Motoo Araki, Yuki Maruyama, Kasumi Yoshinaga, Takuya Sadahira, Koichiro Wada, Katsuyuki Tanabe, Masashi Kitagawa, Yasuyuki Kobayashi, Masami Watanabe, Toyohiko Watanabe, Yasutomo Nasu

    Transplantation proceedings   52 ( 3 )   740 - 747   2020年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    BACKGROUND AND AIMS: Preemptive kidney transplantation (PEKT) is recognized as the best therapy to avoid dialysis. However, it is not clear whether PEKT recipients experience an improvement in quality of life (QoL) after kidney transplantation (KT) that exceeds that of non-PEKT recipients, since PEKT recipients have not experienced the heavy burden of dialysis. The aim of this study was to compare the changes in QoL for PEKT and non-PEKT recipients following transplantation. METHODS: Patients included in this study underwent living donor KT in our hospital. We excluded patients with incomplete SF-36 scores and with factors that could affect QoL, such as complications or rejection. QoL was assessed by the Short Form 36-Item Health Survey version 2.0 preoperatively and 3 and 12 months postoperatively. RESULTS: Eighty-eight patients underwent living donor KT in our hospital. Twelve PEKT and 20 non-PEKT recipients were enrolled in this retrospective study. In the non-PEKT group, both the physical and mental domain scores dramatically improved from baseline at 3 months, and remained at a similar level at 12 months. In contrast, in the PEKT group, only 1 domain of the physical and mental score improved at 3 months, and the social functioning score gradually improved at 12 months. Although the mental component score showed significant improvement in the non-PEKT group, it did not change in the PEKT group. CONCLUSIONS: The improvement of QoL after transplantation is more evident in the non-PEKT group. PEKT recipients have less mental satisfaction than non-PEKT recipients.

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  • Robotic Renal Autotransplantation: A Feasibility Study in a Porcine Model. 査読

    Risa Kubota, Motoo Araki, Koichiro Wada, Kasumi Kawamura, Yuki Maruyama, Yosuke Mitsui, Takuya Sadahira, Yuichi Ariyoshi, Takehiro Iwata, Shingo Nishimura, Atsushi Takamoto, Tomoko Sako, Kohei Edamura, Yasuyuki Kobayashi, Yuzuki Kano, Masashi Kitagawa, Katsuyuki Tanabe, Hitoshi Sugiyama, Jun Wada, Masami Watanabe, Toyohiko Watanabe, Yasutomo Nasu

    Acta medica Okayama   74 ( 1 )   53 - 58   2020年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    We investigated the feasibility of robotic renal autotransplantation (RAT) in a porcine model to reduce invasiveness of RAT. Five pigs underwent robotic RAT using the da Vinci® robotic system. A robotic left nephrectomy was performed in all cases. Robotic RAT was performed on the left side in all but one case. Four ports were used. In 3 cases, the kidney was taken out through the GelPort® and irrigated on ice with Ringer's solution. In 2 cases, a complete intracorporeal robotic RAT was performed. An end-to-side anastomosis was performed between the renal vein and the external iliac vein and between the renal artery and the external iliac artery. Ureteroneocystostomy was also performed in 2 cases. All cases were performed robotically without open conversion. The median (IQR) console time was 3.1 (0.7) h, and the operative time was 3.8 (1.1) h. The estimated blood loss was 30 (0) ml. The warm ischemia time was 4.0 (0.2) min, and the cold ischemia time was 97 (17) min. Intracorporeal transarterial hypothermic renal perfusion was feasible in the 2 complete intracorporeal robotic RAT cases by using a perfusion catheter through a laparoscopic port. Robotic RAT has the potential to be a new minimally invasive substitute for conventional open surgery.

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  • Podocyte autophagy is associated with foot process effacement and proteinuria in patients with minimal change nephrotic syndrome. 査読 国際誌

    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年1月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    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.

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  • Urine 5MedC, a Marker of DNA Methylation, in the Progression of Chronic Kidney Disease. 査読 国際誌

    Onishi A, Sugiyama H, Kitagawa M, Yamanari T, Tanaka K, Ogawa-Akiyama A, Kano Y, Mise K, Tanabe K, Morinaga H, Kinomura M, Uchida HA, Wada J

    Disease markers   2019   5432453 - 5432453   2019年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1155/2019/5432453

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  • Capnocytophaga canimorsus peritonitis diagnosed by mass spectrometry in a diabetic patient undergoing peritoneal dialysis: a case report. 査読

    Tanabe K, Okamoto S, Hiramatsu Asano S, Wada J

    BMC nephrology   20 ( 1 )   219   2019年6月

  • Contrast-enhanced Computed Tomography-Guided Percutaneous Cryoablation of Renal Cell Carcinoma in a Renal Allograft: First Case in Asia. 査読

    Tsuboi I, Araki M, Fujiwara H, Iguchi T, Hiraki T, Arichi N, Kawamura K, Maruyama Y, Mitsui Y, Sadahira T, Kubota R, Nishimura S, Sako T, Takamoto A, Wada K, Kobayashi Y, Watanabe T, Yanai H, Kitagawa M, Tanabe K, Sugiyama H, Wada J, Shiina H, Kanazawa S, Nasu Y

    Acta medica Okayama   73 ( 3 )   269 - 272   2019年6月

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    記述言語:英語  

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  • Renal tubular injury exacerbated by Vasohibin-1 deficiency in a murine cisplatin-induced acute kidney injury model. 査読

    Tanimura S, Tanabe K, Miyake H, Masuda K, Tsushida K, Morioka T, Sugiyama H, Sato Y, Wada J

    American journal of physiology. Renal physiology   317 ( 2 )   F264 - F274   2019年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1152/ajprenal.00045.2019

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  • Exogenous Vasohibin-2 Exacerbates Angiotensin II-Induced Ascending Aortic Dilation in Mice 査読

    Okuyama M, Uchida HA, Hada Y, Kakio Y, Otaka N, Umebayashi R, Tanabe K, Fujii Y, Kasahara S, Subramanian V, Daugherty A, Sato Y, Wada J

    Circulation reports   1 ( 4 )   155 - 161   2019年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    DOI: 10.1253/circrep.cr-19-0008

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  • Renal expression of trefoil factor 3 mRNA in association with tubulointerstitial fibrosis in IgA nephropathy. 査読

    Tanaka K, Sugiyama H, Yamanari T, Mise K, Morinaga H, Kitagawa M, Onishi A, Ogawa-Akiyama A, Tanabe K, Eguchi J, Ohmoto Y, Shikata K, Wada J

    Nephrology (Carlton, Vic.)   23 ( 9 )   855 - 862   2018年9月

  • Endogenous antiangiogenic factors in chronic kidney disease: Potential biomarkers of progression 査読

    Katsuyuki Tanabe, Yasufumi Sato, Jun Wada

    International Journal of Molecular Sciences   19 ( 7 )   1859   2018年7月

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    記述言語:英語   出版者・発行元:MDPI AG  

    Chronic kidney disease (CKD) is a major global health problem. Unless intensive intervention is initiated, some patients can rapidly progress to end-stage kidney disease. However, it is often difficult to predict renal outcomes using conventional laboratory tests in individuals with CKD. Therefore, many researchers have been searching for novel biomarkers to predict the progression of CKD. Angiogenesis is involved in physiological and pathological processes in the kidney and is regulated by the balance between a proangiogenic factor, vascular endothelial growth factor (VEGF)-A, and various endogenous antiangiogenic factors. In recent reports using genetically engineered mice, the roles of these antiangiogenic factors in the pathogenesis of kidney disease have become increasingly clear. In addition, recent clinical studies have demonstrated associations between circulating levels of antiangiogenic factors and renal dysfunction in CKD patients. In this review, we summarize recent advances in the study of representative endogenous antiangiogenic factors, including soluble fms-related tyrosine kinase 1, soluble endoglin, pigment epithelium-derived factor, VEGF-A165 b, endostatin, and vasohibin-1, in associations with kidney diseases and discuss their predictive potentials as biomarkers of progression of CKD.

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  • Anti-MuSK Antibody-positive Myasthenia Gravis Successfully Treated with Outpatient Periodic Weekly Blood Purification Therapy. 査読

    Kentaro Deguchi, Kosuke Matsuzono, Yumiko Nakano, Syoichiro Kono, Kota Sato, Shoko Deguchi, Katsuyuki Tanabe, Nozomi Hishikawa, Yasuyuki Ota, Toru Yamashita, Kiyoe Ohta, Masakatsu Motomura, Koji Abe

    Internal medicine (Tokyo, Japan)   57 ( 10 )   1455 - 1458   2018年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    A 37-year-old man with anti-muscle-specific tyrosine kinase (MuSK) antibody-positive myasthenia gravis (MG) presented with subacute progressive dysphagia and muscle weakness of the neck and bilateral upper extremities. Conventional immune-suppressive treatments and high-dose intravenous immunoglobulin were ineffective. He then displayed repeated exacerbations and remissions over the course of two years, despite two to four sessions of plasma exchange (PE) every two months. The patient was successfully treated with outpatient periodic weekly blood purification therapy with alternative PE and double-filtration plasmapheresis using an internal shunt. This case report suggests the benefits of blood purification therapy with an internal shunt against anti-MuSK antibody-positive MG.

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  • Estrogen-related receptor α is essential for maintaining mitochondrial integrity in cisplatin-induced acute kidney injury. 査読

    Tsushida K, Tanabe K, Masuda K, Tanimura S, Miyake H, Arata Y, Sugiyama H, Wada J

    Biochemical and biophysical research communications   498 ( 4 )   918 - 924   2018年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

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  • Deletion of pro-angiogenic factor vasohibin-2 ameliorates glomerular alterations in a mouse diabetic nephropathy model 査読

    Kana Masuda, Katsuyuki Tanabe, Haruyo Ujike, Norikazu Hinamoto, Hiromasa Miyake, Satoshi Tanimura, Hitoshi Sugiyama, Yasufumi Sato, Yohei Maeshima, Jun Wada

    PLoS ONE   13 ( 4 )   e0195779   2018年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Public Library of Science  

    Angiogenesis has been implicated in glomerular alterations in the early stage of diabetic nephropathy. We previously reported the renoprotective effects of vasohibin-1 (VASH1), which is a novel angiogenesis inhibitor derived from endothelial cells, on diabetic nephropathy progression. Vasohibin-2 (VASH2) was originally identified as a VASH1 homolog and possesses pro-angiogenic activity in contrast to VASH1. In addition, VASH2 was recently shown to promote epithelial-to-mesenchymal transition via enhanced transforming growth factor (TGF)-β signaling in cancer cells. Herein, we investigated the pathogenic roles of VASH2 in diabetic nephropathy using VAHS2-deficient mice. The type 1 diabetes model was induced by intraperitoneal injections of streptozoto-cin in VASH2 homozygous knockout (VASH2LacZ/LacZ) or wild-type mice. These mice were euthanized 16 weeks after inducing hyperglycemia. Increased urine albumin excretion and creatinine clearance observed in diabetic wild-type mice were significantly prevented in diabetic VASH2-deficient mice. Accordingly, diabetes-induced increase in glomerular volume and reduction in glomerular slit-diaphragm density were significantly improved in VASH2 knockout mice. Increased glomerular endothelial area was also suppressed in VASH2-deficient mice, in association with inhibition of enhanced vascular endothelial growth factor (VEGF) receptor 2 (VEGFR2), but not VEGF level. Furthermore, glomerular accumulation of mesangial matrix, including type IV collagen, and increased expression of TGF-β were improved in diabetic VASH2 knockout mice compared with diabetic wild-type mice. Based on the immunofluorescence findings, endogenous VASH2 localization in glomeruli was consistent with mesangial cells. Human mesangial cells (HMCs) were cultured under high glucose condition in in vitro experiments. Transfection of VASH2 small interfering RNA (siRNA) into the HMCs resulted in the suppression of type IV collagen production induced by high glucose compared with control siRNA. These results indicate that VASH2 may be involved in diabetes-induced glomerular alterations, particularly impaired filtration barrier and mesangial expansion. Therefore, VASH2 is likely to represent a promising therapeutic target for diabetic nephropathy.

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  • Primary peritoneal carcinosarcoma in a dialysis patient 査読

    Keiko Tanaka, Katsuyuki Tanabe, Naoko Nishii, Kana Masuda, Yuka Arata, Akifumi Ohnishi, Masaru Kinomura, Hitoshi Sugiyama, Jun Wada

    NEPHROLOGY   22 ( 11 )   925 - 925   2017年11月

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    記述言語:英語   出版者・発行元:WILEY  

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  • Immunohistochemistry of Vasohibin-2 in Human Kidney Disease: Implications in Impaired Glucose Tolerance and Reduced Renal Function 査読

    Yuka Arata, Katsuyuki Tanabe, Norikazu Hinamoto, Hiroko Yamasaki, Hitoshi Sugiyama, Yohei Maeshima, Naoki Kanomata, Yasufumi Sato, Jun Wada

    ACTA MEDICA OKAYAMA   71 ( 5 )   369 - 380   2017年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OKAYAMA UNIV MED SCHOOL  

    Several angiogenesis-related factors are known to play important roles in the pathogenesis of kidney disease. Vasohibin-2 (VASH-2) was recently reported as a novel proangiogenic factor. Although VASH-2 was demonstrated to accelerate tumor angiogenesis, its roles in non-tumor processes including renal disease have not been well elucidated yet. Here, we performed a retrospective study including an immunohistochemical analysis of human kidney biopsy specimens from 82 Japanese patients with a variety of kidney diseases, and we evaluated the correlations between the immunoreactivity of VASH-2 and the patients' clinicopathological parameters. VASH-2 immunoreactivity was detected in varying degrees in renal tubules as well as in peritubular capillaries and vasa recta. The cortical and medullary tubule VASH-2(+) scores were correlated with the presence of hypertension, and the medullary tubule VASH-2(+) score was significantly correlated with the blood glucose (p=0.029, r=0.35) and hemoglobin A1c levels (p=0.0066, r=0.39). Moreover, decreased VASH-2(+) scores in the vasa recta were associated with reduced renal function (p=0.0003). These results suggest that VASH-2 could play an important role in the pathogenesis of renal diseases, and that VASH-2 is closely associated with hypertension and impaired glucose tolerance.

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  • An angiotensin II type 1 receptor binding molecule has a critical role in hypertension in a chronic kidney disease model 査読

    Ryu Kobayashi, Hiromichi Wakui, Kengo Azushima, Kazushi Uneda, Sona Haku, Kohji Ohki, Kotaro Haruhara, Sho Kinguchi, Miyuki Matsuda, Masato Ohsawa, Yoshiyuki Toya, Akira Nishiyama, Akio Yamashita, Katsuyuki Tanabe, Yohei Maeshima, Satoshi Umemura, Kouichi Tamura

    KIDNEY INTERNATIONAL   91 ( 5 )   1115 - 1125   2017年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE INC  

    Angiotensin II type 1 receptor-associated protein (ATRAP) promotes AT1R internalization along with suppression of hyperactivation of tissue AT1R signaling. Here, we provide evidence that renal ATRAP plays a critical role in suppressing hypertension in a mouse remnant kidney model of chronic kidney disease. The effect of 5/6 nephrectomy on endogenous ATRAP expression was examined in the kidney of C57BL/6 and 129/Sv mice. While 129/Sv mice with a remnant kidney showed decreased renal ATRAP expression and developed hypertension, C57BL/6 mice exhibited increased renal ATRAP expression and resistance to progressive hypertension. Consequently, we hypothesized that downregulation of renal ATRAP expression is involved in pathogenesis of hypertension in the remnant kidney model of chronic kidney disease. Interestingly, 5/6 nephrectomy in ATRAP-knockout mice on the hypertension resistant C57BL/6 background caused hypertension with increased plasma volume. Moreover, in knockout compared to wild-type C57BL/6 mice after 5/6 nephrectomy, renal expression of the epithelial sodium channel cc-subunit and tumor necrosis factor-alpha was significantly enhanced, concomitant with increased plasma membrane angiotensin II type 1 receptor in the kidneys. Thus, renal ATRAP downregulation is involved in the onset and progression of blood pressure elevation caused by renal mass reduction, and implicates ATRAP as a therapeutic target for hypertension in chronic kidney disease.

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  • Antiangiogenic Therapy for Diabetic Nephropathy 査読

    Katsuyuki Tanabe, Yohei Maeshima, Yasufumi Sato, Jun Wada

    BIOMED RESEARCH INTERNATIONAL   2017   5724069   2017年

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    記述言語:英語   出版者・発行元:HINDAWI LTD  

    Angiogenesis has been shown to be a potential therapeutic target for early stages of diabetic nephropathy in a number of animal experiments. Vascular endothelial growth factor (VEGF) is the main mediator for abnormal angiogenesis in diabetic glomeruli. Although beneficial effects of anti-VEGF antibodies have previously been demonstrated in diabetic animal experiments, recent basic and clinical evidence has revealed that the blockade of VEGF signaling resulted in proteinuria and renal thrombotic microangiopathy, suggesting the importance of maintaining normal levels of VEGF in the kidneys. Therefore, antiangiogenic therapy for diabetic nephropathy should eliminate excessive glomerular angiogenic response without accelerating endothelial injury. Some endogenous antiangiogenic factors such as endostatin and tumstatin inhibit overactivation of endothelial cells but do not specifically block VEGF signaling. In addition, the novel endothelium-derived antiangiogenic factor vasohibin-1 enhances stress tolerance and survival of the endothelial cells, while inhibiting excess angiogenesis. These factors have been demonstrated to suppress albuminuria and glomerular alterations in a diabetic mouse model. Thus, antiangiogenic therapy with promising candidates will possibly improve renal prognosis in patients with early stages of diabetic nephropathy.

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  • Sustained Tubulointerstitial Inflammation in Kidney with Severe Leptospirosis 査読

    Keiko Tanaka, Katsuyuki Tanabe, Naoko Nishii, Keiichi Takiue, Hitoshi Sugiyama, Jun Wada

    INTERNAL MEDICINE   56 ( 10 )   1179 - 1184   2017年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:JAPAN SOC INTERNAL MEDICINE  

    Leptospirosis is frequently associated with acute kidney injury. Some survivors are known to progress to chronic kidney disease due to sustained tubulointerstitial inflammation. We present a case of severe leptospirosis with acute renal failure. Although antibiotic therapy resolved the infection, moderate renal dysfunction remained. A renal biopsy demonstrated marked inflammatory infiltration in the tubules and interstitium. Many of the inflammatory cells were CD68-positive monocytes/macrophages, predominantly M1 phenotype. An intermediate dose of oral corticosteroids normalized the patient's serum creatinine levels. We suggest that corticosteroid therapy may be a therapeutic option for some patients with sustained tubulointerstitial nephritis who survive severe leptospirosis.

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  • The Efficacy of Rituximab in High-risk Renal Transplant Recipients 査読

    Motoo Araki, Koichiro Wada, Yosuke Mitsui, Risa Kubota, Takashi Yoshioka, Yuichi Ariyoshi, Yasuyuki Kobayashi, Masashi Kitagawa, Katsuyuki Tanabe, Hiroshi Sugiyama, Jun Wada, Masami Watanabe, Toyohiko Watanabe, Katsuyuki Hotta, Yasutomo Nasu

    ACTA MEDICA OKAYAMA   70 ( 4 )   295 - 297   2016年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OKAYAMA UNIV MED SCHOOL  

    Although graft survival following renal transplantation (RTx) has improved, outcomes following highrisk RTx are variable. Preexisting antibodies, including donor-specific antibodies (DSA), play an important role in graft dysfunction and survival. We have designed a study to investigate the safety and efficacy of anti-CD20 monoclonal antibodies (rituximab) in high-risk RTx recipients. Major eligibility criteria include: 1) major and minor ABO blood group mismatch, 2) positive DSA. Thirty-five patients will receive 200 mg/body of rituximab. The primary endpoint is the incidence of B cell depletion. This study will clarify whether rituximab is efficacious in improving graft survival in high-risk RTx recipients.

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  • The urinary levels of prostanoid metabolites predict acute kidney injury in heterogeneous adult Japanese ICU patients: a prospective observational study 査読

    Haruyo Ujike-Omori, Yohei Maeshima, Masaru Kinomura, Katsuyuki Tanabe, Kiyoshi Mori, Hiroyuki Watatani, Norikazu Hinamoto, Hitoshi Sugiyama, Yoshiki Sakai, Hiroshi Morimatsu, Hirofumi Makino

    CLINICAL AND EXPERIMENTAL NEPHROLOGY   19 ( 6 )   1024 - 1036   2015年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:SPRINGER  

    Background Acute kidney injury (AKI) is frequently observed in critically ill patients in the intensive care unit (ICU) and is associated with increased mortality. Prostanoids regulate numerous biological functions, including hemodynamics and renal tubular transport. We herein investigated the ability of urinary prostanoid metabolites to predict the onset of AKI in critically ill adult patients.
    Methods The current study was conducted as a prospective observational study. Urine of patients admitted to the ICU at Okayama University Hospital was collected and the urinary levels of prostaglandin E-2 (PGE(2)), PGI(2) metabolite (2,3-dinor-6-OXO-PGF(1 alpha)), thromboxane A(2) (TXA(2)) metabolite (11-dehydro-TXB2) were determined.
    Results Of the 93 patients, 24 developed AKI (AKIN criteria). Surgical intervention (93, 75 %) was the leading cause of ICU admission. Overall, the ratio of the level of serum Cr on Day 1 after ICU admission to that observed at baseline positively correlated with the urinary 2,3-dinor-6-OXO-PGF(1 alpha)/Cr (r = 0.57, p &lt; 0.0001) and 11-dehydro-TXB2/Cr (r = 0.47, p &lt; 0.0001) ratios. In 16 cases of de novo AKI, the urinary 2,3-dinor-6-OXO-PGF(1 alpha)/Cr and 11-dehydro-TXB2/Cr values were significantly elevated compared with that observed in the non-AKI group, whereas the urinary PGE(2)/Cr values were not. The urinary 2,3-dinor-6-OXO-PGF(1 alpha)/Cr ratio exhibited the best diagnostic and predictive performance among the prostanoid metabolites according to the receiver operating characteristic (ROC) analysis [ROC-area under the curve (AUC): 0.75].
    Conclusions Taken together, these results demonstrate that the urinary 2,3-dinor-6-OXO-PGF(1 alpha)/Cr and 11-dehydro-TXB2/Cr ratios are associated with the subsequent onset of AKI and poor outcomes in adult heterogeneous ICU patients.

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  • ONO-1301, a Sustained-Release Prostacyclin Analog, Ameliorates the Renal Alterations in a Mouse Type 2 Diabetes Model Possibly Through Its Protective Effects on Mesangial Cells 査読

    Hiroyuki Watatani, Hiroko Yamasaki, Yohei Maeshima, Tatsuyo Nasu, Norikazu Hinamoto, Haruyo Ujike, Hitoshi Sugiyama, Yoshiki Sakai, Katsuyuki Tanabe, Hirofumi Makino

    ACTA MEDICA OKAYAMA   69 ( 1 )   1 - 15   2015年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OKAYAMA UNIV MED SCHOOL  

    Diabetic nephropathy is the most common pathological disorder predisposing patients to end-stage renal disease. Considering the increasing prevalence of type 2 diabetes mellitus worldwide, novel therapeutic approaches are urgently needed. ONO-1301 is a novel sustained-release prostacyclin analog that inhibits thromboxane A(2) synthase. Here we examined the therapeutic effects of the intermittent administration of slow-release ONO-1301 (SR-ONO) on diabetic nephropathy in obese type 2 diabetes mice, as well as its direct effects on mesangial cells. The subcutaneous injection of SR-ONO (3mg/kg) every 3 wks did not affect the obesity or hyperglycemia in the db/db obese mice used as a model of type 2 diabetes, but it significantly ameliorated their albuminuria, glomerular hypertrophy, glomerular accumulation of type IV collagen, and monocyte/macrophage infiltration, and also the increase of TGF-beta 1, a-smooth muscle actin (alpha-SMA) and MCP-1 compared to vehicle treatment. In cultured mouse mesangial cells, ONO-1301 concentration-dependently suppressed the increases in TGF-beta, type IV collagen, alpha-SMA, MCP-1 and fibronectin induced by high ambient glucose, at least partly through prostacyclin (PGI(2)) receptor-mediated signaling. Taken together, these results suggest the potential therapeutic efficacy of the intermittent administration of SR-ONO against type 2 diabetic nephropathy, possibly through protective effects on mesangial cells.

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  • Endogenous Fructose Production and Fructokinase Activation Mediate Renal Injury in Diabetic Nephropathy 査読

    Miguel A. Lanaspa, Takuji Ishimoto, Christina Cicerchi, Yoshifuru Tamura, Carlos A. Roncal-Jimenez, Wei Chen, Katsuyuki Tanabe, Ana Andres-Hernando, David J. Orlicky, Esteban Finol, Shinichiro Inaba, Nanxing Li, Christopher J. Rivard, Tomoki Kosugi, Laura G. Sanchez-Lozada, J. Mark Petrash, Yuri Y. Sautin, A. Ahsan Ejaz, Wataru Kitagawa, Gabriela E. Garcia, David T. Bonthron, Aruna Asipu, Christine P. Diggle, Bernardo Rodriguez-Iturbe, Takahiko Nakagawa, Richard J. Johnson

    JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY   25 ( 11 )   2526 - 2538   2014年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER SOC NEPHROLOGY  

    Diabetes is associated with activation of the polyol pathway, in which glucose is converted to sorbitol by aldose reductase. Previous studies focused on the role of sorbitol in mediating diabetic complications. However, in the proximal tubule, sorbitol can be converted to fructose, which is then metabolized largely by fructokinase, also known as ketohexokinase, leading to ATP depletion, proinflammatory cytokine expression, and oxidative stress. We and others recently identified a potential deleterious role of dietary fructose in the generation of tubulointerstitial injury and the acceleration of CKD. In this study, we investigated the potential role of endogenous fructose production, as opposed to dietary fructose, and its metabolism through fructokinase in the development of diabetic nephropathy. Wild-type mice with streptozotocin-induced diabetes developed proteinuria, reduced GFR, and renal glomerular and proximal tubular injury. Increased renal expression of aldose reductase; elevated levels of renal sorbitol, fructose, and uric acid; and low levels of ATP confirmed activation of the fructokinase pathway. Furthermore, renal expression of inflammatory cytokines with macrophage infiltration was prominent. In contrast, diabetic fructokinase-deficient mice demonstrated significantly less proteinuria, renal dysfunction, renal injury, and inflammation. These studies identify fructokinase as a novel mediator of diabetic nephropathy and document a novel role for endogenous fructose production, or fructoneogenesis, in driving renal disease.

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  • Exacerbation of Diabetic Renal Alterations in Mice Lacking Vasohibin-1 査読

    Norikazu Hinamoto, Yohei Maeshima, Hiroko Yamasaki, Tatsuyo Nasu, Daisuke Saito, Hiroyuki Watatani, Haruyo Ujike, Katsuyuki Tanabe, Kana Masuda, Yuka Arata, Hitoshi Sugiyama, Yasufumi Sato, Hirofumi Makino

    PLOS ONE   9 ( 9 )   e107934   2014年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PUBLIC LIBRARY SCIENCE  

    Vasohibin-1 (VASH1) is a unique endogenous inhibitor of angiogenesis that is induced in endothelial cells by pro-angiogenic factors. We previously reported renoprotective effect of adenoviral delivery of VASH1 in diabetic nephropathy model, and herein investigated the potential protective role of endogenous VASH1 by using VASH1-deficient mice. Streptozotocininduced type 1 diabetic VASH1 heterozygous knockout mice (VASH1(+/-)) or wild-type diabetic mice were sacrificed 16 weeks after inducing diabetes. In the diabetic VASH1(+/-) mice, albuminuria were significantly exacerbated compared with the diabetic wild-type littermates, in association with the dysregulated distribution of glomerular slit diaphragm related proteins, nephrin and ZO-1, glomerular basement membrane thickning and reduction of slit diaphragm density. Glomerular monocyte/macrophage infiltration and glomerular nuclear translocation of phosphorylated NF-kappa B p65 were significantly exacerbated in the diabetic VASH1(+/-) mice compared with the diabetic wild-type littermates, accompanied by the augmentation of VEGF-A, M1 macrophage-derived MCP-1 and phosphorylation of I kappa B alpha, and the decrease of angiopoietin-1/2 ratio and M2 macrophage-derived Arginase-1. The glomerular CD31(+) endothelial area was also increased in the diabetic VASH1(+/-) mice compared with the diabetic-wild type littermates. Furthermore, the renal and glomerular hypertrophy, glomerular accumulation of mesangial matrix and type IV collagen and activation of renal TGF-beta(1)/Smad3 signaling, a key mediator of renal fibrosis, were exacerbated in the diabetic VASH1(+/-) mice compared with the diabetic wild-type littermates. In conditionally immortalized mouse podocytes cultured under high glucose condition, transfection of VASH1 small interfering RNA (siRNA) resulted in the reduction of nephrin, angiopoietin-1 and ZO-1, and the augmentation of VEGF-A compared with control siRNA. These results suggest that endogenous VASH1 may regulate the development of diabetic renal alterations, partly via direct effects on podocytes, and thus, a strategy to recover VASH1 might potentially lead to the development of a novel therapeutic approach for diabetic nephropathy.

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  • Uric acid-dependent inhibition of AMP kinase induces hepatic glucose production in diabetes and starvation: evolutionary implications of the uricase loss in hominids 査読

    Christina Cicerchi, Nanxing Li, James Kratzer, Gabriela Garcia, Carlos A. Roncal-Jimenez, Katsuyuki Tanabe, Brandi Hunter, Christopher J. Rivard, Yuri Y. Sautin, Eric A. Gaucher, Richard J. Johnson, Miguel A. Lanaspa

    FASEB JOURNAL   28 ( 8 )   3339 - 3350   2014年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:FEDERATION AMER SOC EXP BIOL  

    Reduced AMP kinase (AMPK) activity has been shown to play a key deleterious role in increased hepatic gluconeogenesis in diabetes, but the mechanism whereby this occurs remains unclear. In this article, we document that another AMP-dependent enzyme, AMP deaminase (AMPD) is activated in the liver of diabetic mice, which parallels with a significant reduction in AMPK activity and a significant increase in intracellular glucose accumulation in human HepG2 cells. AMPD activation is induced by a reduction in intracellular phosphate levels, which is characteristic of insulin resistance and diabetic states. Increased gluconeogenesis is mediated by reduced TORC2 phosphorylation at Ser171 by AMPK in these cells, as well as by the up-regulation of the rate-limiting enzymes PEPCK and G6Pc. The mechanism whereby AMPD controls AMPK activation depends on the production of a specific AMP downstream metabolite through AMPD, uric acid. In this regard, humans have higher uric acid levels than most mammals due to a mutation in uricase, the enzyme involved in uric acid degradation in most mammals, that developed during a period of famine in Europe 1.5 x 10(7) yr ago. Here, working with resurrected ancestral uricases obtained from early hominids, we show that their expression on HepG2 cells is enough to blunt gluconeogenesis in parallel with an up-regulation of AMPK activity. These studies identify a key role AMPD and uric acid in mediating hepatic gluconeogenesis in the diabetic state, via a mechanism involving AMPK down-regulation and overexpression of PEPCK and G6Pc. The uricase mutation in the Miocene likely provided a survival advantage to help maintain glucose levels under condi-tions of near starvation, but today likely has a role in the pathogenesis of diabetes.

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  • Urinary and Plasma Levels of Vasohibin-1 Can Predict Renal Functional Deterioration in Patients with Renal Disorders 査読

    Norikazu Hinamoto, Yohei Maeshima, Daisuke Saito, Hiroko Yamasaki, Katsuyuki Tanabe, Tatsuyo Nasu, Hiroyuki Watatani, Haruyo Ujike, Masaru Kinomura, Hitoshi Sugiyama, Hikaru Sonoda, Yasufumi Sato, Hirofumi Makino

    PLOS ONE   9 ( 6 )   e96932   2014年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:PUBLIC LIBRARY SCIENCE  

    Vasohibin-1 (VASH-1) is a negative feedback regulator of angiogenesis, and a small vasohibin-binding protein (SVBP) serves as its secretory chaperone and contributes to its antiangiogenic effects. In the present study, we aimed to define the clinical significance of VASH-1 and SVBP in patients with chronic kidney disease (CKD). We recruited 67 Japanese hospitalized patients with renal disorders with (n = 45) or without (n = 22) renal biopsy samples and 10 Japanese healthy controls. We evaluated the correlations between the plasma and urinary levels of VASH-1/VASH-1-SVBP complex/SVBP and the clinicopathological parameters. The plasma levels of VASH-1 were inversely correlated with age and systolic and diastolic blood pressure and positively correlated with crescent formation. Increased plasma and urinary levels of VASH-1 and VASH-1-SVBP complex were significantly correlated with worse renal outcomes. These results demonstrate an association between elevated urinary and plasma levels of VASH-1 and progressive decline of the renal function, thus suggesting a potential role for VASH-1 in predicting a worse renal prognosis in patients with renal disease, including CKD.

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  • Renal distribution of Vasohibin-1 in patients with chronic kidney disease 査読

    Norikazu Hinamoto, Yohei Maeshima, Daisuke Saito, Hiroko Yamasakr, Katsuyuki Tanabe, Tatsuyo Nasu, Hiroyuki Watatani, Haruyo Ujike, Masaru Kinomura, Hitoshi Sugiyama, Hikaru Sonoda, Naoki Kanomata, Yasufumi Sate, Hirofumi Makino

    Acta Medica Okayama   68 ( 4 )   219 - 233   2014年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:Okayama University  

    Experimental studies have demonstrated the involvement of angiogenesis-related factors in the progression of chronic kidney disease (CKD). There have so far been no reports investigating the distribution and clinical roles of Vasohibin-1 (VASH-1), a negative feedback regulator of angiogenesis, in CKD. We recruited 54 Japanese CKD patients and 6 patients who had normal renal tissues excised due to localized renal cell carcinoma. We evaluated the correlations between the renal expression level of VASH-1 and the clinical/histological parameters. VASH-1 was observed in renal endothelial/mesangial cells, crescentic lesions and interstitial inflammatory cells. Significant positive correlations were observed between 1) crescent formation and the number of VASH-1+ cells in the glomerulus (r=0.48, /&gt
    = 0.001) or cortex (r = 0.64, p&lt
    0.0001), 2) interstitial cell infiltration and the number of VASH-1+ cells in the cortex (r = 0.34, p = 0.02), 3) the glomerular VEGFR-2+ area and the number of VASH 1+ cells in the glomerulus (r = 0.44, p = 0.01) or medulla (r = 0.63, p = 0.01). These results suggest that the renal levels of VASH-1 may be affected by local inflammation, crescentic lesions and VEGFR-2. © 2014 by Okayama University Medical School.

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  • Vasohibin-1 deficiency enhances renal fibrosis and inflammation after unilateral ureteral obstruction 査読

    Hiroyuki Watatani, Yohei Maeshima, Norikazu Hinamoto, Hiroko Yamasaki, Haruyo Ujike, Katsuyuki Tanabe, Hitoshi Sugiyama, Fumio Otsuka, Yasufumi Sato, Hirofumi Makino

    Physiological Reports   2 ( 6 )   2014年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:American Physiological Society  

    Tubulointerstitial injuries are known to predict the deterioration of renal function in chronic kidney disease (CKD). We recently reported the protective role of Vasohibin-1(VASH-1), a negative feedback regulator of angiogenesis, in diabetic nephropathy, but its impact on tubulointerstitial injuries remains to be elucidated. In the present study, we evaluated the role of endogenous VASH-1 in regulating the tubulointerstitial alterations induced by unilateral ureteral obstruction (UUO), and assessed its role on fibrogenesis and the activation of Smad3 signaling in renal fibroblasts. UUO was induced in female Vasohibin-1 heterozygous knockout mice (VASH-1+/-) or wild-type (WT) (VASH-1+/+) littermates. Mice were sacrificed on Day 7 after left ureter ligation, and the kidney tissue was obtained. Interstitial fibrosis, the accumulation of type I and type III collagen and monocytes/macrophages infiltration in the obstructed kidneys (OBK) were significantly exacerbated in VASH-1+/- mice compared with WT mice (Day 7). The increases in the renal levels of TGF-β1, pSmad3, NF-jB pp65, CCL2 mRNA, and the number of interstitial fibroblast-specific protein-1 (FSP-1)+ fibroblasts in the OBK were significantly aggravated in VASH-1+/- mice. In addition, treatment with VASH-1 siRNA enhanced the TGF-β1-induced phosphorylation of Smad3, the transcriptional activation of the Smad3 pathway and the production of type I/type III collagen in fibroblasts, in vitro. Taken together, our findings demonstrate a protective role for endogenous VASH-1 on tubulointerstitial alterations via its regulation of inflammation and fibrosis and also show the direct anti-fibrotic effects of VASH-1 on renal fibroblasts through its modulation of TGF-β1 signaling.

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  • Umami: The Taste That Drives Purine Intake 査読

    Richard J. Johnson, Takahiko Nakagawa, L. Gabriela Sanchez-Lozada, Miguel A. Lanaspa, Yoshifuru Tamura, Katsuyuki Tanabe, Takuji Ishimoto, Jeffrey Thomas, Shinichiro Inaba, Wataru Kitagawa, Christopher J. Rivard

    JOURNAL OF RHEUMATOLOGY   40 ( 11 )   1794 - 1796   2013年11月

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    記述言語:英語   出版者・発行元:J RHEUMATOL PUBL CO  

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  • Epicatechin limits renal injury by mitochondrial protection in cisplatin nephropathy 査読

    Katsuyuki Tanabe, Yoshifuru Tamura, Miguel A. Lanaspa, Makoto Miyazaki, Norihiko Suzuki, Waichi Sato, Yohei Maeshima, George F. Schreiner, Francisco J. Villarreal, Richard J. Johnson, Takahiko Nakagawa

    American Journal of Physiology - Renal Physiology   303 ( 9 )   F1264 - F1274   2012年11月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Cisplatin nephropathy can be regarded as a mitochondrial disease. Intervention to halt such deleterious injury is under investigation. Recently, the flavanol (-)-epicatechin emerges as a novel compound to protect the cardiovascular system, owing in part to mitochondrial protection. Here, we have hypothesized that epicatechin prevents the progression of cisplatininduced kidney injury by protecting mitochondria. Epicatechin was administered 8 h after cisplatin injury was induced in the mouse kidney. Cisplatin significantly induced renal dysfunction and tubular injury along with an increase in oxidative stress. Mitochondrial damages were also evident as a decrease in loss of mitochondrial mass with a reduction in the oxidative phosphorylation complexes and low levels of MnSOD. The renal damages and mitochondrial injuries were significantly prevented by epicatechin treatment. Consistent with these observations, an in vitro study using cultured mouse proximal tubular cells demonstrated that cisplatin-induced mitochondrial injury, as revealed by a decrease in mitochondrial succinate dehydrogenase activity, an induction of cytochrome c release, mitochondrial fragmentation, and a reduction in complex IV protein, was prevented by epicatechin. Such a protective effect of epicatechin might be attributed to decreased oxidative stress and reduced ERK activity. Finally, we confirmed that epicatechin did not perturb the anticancer effect of cisplatin in HeLa cells. In conclusion, epicatechin exhibits protective effects due in part to its ability to prevent the progression of mitochondrial injury in mouse cisplatin nephropathy. Epicatechin may be a novel option to treat renal disorders associated with mitochondrial dysfunction. © 2012 the American Physiological Society.

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  • Nicorandil, a K atp channel opener, alleviates chronic renal injury by targeting podocytes and macrophages 査読

    Yoshifuru Tamura, Katsuyuki Tanabe, Wataru Kitagawa, Shunya Uchida, George F. Schreiner, Richard J. Johnson, Takahiko Nakagawa

    American Journal of Physiology - Renal Physiology   303 ( 3 )   F339 - F349   2012年8月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Nicorandil exhibits a protective effect in the vascular system, which is thought to be due to vasodilatation from opening ATP-dependent potassium channels and donation of nitric oxide. Recently, nicorandil was shown to be renoprotective in models of acute kidney injury and glomerulone-phritis. However, the specific mechanisms of renoprotection are unclear. We evaluated the effect of nicorandil on the rat remnant kidney model of chronic kidney disease. Blood pressure was unchanged by a 10-wk course of nicorandil, while albuminuria was significantly reduced. Glomerular injury and tubulointerstitial injury were also ameliorated by nicorandil. Oxidative stress, as noted by renal nitrotyrosine level and urine 8-hydroxy-2′-deoxyguanosine, were elevated in this model and was significantly reduced by nic-orandil treatment. Treatment was associated with maintenance of the mitochondrial antioxidant, manganese SOD, in podocytes and with suppression of xanthine oxidase expression in infiltrating macro-phages. Interestingly, these two cell types express sulfonylurea receptor 2 (SUR2), a binding site of nicorandil in the ATP-dependent K channel. Consistently, we found that stimulating SUR2 with nic-orandil prevented angiotensin II-mediated upregulation of xanthine oxidase in the cultured macrophage, while xanthine oxidase expression was rather induced by blocking SUR2 with glibenclamide. In conclusion, nicorandil reduces albuminuria and ameliorates renal injury by blocking oxidative stress in chronic kidney disease. © 2012 the American Physiological Society.

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  • Sustained-release prostacyclin analog ONO-1301 ameliorates tubulointerstitial alterations in a mouse obstructive nephropathy model 査読

    Tatsuyo Nasu, Masaru Kinomura, Katsuyuki Tanabe, Hiroko Yamasaki, Su le Htay, Daisuke Saito, Norikazu Hinamoto, Hiroyuki Watatani, Haruyo Ujike, Yoshinori Suzuki, Takeshi Sugaya, Hitoshi Sugiyama, Yoshiki Sakai, Kunio Matsumoto, Yohei Maeshima, Hirofumi Makino

    American Journal of Physiology - Renal Physiology   302 ( 12 )   F1616 - F1629   2012年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Tubulointerstitial injuries are crucial histological alterations that predict the deterioration of renal function in chronic kidney disease. ONO-1301, a novel sustained-release prostacyclin analog, accompanied by thromboxane synthase activity, exerts therapeutic effects on experimental pulmonary hypertension, lung fibrosis, cardiomyopathy, and myocardial ischemia, partly associated with the induction of hepatocyte growth factor (HGF). In the present study, we examined the therapeutic efficacies of ONO-1301 on tubulointerstitial alterations induced by unilateral ureteral obstruction (UUO). After inducing unilateral ureteral obstruction in C57/BL6J mice, a single injection of sustained-release ONO-1301 polymerized with poly (D,L-lactic-co-glycolic acid) sustained-release ONO-1301 (SR-ONO) significantly suppressed interstitial fibrosis, accumulation of types I and III collagen, increase in the number of interstitial fibroblast-specific protein-1 (FSP-1)+ cells, and interstitial infiltration of monocytes/macrophages (F4/80+) in the obstructed kidneys (OBK
    day 7). Treatment with SR-ONO significantly suppressed the increase of the renal levels of profibrotic factor TGF-β and phosphorylation of Smad2/3, and elevated the renal levels of HGF in the OBK. In cultured mouse proximal tubular epithelial cells (mProx24), ONO-1301 significantly ameliorated the expression of fibroblast-specific protein-1 and α-smooth muscle actin as well as phosphorylation of Smad3 and increased the expression of zonula occludens-1 and E-cadherin in the presence of TGF-β1 as detected by immunoblot and immunocytochemistry, partly dependent on PGI2 receptor-mediated signaling. Administration of rabbit anti-HGF antibodies, but not the control IgG, partly reversed the suppressive effects of SR-ONO on tubulointerstitial injuries in the OBK. Taken together, our findings suggest the potential therapeutic efficacies of ONO-1301 in suppressing tubulointerstitial alterations partly mediated via inducing HGF, an antifibrotic factor counteracting TGF-β. © 2012 the American Physiological Society.

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  • Nicorandil as a novel therapy for advanced diabetic nephropathy in the eNOS-deficient mouse 査読

    Katsuyuki Tanabe, Miguel A. Lanaspa, Wataru Kitagawa, Christopher J. Rivard, Makoto Miyazaki, Jelena Klawitter, George F. Schreiner, Moin A. Saleem, Peter W. Mathieson, Hirofumi Makino, Richard J. Johnson, Takahiko Nakagawa

    American Journal of Physiology - Renal Physiology   302 ( 9 )   F1151 - F1161   2012年5月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Nicorandil is an orally available drug that can act as a nitric oxide donor, an antioxidant, and an ATP-dependent K channel activator. We hypothesized that it may have a beneficial role in treating diabetic nephropathy. We administered nicorandil to a model of advanced diabetic nephropathy (the streptozotocin-induced diabetes in mice lacking endothelial nitric oxide synthase, eNOSKO)
    controls included diabetic eNOS KO mice without nicorandil and nondiabetic eNOS KO mice treated with either nicorandil or vehicle. Mice were treated for 8 wk. Histology, blood pressure, and renal function were determined. Additional studies involved examining the effects of nicorandil on cultured human podocytes. Here, we found that nicorandil did not affect blood glucose levels, blood pressure, or systemic endothelial function, but significantly reduced proteinuria and glomerular injury (mesangiolysis and glomerulosclerosis). Nicorandil protected against podocyte loss and podocyte oxidative stress. Studies in cultured podocytes showed that nicorandil likely protects against glucose-mediated oxidant stress via the ATP-dependent K channel as opposed to its NO-stimulating effects. In conclusion, nicorandil may be beneficial in diabetic nephropathy by preserving podocyte function. We recommend clinical trials to determine whether nicorandil may benefit diabetic nephropathy or other conditions associated with podocyte dysfunction. © 2012 the American Physiological Society.

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  • Sucrose induces fatty liver and pancreatic inflammation in male breeder rats independent of excess energy intake 査読

    Carlos A. Roncal-Jimenez, Miguel A. Lanaspa, Christopher J. Rivard, Takahiko Nakagawa, L. Gabriela Sanchez-Lozada, Diana Jalal, Ana Andres-Hernando, Katsuyuki Tanabe, Magdalena Madero, Nanxing Li, Christina Cicerchi, Kim Mc Fann, Yuri Y. Sautin, Richard J. Johnson

    METABOLISM-CLINICAL AND EXPERIMENTAL   60 ( 9 )   1259 - 1270   2011年9月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:W B SAUNDERS CO-ELSEVIER INC  

    Fructose induces metabolic syndrome in rats; but studies have been criticized for using high concentrations of fructose that are not physiologic, for using only pure fructose, and for not controlling for energy intake. We tested the hypothesis that a 40% sucrose diet (containing 20% fructose) might induce features of metabolic syndrome in male breeder rats independent of excess energy intake. Male Sprague-Dawley breeder rats were pair fed 40% sucrose or isocaloric starch diet for 4 months and evaluated for metabolic syndrome and diabetes. In vitro studies were performed in rat insulinoma cells (RIN-m5F) exposed to uric acid, and markers of inflammation were assessed. Rats fed a 40% sucrose diet developed accelerated features of metabolic syndrome with up-regulation of fructose-dependent transporter Glut5 and fructokinase. Fatty liver and low-grade pancreatic inflammation also occurred. Uric acid was found to stimulate inflammatory mediators and oxidative stress in islet cells in vitro. Sucrose, at concentrations ingested by a subset of Americans, can accelerate metabolic syndrome, fatty liver, and type 2 diabetes mellitus in male breeder rats; and the effects are independent of excess energy intake. (C) 2011 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.metabol.2011.01.008

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  • Selective Stimulation of VEGFR2 Accelerates Progressive Renal Disease 査読

    Waichi Sato, Katsuyuki Tanabe, Tomoki Kosugi, Kelly Hudkins, Miguel A. Lanaspa, Li Zhang, Martha Campbell-Thompson, Qiuhong Li, David A. Long, Charles E. Alpers, Takahiko Nakagawa

    AMERICAN JOURNAL OF PATHOLOGY   179 ( 1 )   155 - 166   2011年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCIENCE INC  

    Vascular endothelial growth factor A (VEGF-A) can play both beneficial and deleterious roles in renal diseases, where its specific function might be determined by nitric oxide bioavailability. The complexity of VEGF-A in renal disease could in part be accounted for by the distinct roles of its two receptors; VEGFR1 is involved in the inflammatory responses, whereas VEGFR2 predominantly mediates angiogenesis. Because nondiabetic chronic renal disease is associated with capillary loss, we hypothesized that selective stimulation of VEGFR2 could be beneficial in this setting. However, VEGFR2 activation may be deleterious in the presence of nitric oxide deficiency. We systematically overexpressed a mutant form of VEGF-A binding only VEGFR2 (Flk-sel) using an adeno-associated virus-1 vector in wild-type and eNOS knockout mice and then induced renal injury by uninephrectomy. Flksel treatment increased angiogenesis and lowered blood pressure in both mouse types. Flk-set overexpression caused mesangial injury with increased proliferation associated with elevated expression of PDGF, PDGF-beta receptor, and VEGFR2; this effect was greater in eNOS knockout than in wild-type mice. Flk-sel also induced tubulointerstitial injury, with some tubular epithelial cells expressing alpha-smooth muscle actin, indicating a phenotypic evolution toward myofibroblasts. In conclusion, prestimulation of VEGFR2 can potentiate subsequent renal injury in mice, an effect enhanced in the setting of nitric oxide deficiency. Pathol 2011, 179: 155-166. DOI: 10.1016/j.ajpath.2011.03.024)

    DOI: 10.1016/j.ajpath.2011.03.024

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  • Unexpected occurrence of adrenal Cushing&apos;s syndrome in a patient with systemic lupus erythematosus 査読

    Akihiro Katayama, Fumio Otsuka, Katsuyuki Tanabe, Naoko Tsukamoto, Ryutaro Yamanaka, Yoshinori Matsumoto, Yasutomo Nasu, Hirofumi Makino

    HYPERTENSION RESEARCH   34 ( 5 )   662 - 663   2011年5月

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    記述言語:英語   出版者・発行元:NATURE PUBLISHING GROUP  

    DOI: 10.1038/hr.2011.13

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  • Amelioration of renal alterations in obese type 2 diabetic mice by vasohibin-1, a negative feedback regulator of angiogenesis 査読

    Daisuke Saito, Yohei Maeshima, Tatsuyo Nasu, Hiroko Yamasaki, Katsuyuki Tanabe, Hitoshi Sugiyama, Hikaru Sonoda, Yasufumi Sato, Hirofumi Makino

    AMERICAN JOURNAL OF PHYSIOLOGY-RENAL PHYSIOLOGY   300 ( 4 )   F873 - F886   2011年4月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER PHYSIOLOGICAL SOC  

    Saito D, Maeshima Y, Nasu T, Yamasaki H, Tanabe K, Sugiyama H, Sonoda H, Sato Y, Makino H. Amelioration of renal alterations in obese type 2 diabetic mice by vasohibin-1, a negative feedback regulator of angiogenesis. Am J Physiol Renal Physiol 300: F873-F886, 2011. First published January 12, 2011; doi:10.1152/ajprenal.00503.2010.-The involvement of VEGF-A as well as the therapeutic efficacy of angiogenesis inhibitors in diabetic nephropathy have been reported. We recently reported the therapeutic effects of vasohibin-1 (VASH-1), an endogenous angiogenesis inhibitor, in a type 1 diabetic nephropathy model (Nasu T, Maeshima Y, Kinomura M, Hirokoshi-Kawahara K, Tanabe K, Sugiyama H, Sonoda H, Sato Y, Makino H. Diabetes 58: 2365-2375, 2009). In this study, we investigated the therapeutic efficacy of VASH-1 on renal alterations in obese mice with type 2 diabetes. Diabetic db/db mice received intravenous injections of adenoviral vectors encoding human VASH-1 (AdhVASH-1) and were euthanized 8 wk later. AdhVASH-1 treatment resulted in significant suppression of glomerular hypertrophy, glomerular hyperfiltration, albuminuria, increase in the CD31(+) glomerular endothelial area, F4/80(+) monocyte/macrophage infiltration, the accumulation of type IV collagen, and mesangial matrix. An increase in the renal levels of VEGF-A, VEGFR-2, transforming growth factor (TGF)-beta 1, and monocyte chemoattractant protein-1 in diabetic animals was significantly suppressed by AdhVASH-1 (immunoblotting). AdhVASH-1 treatment significantly recovered the loss and altered the distribution patterns of nephrin and zonula occludens (ZO)-1 and suppressed the increase in the number of fibroblast-specific protein-1 (FSP-1(+)) and desmin(+) podocytes in diabetic mice. In vitro, recombinant human VASH-1 (rhVASH-1) dose dependently suppressed the upregulation of VEGF induced by high ambient glucose (25 mM) in cultured mouse podocytes. In addition, rhVASH-1 significantly recovered the mRNA levels of nephrin and the protein levels of ZO-1 and P-cadherin and suppressed the increase in protein levels of desmin, FSP-1, Snail, and Slug in podocytes under high-glucose condition. Taken together, these results suggest the potential use of VASH-1 as a novel therapeutic agent in type 2 diabetic nephropathy mediated via antiangiogenic effects and maintenance of podocyte phenotype in association with antiproteinuric effects.

    DOI: 10.1152/ajprenal.00503.2010

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  • Effects of eplerenone on nephrotic syndrome in a patient with renovascular hypertension 査読

    Jiro Suzuki, Fumio Otsuka, Kenichi Inagaki, Katsuyuki Tanabe, Naoko Tsukamoto, Tomoko Miyoshi, Eri Nakamura, Toshio Ogura, Isao Kumagai, Hirofumi Makino

    HYPERTENSION RESEARCH   34 ( 3 )   404 - 406   2011年3月

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    記述言語:英語   出版者・発行元:NATURE PUBLISHING GROUP  

    DOI: 10.1038/hr.2010.249

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  • Intermittent administration of a sustained-release prostacyclin analog ONO-1301 ameliorates renal alterations in a rat type 1 diabetes model 査読

    H. Yamasaki, Y. Maeshima, T. Nasu, D. Saito, K. Tanabe, K. Hirokoshi-Kawahara, H. Sugiyama, Y. Sakai, H. Makino

    PROSTAGLANDINS LEUKOTRIENES AND ESSENTIAL FATTY ACIDS   84 ( 3-4 )   99 - 107   2011年3月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:ELSEVIER SCI LTD  

    Diabetic nephropathy is the most common pathological disorder predisposing end-stage renal disease. ONO-1301 is a novel sustained-release prostacyclin analog possessing thromboxane (T)() synthase inhibitory activity. Here, we aimed to investigate the therapeutic efficacies of ONO-1301 in a rat type 1 diabetic nephropathy model. Streptozotocin (STZ)-induced diabetic rats received injections of slow-release form of ONO-1301 (SR-ONO) every 3 weeks. Animals were sacrificed at Week 14. SR-ONO significantly suppressed albuminuria, glomerular hypertrophy, mesangial matrix accumulation, glomerular accumulation of monocyte/macrophage, increase in glomerular levels of pro-fibrotic factor transforming growth factor (TGF)-beta1 and the number of glomerular alpha-smooth muscle actin (SMA). cells in diabetic animals. The glomerular levels of hepatocyte growth factor (HGF) were significantly increased in SR-ONO-treated diabetic animals. Taken together, these results suggest the potential therapeutic efficacy of intermittent administration of SR-ONO in treating diabetic nephropathy potentially via inducing HGF, thus counteracting the pro-fibrotic effects of TGF-beta1. (C) 2010 Elsevier Ltd. All rights reserved.

    DOI: 10.1016/j.plefa.2010.11.005

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  • Endothelial dysfunction as a potential contributor in diabetic nephropathy 査読

    Takahiko Nakagawa, Katsuyuki Tanabe, Byron P. Croker, Richard J. Johnson, Maria B. Grant, Tomoki Kosugi, Qiuhong Li

    NATURE REVIEWS NEPHROLOGY   7 ( 1 )   36 - 44   2011年1月

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    記述言語:英語   出版者・発行元:NATURE PUBLISHING GROUP  

    The mechanisms that drive the development of diabetic nephropathy remain undetermined. Only 30-40% of patients with diabetes mellitus develop overt nephropathy, which suggests that other contributing factors besides the diabetic state are required for the progression of diabetic nephropathy. Endothelial dysfunction is associated with human diabetic nephropathy and retinopathy, and advanced diabetic glomerulopathy often exhibits thrombotic microangiopathy, including glomerular capillary microaneurysms and mesangiolysis, which are typical manifestations of endothelial dysfunction in the glomerulus. Likewise, diabetic mice with severe endothelial dysfunction owing to deficiency of endothelial nitric oxide synthase develop progressive nephropathy and retinopathy similar to the advanced lesions observed in humans with diabetes mellitus. Additionally, inhibitors of the renin-angiotensin system fail to be renoprotective in some individuals with diabetic nephropathy (due in part to aldosterone breakthrough) and in some mouse models of the disease. In this Review, we discuss the clinical and experimental evidence that supports a role for endothelial nitric oxide deficiency and subsequent endothelial dysfunction in the progression of diabetic nephropathy and retinopathy. If endothelial dysfunction is the key factor required for diabetic nephropathy, then agents that improve endothelial function or raise intraglomerular nitric oxide level could be beneficial in the treatment of diabetic nephropathy.

    DOI: 10.1038/nrneph.2010.152

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  • Inflammatory Cytokine-induced Expression of Vasohibin-1 by Rheumatoid Synovial Fibroblasts 査読

    Kohei Miyake, Keiichiro Nishida, Yasutaka Kadota, Hiroko Yamasaki, Tatsuyo Nasu, Daisuke Saitou, Katsuyuki Tanabe, Hikaru Sonoda, Yasufumi Sato, Yohei Maeshima, Hirofumi Makino

    ACTA MEDICA OKAYAMA   63 ( 6 )   349 - 358   2009年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:OKAYAMA UNIV MED SCHOOL  

    Angriogenesis is an essential event in the development of synovial inflammation in rheumatoid arthritis (RA). The aim of the current study was to investigate the expression of vasohibin-1, a novel endothelium-derived vascular endothelial growth factor (VEGF)-inducible angiogenesis inhibitor, in the RA synovium, and to test the effect of inflammatory cytokines on the expression of vasohibin-1 by RA synovial fibroblasts (RASFs). Synovial tissue samples were obtained at surgery from patients with osteoarthritis (OA) and RA, and subjected to immunohistochemistry to investigate the expression and distribution of vasohibin-1 relevant to the degree of synovial inflammation. In an in vitro analysis, RASFs were used to examine the expression of vasohibin-1 and VEGF mRNA by real-time PCR after stimulation with VEGF or inflammatory cytokines under normoxic or hypoxic conditions. The immunohistochemical results showed that vasohibin-1 was expressed in synovial lining cells, endothelial cells, and synovial fibroblasts. In synovial tissue, there was a significant correlation between the expression of vasohibin-1 and histological inflammation score (p = 0.002, r = 0.842). In vitro, stimulation with VEGF induced the expression of vasohibin-1 mRNA in RASFs under normoxic conditions, and stimulation with cytokines induced vasohibin-1 mRNA expression under a hypoxic condition. These results suggest that vasohibin-1 was expressed in RA synovial tissue and might be regulated by inflammatory cytokines.

    DOI: 10.18926/AMO/31820

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  • Vasohibin-1, a Negative Feedback Regulator of Angiogenesis, Ameliorates Renal Alterations in a Mouse Model of Diabetic Nephropathy 査読

    Tatsuyo Nasu, Yohei Maeshima, Masaru Kinomura, Kumiko Hirokoshi-Kawahara, Katsuyuki Tanabe, Hitoshi Sugiyama, Hikaru Sonoda, Yasufumi Sato, Hirofumi Makino

    DIABETES   58 ( 10 )   2365 - 2375   2009年10月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:AMER DIABETES ASSOC  

    OBJECTIVE-The involvement of proangiogenic factors such as vascular endothelial growth factor as well as the therapeutic efficacy of angiogenesis inhibitors in early diabetic nephropathy has been reported. Vasohibin-1 (VASH-1) is a unique endogenous angiogenesis inhibitor that is induced in endothelial cells by proangiogenic factors. We investigated the therapeutic efficacy of VASH-1 in an early diabetic nephropathy model.
    RESEARCH DESIGN AND METHODS-Streptozotocin-induced type 1 diabetic mice received intravenous injections of adenoviral vectors encoding VASH-1 (AdhVASH-1) or beta-gal (AdLacZ) every other week and were killed after 28 days.
    RESULTS-Treatment with AdhVASH-1 resulted in sustained increase in the protein levels of VASH-1 in the liver and sera, in the absence of any inflammatory alterations. AdhVASH-1 treatment significantly suppressed renal hypertrophy, glomerular hypertrophy, glomerular hyperfiltration, albuminuria, increase of the CD31(+) glomerular endothelial area, F4/80(+) monocyte/macrophage infiltration, the accumulation of type IV collagen, and mesangial matrix compared with AdLacZ-treated diabetic mice. Increase in the renal levels of transforming growth factor-beta 1, monocyte chemoattractant protein-1, and receptor for advanced glycation end products in diabetic animals was significantly suppressed by AdhVASH-1 (real-time PCR and immunoblot). VASH-1 significantly suppressed the increase of transforming growth factor-beta, monocyte chemoattractant protein-1, and receptor for advanced glycation end products, induced by high ambient glucose in cultured mouse mesangial cells. Increased phosphorylation of VEGFR2 was suppressed in AdVASH-1-treated diabetic animals and in cultured glomerular endothelial cells. Endogenous mouse VASH-1 was localized to the mesangial and endothelial area in glomeruli of diabetic mice.
    CONCLUSIONS-These results suggest the potential therapeutic efficacy of VASH-1 in treating early diabetic nephropathy potentially mediated via glomerular endothelial and mesangial cells. Diabetes 58:2365-2375, 2009

    DOI: 10.2337/db08-1790

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  • Amelioration of cisplatin-induced acute renal injury by renal progenitor-like cells derived from the adult rat kidney 査読

    Masaru Kinomura, Shinji Kitamura, Katsuyuki Tanabe, Kunihiro Ichinose, Kumiko Hirokoshi, Yuki Takazawa, Hiroyuki Kitayama, Tatsuyo Nasu, Hitoshi Sugiyama, Yasushi Yamasaki, Takeshi Sugaya, Yohei Maeshima, Hirofumi Makino

    CELL TRANSPLANTATION   17 ( 1-2 )   143 - 158   2008年

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    記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:COGNIZANT COMMUNICATION CORP  

    The replacement of a necrotic tubular epithelium with functional tubular epithelial cells is required for recovery from acute renal failure (ARF). A rat renal progenitor-like (rKS56) cell line was recently established derived from the S3 segment of renal proximal tubules. The therapeutic efficacy of rKS56 cells was examined in a rat model of cisplatin-induced ARE rKS56-lacZ cells expressing P-galactosidase were injected into SD rats either at the subcapsule of the left kidney (rKS-SC) or via the left renal artery (rKS-IA) 2 days after the injection of cisplatin. Bluo-gal(+) rKS56-lacZ cells were observed in the subcapsule in the rKS-SC group on day 5, and were further increased in number on day 9, accompanied by partial distribution in the corticomedullary junction, but not in the rKS-IA group. A portion of Bluo-gal(+) cells coexpressed Ki-67, aquaporin-1, hepatocyte growth factor (HGF), and c-Met. rKS-SC treatment significantly improved the tubular injury scores, ameliorated tubular cell apoptosis, and induced cell proliferation. The renal function also significantly improved in the rKS-SC group on day 5. These results demonstrate that locally implanted rKS56 cells could differentiate into tubular epithelial cells, thereby accelerating the recovery from tubular injury, most likely by producing tubular trophic factors. These results suggest the therapeutic potential of this novel approach for patients with end-stage renal failure.

    DOI: 10.3727/000000008783907008

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  • Endostatin peptide, an inhibitor of angiogenesis, prevents the progression of peritoneal sclerosis in a mouse experimental model 査読

    Katsuyuki Tanabe, Yohei Maeshima, Kunihiro Ichinose, Hiroyuki Kitayama, Yuki Takazawa, Kumiko Hirokoshi, Masaru Kinomura, Hitoshi Sugiyama, Hirofumi Makino

    KIDNEY INTERNATIONAL   71 ( 3 )   227 - 238   2007年2月

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    担当区分:筆頭著者   記述言語:英語   掲載種別:研究論文(学術雑誌)   出版者・発行元:NATURE PUBLISHING GROUP  

    Peritoneal sclerosis is a major and serious complication in patients on long-term continuous ambulatory peritoneal dialysis ( PD). The involvement of angiogenesis and proangiogenic factors such as vascular endothelial growth factor ( VEGF)-A in progressing peritoneal sclerosis has been reported. We previously reported the therapeutic efficacy of endostatin peptide, a potent inhibitor of angiogenesis derived from type XVIII collagen, in a mouse diabetic nephropathy model. Here, we examined the therapeutic effect of endostatin peptide in preventing progression in a mouse peritoneal sclerosis model. Male ICR mice received intraperitoneal injections of chlorhexidine gluconate ( CG) every other day to induce peritoneal sclerosis. Endostatin peptide ( 1 or 4mg/kg/day) was administered via subcutaneously implanted osmotic minipumps. Peritoneal sclerosis ( day 24) was significantly suppressed by endostatin peptide in a dose-dependent manner. Peritoneal accumulation of type III collagen was significantly suppressed by endostatin peptide. Increase in the number of CD31( +) blood vessels, F4/80( +) monocyte/macrophage accumulation, and 5-bromodeoxyuridine(+) proliferating cells was significantly inhibited by endostatin peptide. Increase in peritoneal expression of VEGF-A, profibrotic transforming growth factor-beta 1, and alpha-smooth muscle actin was suppressed by endostatin peptide. Immunoreactivity for endogenous endostatin ( whole molecule) and endostatin receptor alpha 5 beta 1-integrin was increased and colocalized to CD31( +) blood vessels in the thickened peritonea of CG-injected mice. These results demonstrate the potential use of antiangiogenic endostatin peptide as a novel therapeutic agent in preventing peritoneal sclerosis, a severe complication in patients undergoing long-term PD.

    DOI: 10.1038/sj.ki.5002040

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  • 再生誘導剤(セルフリーな再生医療)の展望 月刊BIOINDUSTRY 2020年8月号

    酒井芳紀( 担当: 分担執筆 ,  範囲: YS-1402による慢性腎臓病の治療効果)

    シーエムシー出版  2020年8月 

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MISC

  • 腎移植後に発生し治療により完治したリンパ嚢腫の2例

    窪田 理沙, 荒木 元朗, 和田 耕一郎, 河村 香澄, 丸山 雄樹, 光井 洋介, 西村 慎吾, 山下 里美, 小林 泰之, 渡邉 豊彦, 那須 保友, 加納 弓月, 北川 正史, 田邊 克幸, 和田 淳

    移植   54 ( 総会臨時 )   278 - 278   2019年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 腎虚血再灌流障害における好中球動態の2光子励起顕微鏡を用いた解析

    丸山 雄樹, 荒木 元朗, 城所 研吾, 和田 耕一郎, 河村 香澄, 光井 洋介, 定平 卓也, 窪田 理沙, 西村 慎吾, 渡部 昌実, 渡邉 豊彦, 田邊 克幸, 和田 淳, 柏原 直樹, 那須 保友

    移植   54 ( 総会臨時 )   241 - 241   2019年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 腎移植後に発生し治療により完治したリンパ嚢腫の2例

    窪田 理沙, 荒木 元朗, 和田 耕一郎, 河村 香澄, 丸山 雄樹, 光井 洋介, 西村 慎吾, 山下 里美, 小林 泰之, 渡邉 豊彦, 那須 保友, 加納 弓月, 北川 正史, 田邊 克幸, 和田 淳

    移植   54 ( 総会臨時 )   278 - 278   2019年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 生体腎移植におけるドナー・レシピエントのQoL変化の相違の検討

    光井 洋介, 荒木 元朗, 山下 里美, 丸山 雄樹, 河村 香澄, 窪田 理沙, 西村 慎吾, 和田 耕一郎, 小林 泰之, 渡邉 豊彦, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳, 那須 保友

    移植   54 ( 総会臨時 )   253 - 253   2019年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 生体腎移植におけるドナー・レシピエントのQoL変化の相違の検討

    光井 洋介, 荒木 元朗, 山下 里美, 丸山 雄樹, 河村 香澄, 窪田 理沙, 西村 慎吾, 和田 耕一郎, 小林 泰之, 渡邉 豊彦, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳, 那須 保友

    移植   54 ( 総会臨時 )   253 - 253   2019年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 生体腎移植8年後に回腸末端に発生したPTLDの一例

    和田里 章悟, 荒木 元朗, 河村 香澄, 丸山 雄樹, 光井 洋介, 窪田 理沙, 定平 卓也, 西村 慎吾, 和田 耕一郎, 枝村 康平, 小林 泰之, 渡邉 豊彦, 北川 正史, 田邊 克幸, 那須 保友

    移植   54 ( 総会臨時 )   278 - 278   2019年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 生体腎移植8年後に回腸末端に発生したPTLDの一例

    和田里 章悟, 荒木 元朗, 河村 香澄, 丸山 雄樹, 光井 洋介, 窪田 理沙, 定平 卓也, 西村 慎吾, 和田 耕一郎, 枝村 康平, 小林 泰之, 渡邉 豊彦, 北川 正史, 田邊 克幸, 那須 保友

    移植   54 ( 総会臨時 )   278 - 278   2019年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • Exogenous Vasohibin-2 Influences Development of Angiotensin II-induced Ascending Aortic Aneurysms but Not Abdominal Aortic Aneurysms in Either Normolipidemic or Apolipoprotein E-Deficient Mice

    Nozomu Otaka, Haruhito A. Uchida, MIchihiro Okuyama, Yuki Kakio, Yoshiko Hada, Hidemi Takeuchi, Ryoko Umebayashi, Katsuyuki Tanabe, Yasufumi Sato, Jun Wada

    ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY   39   2019年5月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Web of Science

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  • 腹腔鏡下開窓術を施行した腎移植後リンパ嚢腫の1例

    窪田 理沙, 荒木 元朗, 和田 耕一郎, 河村 香澄, 丸山 雄樹, 光井 洋介, 西村 慎吾, 山下 里美, 小林 泰之, 渡邉 豊彦, 那須 保友, 北川 正史, 田邊 克幸, 和田 淳

    日本臨床腎移植学会プログラム・抄録集   52回   226 - 226   2019年2月

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    記述言語:日本語   出版者・発行元:(一社)日本臨床腎移植学会  

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  • 当院で施行した先行的腎移植の検討

    坪井一朗, 荒木元朗, 河村香澄, 丸山雄樹, 窪田理沙, 定平卓也, 西村慎吾, 和田耕一郎, 小林泰之, 渡邉豊彦, 北川正史, 田邊克幸, 杉山斉, 和田淳, 那須保友

    日本臨床腎移植学会プログラム・抄録集   52nd   142 - 142   2019年2月

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    記述言語:日本語   出版者・発行元:(一社)日本臨床腎移植学会  

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  • 腹腔鏡下開窓術を施行した腎移植後リンパ嚢腫の1例

    窪田 理沙, 荒木 元朗, 和田 耕一郎, 河村 香澄, 丸山 雄樹, 光井 洋介, 西村 慎吾, 山下 里美, 小林 泰之, 渡邉 豊彦, 那須 保友, 北川 正史, 田邊 克幸, 和田 淳

    日本臨床腎移植学会プログラム・抄録集   52回   226 - 226   2019年2月

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    記述言語:日本語   出版者・発行元:(一社)日本臨床腎移植学会  

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  • 当院で施行した先行的腎移植の検討

    坪井 一朗, 荒木 元朗, 河村 香澄, 丸山 雄樹, 窪田 理沙, 定平 卓也, 西村 慎吾, 和田 耕一郎, 小林 泰之, 渡邉 豊彦, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳, 那須 保友

    日本臨床腎移植学会プログラム・抄録集   52回   142 - 142   2019年2月

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    記述言語:日本語   出版者・発行元:(一社)日本臨床腎移植学会  

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  • 生体腎移植レシピエントにおけるCT値を用いた骨密度の変化に関する検討

    丸山 雄樹, 荒木 元朗, 和田 耕一郎, 坪井 一朗, 河村 香澄, 光井 洋介, 窪田 理沙, 西村 慎吾, 小林 泰之, 渡邊 豊彦, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳, 那須 保友

    移植   53 ( 総会臨時 )   490 - 490   2018年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 鰓耳腎症候群の小児に対する生体腎移植の1例

    窪田 理沙, 荒木 元朗, 和田 耕一郎, 河村 香澄, 丸山 雄樹, 光井 洋介, 西村 慎吾, 小林 泰之, 渡邉 豊彦, 那須 保友, 宮井 貴之, 北川 正史, 田邊 克幸, 和田 淳

    移植   53 ( 総会臨時 )   434 - 434   2018年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 鰓耳腎症候群の小児に対する生体腎移植の1例

    窪田 理沙, 荒木 元朗, 和田 耕一郎, 河村 香澄, 丸山 雄樹, 光井 洋介, 西村 慎吾, 小林 泰之, 渡邉 豊彦, 那須 保友, 宮井 貴之, 北川 正史, 田邊 克幸, 和田 淳

    移植   53 ( 総会臨時 )   434 - 434   2018年9月

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  • 生体腎移植におけるリツキシマブ投与の効果と有害事象

    河村 香澄, 荒木 元朗, 丸山 雄樹, 坪井 一朗, 光井 洋介, 窪田 理沙, 西村 真吾, 和田 耕一郎, 小林 泰之, 渡邉 豊彦, 那須 保友, 山下 里美, 北川 正史, 田邉 克幸, 杉山 斉, 和田 淳

    移植   53 ( 総会臨時 )   481 - 481   2018年9月

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  • 生体腎移植におけるリツキシマブ投与の効果と有害事象

    河村 香澄, 荒木 元朗, 丸山 雄樹, 坪井 一朗, 光井 洋介, 窪田 理沙, 西村 真吾, 和田 耕一郎, 小林 泰之, 渡邉 豊彦, 那須 保友, 山下 里美, 北川 正史, 田邉 克幸, 杉山 斉, 和田 淳

    移植   53 ( 総会臨時 )   481 - 481   2018年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 生体腎移植レシピエントにおけるCT値を用いた骨密度の変化に関する検討

    丸山 雄樹, 荒木 元朗, 和田 耕一郎, 坪井 一朗, 河村 香澄, 光井 洋介, 窪田 理沙, 西村 慎吾, 小林 泰之, 渡邊 豊彦, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳, 那須 保友

    移植   53 ( 総会臨時 )   490 - 490   2018年9月

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  • Exogenous Vasohibin-2 Does Not Influence Angiotensin II-induced Abdominal Aortic Aneurysms Formation in Either Normolipidemic or Apolipoprotein E-Deficient Mice

    Nozomu Otaka, Haruhito A. Uchida, Yoshiko Hada, Hidemi Takeuchi, Yuki Kakio, MIchihiro Okuyama, Ryoko Umebayashi, Katsuyuki Tanabe, Yasufumi Sato, Jun Wada

    ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY   38   2018年5月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    DOI: 10.1161/atvb.38.suppl_1.110

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  • 肝腎同時移植における腎保護

    荒木元朗, 和田耕一郎, 山下里美, 丸山雄樹, 光井洋介, 定平卓也, 西村慎吾, 甲斐誠二, 高本篤, 谷本竜太, 杉本盛人, 小林泰之, 渡邉豊彦, 那須保友, 北川正史, 田邊克幸, 和田淳, 楳田祐三, 藤原俊義, 八木孝仁

    日本臨床腎移植学会プログラム・抄録集   51st   97   2018年

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  • Vasohibin-2は大動脈瘤モデルマウスにおいてVEGFとは独立して胸部大動脈瘤を増悪させる

    奥山 倫弘, 内田 治仁, 垣尾 勇樹, 梅林 亮子, 田邊 克幸, 藤井 泰宏, 大澤 晋, 佐藤 靖史, 和田 淳

    脈管学   57 ( Suppl. )   S128 - S128   2017年10月

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  • 抗血管内皮細胞増殖因子(VEGF)薬硝子体内注射による腎障害が示唆された糖尿病性腎症の1例

    大高 望, 川北 智英子, 木野村 賢, 北川 正史, 田邊 克幸, 江口 潤, 内田 治仁, 杉山 斉, 和田 淳, 清水 章

    日本腎臓学会誌   59 ( 6 )   731 - 731   2017年9月

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  • 生体腎移植レシピエントにおける予防的抗菌薬と周術期感染症に関する後ろ向き調査

    和田 耕一郎, 荒木 元朗, 西村 慎吾, 山下 里美, 河村 香澄, 光井 洋介, 吉岡 貴史, 有吉 勇一, 小林 泰之, 渡邉 豊彦, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳, 那須 保友

    移植   52 ( 総会臨時 )   467 - 467   2017年8月

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  • 術前代謝拮抗剤による関節リウマチ増悪を来すもエベロリムスへの変更によって腎移植可能であった一例

    丸山 雄樹, 荒木 元朗, 光井 洋介, 西村 慎吾, 杉本 盛人, 山下 里美, 和田 耕一郎, 小林 泰之, 渡邉 豊彦, 那須 保友, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳

    移植   52 ( 総会臨時 )   502 - 502   2017年8月

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  • 腎移植レシピエントにおける術前皮下脂肪・内臓脂肪体積の術後腎機能への影響

    光井 洋介, 荒木 元朗, 河村 香澄, 丸山 雄樹, 西村 慎吾, 和田 耕一郎, 小林 泰之, 渡辺 豊彦, 北川 正史, 田邊 克幸, 那須 保友

    移植   52 ( 総会臨時 )   354 - 354   2017年8月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 当院で施行した先行的腎移植(Pre-emptive Renal Transplantation:PRT)の検討

    光井 洋介, 荒木 元朗, 山下 里美, 吉岡 貴史, 有吉 勇一, 和田 耕一郎, 小林 泰之, 江原 伸, 渡辺 豊彦, 那須 保友, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳

    日本臨床腎移植学会雑誌   5 ( 1 )   89 - 90   2017年7月

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    記述言語:日本語   出版者・発行元:日本臨床腎移植学会  

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  • Overexpression of Vasohibin-2 Exacerbates Development of Angiotensin II-Induced Thoracic Aortic Aneurysms Independent of VeEGF

    Michihiro Okuyama, Haruhito A. Uchida, Ryoko Umebayashi, Yuki Kakio, Hidemi Takeuchi, Katsuyuki Tanabe, Yasufumi Sato, Jun Wada

    ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY   37   2017年5月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:LIPPINCOTT WILLIAMS & WILKINS  

    Web of Science

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  • 当院における透析導入患者の潜在性結核感染症スクリーニング状況の検討

    加藤 綾子, 大西 章史, 杉山 斉, 森下 美智子, 宮脇 義亜, 荒田 夕佳, 益田 加奈, 秋山 愛由, 梅林 亮子, 山成 俊夫, 森永 裕士, 田邊 克幸, 木野村 賢, 和田 淳

    中国腎不全研究会誌   25   67 - 68   2017年3月

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    記述言語:日本語   出版者・発行元:中国腎不全研究会  

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  • 当院における高齢者の生体腎移植レシピエントの検討

    光井 洋介, 荒木 元朗, 山下 里美, 吉岡 貴史, 有吉 勇一, 和田 耕一郎, 小林 泰之, 江原 伸, 渡辺 豊彦, 那須 保友, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳

    移植   51 ( 6 )   509 - 509   2016年12月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 生体腎移植レシピエントにおける周術期感染に関する後ろ向き調査

    和田 耕一郎, 荒木 元朗, 山下 里美, 光井 洋介, 吉岡 貴史, 有吉 勇一, 西村 慎吾, 小林 泰之, 渡辺 豊彦, 北川 正史, 田邊 克幸, 森永 裕士, 杉山 斉, 和田 淳, 那須 保友

    移植   51 ( 総会臨時 )   414 - 414   2016年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 岡山大学病院における生体腎移植レシピエントの術前ワクチン接種の現状

    光井 洋介, 荒木 元朗, 山下 里美, 吉岡 貴史, 有吉 勇一, 西村 慎吾, 和田 耕一郎, 小林 泰之, 渡辺 豊彦, 那須 保友, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳

    移植   51 ( 総会臨時 )   266 - 266   2016年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 岡山大学病院における腹腔鏡下ドナー腎採取術の検討

    西村 慎吾, 荒木 元朗, 小林 泰之, 有森 千聖, 山下 里美, 光井 洋介, 窪田 理沙, 吉岡 貴史, 有吉 勇一, 和田 耕一郎, 渡辺 豊彦, 北川 正史, 田邊 克幸, 和田 淳, 那須 保友

    移植   51 ( 総会臨時 )   331 - 331   2016年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 長期透析患者に対する腎移植症例の検討

    有吉 勇一, 荒木 元朗, 光井 洋介, 吉岡 貴史, 和田 耕一郎, 小林 泰之, 江原 伸, 渡邉 豊彦, 那須 保友, 山下 里美, 北川 正史, 田邊 克幸, 森永 裕士, 杉山 斉, 和田 淳

    日本臨床腎移植学会雑誌 = Journal of Japanese Society for Clinical Renal Transplantation   4 ( 1 )   113 - 117   2016年7月

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    記述言語:日本語   出版者・発行元:日本臨床腎移植学会  

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  • 生体腎移植レシピエントにおける周術期感染症に関する検討

    和田 耕一郎, 定平 卓也, 山本 満寿美, 石井 亜矢乃, 渡辺 豊彦, 那須 保友, 荒木 元朗, 山下 里美, 吉岡 貴史, 有吉 勇一, 光畑 律子, 山成 俊夫, 北川 正史, 田邊 克幸, 森永 裕士, 杉山 斉, 和田 淳

    日本化学療法学会雑誌   64 ( Suppl.A )   177 - 177   2016年5月

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    記述言語:日本語   出版者・発行元:(公社)日本化学療法学会  

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  • 維持血液透析を要したFontan術後成人先天性心疾患(ACHD)の1症例と透析管理の特徴

    木野村 賢, 森下 美智子, 宮脇 義亜, 益田 加奈, 荒田 夕佳, 秋山 愛由, 大西 章史, 山成 俊夫, 田邊 克幸, 杉山 斉, 赤木 禎治, 和田 淳

    日本透析医学会雑誌   49 ( Suppl.1 )   715 - 715   2016年5月

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    記述言語:日本語   出版者・発行元:(一社)日本透析医学会  

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  • 当院における透析導入患者の潜在性結核感染症スクリーニング状況の検討

    大西 章史, 杉山 斉, 森下 美智子, 宮脇 義亜, 荒田 夕佳, 益田 加奈, 秋山 愛由, 梅林 亮子, 山成 俊夫, 森永 裕士, 田邊 克幸, 木野村 賢, 和田 淳

    日本透析医学会雑誌   49 ( Suppl.1 )   807 - 807   2016年5月

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    記述言語:日本語   出版者・発行元:(一社)日本透析医学会  

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  • 不明熱の原因として非結核性抗酸菌(NTM)症が考えられた血液透析患者の1例.

    益田 加奈, 木野村 賢, 竹内 英実, 森下 美智子, 荒田 夕佳, 秋山 愛由, 大西 章史, 田邊 克幸, 佐田 憲映, 谷口 暁彦, 杉山 斉, 和田 淳

    中国腎不全研究会誌   24   183 - 184   2016年

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  • 生体腎移植後に移植尿管結石、一時的尿管狭窄を生じた症例

    光井 洋介, 荒木 元朗, 山下 里美, 吉岡 貴史, 有吉 勇一, 和田 耕一郎, 小林 泰之, 江原 伸, 渡邉 豊彦, 那須 保友, 北川 正史, 田辺 克幸, 杉山 斉

    西日本泌尿器科   77 ( 増刊 )   127 - 127   2015年10月

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    記述言語:日本語   出版者・発行元:西日本泌尿器科学会  

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  • 当院で施行した先行的腎移植(preemptive renal transplantation:PRT)の検討

    光井 洋介, 荒木 元朗, 山下 里美, 吉岡 貴史, 有吉 勇一, 和田 耕一郎, 小林 泰之, 江原 伸, 渡辺 豊彦, 那須 保友, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳

    移植   50 ( 総会臨時 )   316 - 316   2015年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 生体腎移植レシピエントにおける周術期感染症に関する検討

    和田 耕一郎, 荒木 元朗, 山下 里美, 吉岡 貴史, 有吉 勇一, 小林 泰之, 江原 伸, 渡辺 豊彦, 山成 俊夫, 北川 正史, 田邊 克幸, 杉山 斉, 和田 淳, 那須 保友

    移植   50 ( 総会臨時 )   299 - 299   2015年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 生体腎移植におけるリツキシマブの効果と有害事象の検討

    荒木 元朗, 和田 耕一郎, 宗石 理沙, 吉岡 貴史, 有吉 勇一, 山下 里美, 小林 泰之, 江原 伸, 渡辺 豊彦, 那須 保友, 田邊 克幸, 北川 正史, 杉山 斉, 和田 淳

    移植   50 ( 総会臨時 )   475 - 475   2015年9月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • 当科で施行した生体腎移植レシピエント、ドナーのQOL評価

    有吉 勇一, 荒木 元朗, 宗石 理沙, 吉岡 貴史, 和田 耕一郎, 小林 泰之, 佐々木 克己, 江原 伸, 渡辺 豊彦, 那須 保友, 公文 裕巳, 有森 千聖, 北川 正史, 田邊 克幸, 森永 裕士, 菊本 陽子, 内田 治仁, 喜多村 真治, 前島 洋平, 杉山 斉, 槇野 博史

    移植   49 ( 4-5 )   377 - 377   2014年11月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • マウス慢性腎臓病病態モデルにおけるAT1受容体結合因子ATRAP発現調節についての検討

    小林 竜, 田村 功一, 涌井 広道, 大澤 正人, 小豆島 健護, 畝田 一司, 大城 光二, 出島 徹, 前田 晃延, 戸谷 義幸, 山下 暁朗, 田邉 克幸, 前島 洋平, 槇野 博史, 梅村 敏

    日本高血圧学会総会プログラム・抄録集   37回   401 - 401   2014年10月

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    記述言語:日本語   出版者・発行元:(NPO)日本高血圧学会  

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  • 腎線維化におけるAT1受容体結合因子ATRAPの発現調節についての検討

    大友 優太, 涌井 広道, 田村 功一, 大澤 正人, 小豆島 健護, 畝田 一司, 小林 竜, 大城 光二, 戸谷 義幸, 山下 暁朗, 田邊 克幸, 前島 洋平, 槇野 博史, 梅村 敏

    日本高血圧学会総会プログラム・抄録集   37回   337 - 337   2014年10月

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    記述言語:日本語   出版者・発行元:(NPO)日本高血圧学会  

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  • 岡山大学泌尿器科におけるpreemptive腎移植症例の検討

    有吉 勇一, 荒木 元朗, 宗石 理沙, 吉岡 貴史, 和田 耕一郎, 小林 泰之, 佐々木 克己, 江原 伸, 渡辺 豊彦, 那須 保友, 公文 裕巳, 清水 千聖, 赤木 滋, 森永 裕士, 田邊 克幸, 北川 正史, 杉山 斉, 和田 淳, 槇野 博史

    移植   49 ( 1 )   167 - 167   2014年5月

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    記述言語:日本語   出版者・発行元:(一社)日本移植学会  

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  • LACK OF VASOHIBIN-1 EXACERBATES RENAL ALTERATIONS INDUCED BY INFUSION OF ANGIOTENSIN-II

    Hinamoto Norikazu, Maeshima Yohei, Yamasaki Hiroko, Watatani Hiroyuki, Ujike Haruyo, Tanabe Katsuyuki, Masuda Kana, Sugiyama Hitoshi, Sato Yasufumi, Makino Hirofumi

    NEPHROLOGY   19   106 - 106   2014年5月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:WILEY-BLACKWELL  

    Web of Science

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  • REDUCTION OF PROTEINURIA IN THE STREPTOZOTOCIN-INDUCED DIABETIC MICE LACKING ENDOGENOUS VASOHIBIN-2

    Ujike Haruyo, Maeshima Yohei, Hinamoto Norikazu, Watatani Hiroyuki, Tanabe Katsuyuki, Masuda Kana, Sugiyama Hitoshi, Sato Yasufumi, Makino Hirofumi

    NEPHROLOGY   19   43 - 44   2014年5月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:WILEY-BLACKWELL  

    Web of Science

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  • ORAL ADMINISTRATION OF A PROSTACYCLIN ANALOG ONO-1301 AMELIORATES VASCULAR CALCIFICATION IN A RAT MODEL OF ADENINE-INDUCED CHRONIC KIDNEY DISEASE

    Watatani Hiroyuki, Maeshima Yohei, Hinamoto Norikazu, Ujike Haruyo, Tanabe Katsuyuki, Masuda Kana, Sugiyama Hitoshi, Sakai Yoshiki, Makino Hirofumi

    NEPHROLOGY   19   172 - 172   2014年5月

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    記述言語:英語   掲載種別:研究発表ペーパー・要旨(国際会議)   出版者・発行元:WILEY-BLACKWELL  

    Web of Science

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  • 尿酸代謝におけるUp-to-Date(第8回) 尿酸とフルクトース

    仲川 孝彦, 中山 隆弘, 小杉 智規, 田村 好古, 北川 渡, 田邊 克幸, 佐藤 和一, Johnson Richard J.

    医薬の門   53 ( 2 )   68 - 73   2013年5月

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    記述言語:日本語   出版者・発行元:鳥居薬品(株)  

    臨床検討にて、近年のフルクトース消費増加とメタボリックシンドローム発症の間に相関を認める。また動物モデルにおいても、フルクトースにより、初期には高尿酸血症を伴う高血圧、高中性脂肪血症、インスリン抵抗性、腎臓尿細管障害を認め、晩期にはインスリン分泌低下や脂肪肝の発症を認める。しかしながら、高尿酸血症治療により初期のメタボリックシンドローム様症状は軽減されうる。最近のわれわれの実験結果を中心に、メタボリックシンドロームにおけるフルクトースと尿酸の役割を紹介したい。(著者抄録)

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  • 急性腎不全で発症し透析を離脱し得たSLEの1例

    大西章史, 森永裕士, 赤木滋, 北川正史, 井上章子, 寺見直人, 山成俊夫, 辻憲二, 氏家はる代, 小川愛由, 中山和典, 綿谷博雪, 井上淳子, 田邊克幸, 杉山斉, 槇野博史

    日本腎臓学会誌   55 ( 6 )   2013年

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  • 平成21年度岡山医学会賞(砂田賞)受賞論文 血管新生negative feedback制御因子Vasohibin-1によるマウス糖尿病性腎症進展制御効果の検討

    那須 達世, 前島 洋平, 木野村 賢, 川原(広越, 久美子, 田邊 克幸, 杉山 斉, 園田 光, 佐藤 靖史, 槇野 博史

    岡山医学会雑誌   123 ( 1 )   19 - 25   2011年4月

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    記述言語:日本語   出版者・発行元:岡山医学会  

    CiNii Article

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  • 血管新生関連因子の遺伝子導入アプローチを用いた腹膜線維化進展機序の解明と新規治療法開発の基礎的検討.

    前島洋平, 田邉克幸, 杉山 斉, 槇野博史

    腎と透析   69   142 - 145   2010年

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  • PREVEND IT Prevention of Renal and Vascular Endstage Disease Intervention Trial.

    田邉克幸, 前島洋平, 槇野博史

    DATA UPDATE 循環系 第4版   344 - 345   2009年

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  • 腹膜再生プログラムの進歩 血管新生抑制因子vasohibinによる腹膜硬化症抑制効果の検討

    田邊 克幸, 前島 洋平, 那須 達世, 高沢 有紀, 木野村 賢, 広越 久美子, 井上 達之, 斉藤 大輔, 杉山 斉, 園田 光, 佐藤 靖史, 槇野 博史

    腎と透析   65 ( 別冊 腹膜透析2008 )   84 - 87   2008年8月

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    記述言語:日本語   出版者・発行元:(株)東京医学社  

    腹膜硬化症モデルマウスを用いてvasohibinの効果を組織学的、免疫組織化学的に検討した。結果、vasohibinは抗血管新生作用、抗炎症作用、抗線維化作用を介して腹膜硬化症の進展を抑制することが示唆された。

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  • 診療controversy medical decision makingのために ループス腎炎に対する免疫抑制療法 慎重な立場から

    田邊 克幸, 佐田 憲映, 槇野 博史

    内科   99 ( 4 )   697 - 700   2007年4月

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    記述言語:日本語   出版者・発行元:(株)南江堂  

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  • わが国の慢性腎臓病(CKD)対策の最前線 CKDの定義と分類

    田邊 克幸, 前島 洋平, 槇野 博史

    腎臓   29 ( 2 )   78 - 81   2006年10月

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    記述言語:日本語   出版者・発行元:(公財)日本腎臓財団  

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  • NM-3による糖尿病腎症進展抑制機序の検討

    一瀬邦弘, 前島洋平, 山本佳彦, 縣直樹, 來山浩之, 高沢有紀, 木野村賢, 広越久美子, 田邊克幸, 杉山斉, 山崎康司, 槙野博史

    日本腎臓学会誌   48 ( 3 )   2006年

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  • アデノウイルスを用いたangiopoietin-1遺伝子治療による尿細管間質病変制御効果の検討

    高沢有紀, 前島洋平, 一瀬邦弘, 田邊克幸, 来山浩之, 広越久美子, 木野村賢, 山本佳彦, 杉山斉, 伊藤克礼, 滝正樹, 藤原俊義, 濱田洋文, 槇野博史

    日本腎臓学会誌   48 ( 3 )   2006年

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  • 血管新生抑制因子endostatin peptideによる腹膜硬化症抑制効果の検討

    田邊克幸, 前島洋平, 一瀬邦弘, 高沢有紀, 來山浩之, 広越久美子, 木野村賢, 杉山斉, 槇野博史

    日本腎臓学会誌   48 ( 3 )   2006年

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  • シスプラチン誘導急性腎不全モデルにおけるラット腎幹/前駆細胞(rKS56)治療効果の検討

    木野村賢, 前島洋平, 喜多村真治, 一瀬邦弘, 高沢有紀, 來山浩之, 広越久美子, 田邉克幸, 菅谷健, 山崎康司, 杉山斉, 槇野博史

    日本腎臓学会誌   48 ( 3 )   2006年

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講演・口頭発表等

  • 慢性腎臓病の進行における腎Vasohibin発現の関与の解明

    田邊克幸, 森岡朋代, 谷村智史

    第14回Vasohibin研究会  2019年2月17日 

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    記述言語:日本語   会議種別:口頭発表(一般)  

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  • Estrogen-related receptor α欠損はシスプラチン腎症におけるミトコンドリア障害を促進する

    田邊克幸, 津志田圭吾, 三宅広将, 益田加奈, 谷村智史, 杉山斉, 和田淳

    第61回日本腎臓学会  2018年6月10日 

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    記述言語:日本語   会議種別:ポスター発表  

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  • 腎疾患におけるVasohibin-2の役割に関する検討

    田邊克幸, 益田加奈, 谷村智史, 三宅広将, 津志田圭吾

    第13回Vasohibin研究会  2018年2月24日 

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    記述言語:日本語   会議種別:口頭発表(一般)  

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  • 当院での腎移植後低リン血症とPTHレベルとの関連性の検討

    田邊克幸, 北川正史, 荒木元朗, 和田耕一郎, 西村慎吾, 光井洋介, 丸山雄樹, 那須保友, 和田淳

    第51回日本臨床腎移植学会  2018年2月16日 

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    記述言語:日本語   会議種別:ポスター発表  

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  • 急性腎障害におけるVasohibin-1及び-2の発現意義についての検討

    田邊克幸, 三宅広将, 益田加奈, 谷村智史, 津志田圭吾

    第12回Vasohibin研究会  2017年2月4日 

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    記述言語:日本語   会議種別:口頭発表(一般)  

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  • Genetic Deletion of Endogenous Proangiogenic Factor Vasohibin-2 Exacerbates Renal Ischemic Reperfusion Injury

    Tanabe K, Masuda K, Arata Y, Sugiyama H, Wada J

    American Society of Nephrology Kidney Week 2016  2016年11月17日 

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    記述言語:英語   会議種別:ポスター発表  

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  • 急性腎障害における内因性血管新生促進因子Vasohibin-2の役割に関する検討

    田邊克幸, 益田加奈, 荒田夕佳, 三宅広将, 杉山斉, 佐藤靖史, 和田淳

    第59回日本腎臓学会  2016年6月18日 

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    記述言語:日本語   会議種別:ポスター発表  

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  • 急性及び慢性の腎障害におけるVasohibin-2の発現意義についての検討

    田邊克幸, 益田加奈, 荒田夕佳, 三宅広将

    第11回Vasohibin研究会  2016年1月23日 

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    記述言語:日本語   会議種別:口頭発表(一般)  

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産業財産権

  • バソヒビン含有治療剤

    佐藤 靖史, 前島 洋平, 那須 達世, 田邊 克幸, 槇野 博史

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    出願人:国立大学法人 岡山大学, 塩野義製薬株式会社

    出願番号:JP2008055744  出願日:2008年3月26日

    公開番号:WO2008-123308  公開日:2008年10月16日

    J-GLOBAL

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  • バソヒビン含有治療剤

    佐藤 靖史, 前島 洋平, 那須 達世, 田邊 克幸, 槇野 博史

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    出願人:国立大学法人 岡山大学, 塩野義製薬株式会社

    出願番号:特願2009-509145  出願日:2008年3月26日

    特許番号/登録番号:特許第5256192号  発行日:2013年4月26日

    J-GLOBAL

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社会貢献活動

  • 岡山県看護協会研修

    役割:講師

    №31 慢性腎臓病(CKD)患者の看護  2021年11月18日

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