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  <Article>
    <Journal>
      <PublisherName>Springer Science and Business Media LLC</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1342-1751</Issn>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2026</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Optimizing low-dose rituximab protocol for ABO-mismatched kidney transplantation: long-term outcomes in a single-center retrospective cohort study</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tomoaki</FirstName>
        <LastName>Yamanoi</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takanori</FirstName>
        <LastName>Sekito</LastName>
        <Affiliation>Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Moto</FirstName>
        <LastName>Tokunaga</LastName>
        <Affiliation>Department of Urology, NHO Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ichiro</FirstName>
        <LastName>Tsuboi</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kasumi</FirstName>
        <LastName>Yoshinaga</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuki</FirstName>
        <LastName>Maruyama</LastName>
        <Affiliation>Department of Inflammation and Immunity, Lerner Research Institute, Cleveland Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tatsushi</FirstName>
        <LastName>Kawada</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Risa</FirstName>
        <LastName>Kubota</LastName>
        <Affiliation>Department of Urology, NHO Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yusuke</FirstName>
        <LastName>Tominaga</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takuya</FirstName>
        <LastName>Sadahira</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Katayama</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takehiro</FirstName>
        <LastName>Iwata</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shingo</FirstName>
        <LastName>Nishimura</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kensuke</FirstName>
        <LastName>Bekku</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuhiro</FirstName>
        <LastName>Onishi</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hidemi</FirstName>
        <LastName>Takeuchi</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Morinaga</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koichiro</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Urology, Shimane University Faculty of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Motoo</FirstName>
        <LastName>Araki</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background ABO-mismatched kidney transplantation (KTx) expands donor availability but increases risks of antibody-mediated rejection and passenger lymphocyte syndrome (PLS). While rituximab (Rit) potentially mitigates these complications, conventional high-dose regimens (375 mg/m2) elevate infectious and hematologic toxicity. We implemented low-dose Rit induction (200 mg/body) for desensitization in minor/major ABO-mismatched and DSA-positive KTx, evaluating its efficacy and safety over 15-years.&lt;br&gt;
Methods This single-center retrospective cohort (May 2009&#8211;April 2024) analyzed 161 adult KTx recipients: Rit (n&#8201;=&#8201;107) and Non-Rit (n&#8201;=&#8201;54) groups. All received tacrolimus, mycophenolate mofetil, prednisolone, and basiliximab; high-risk patients also underwent plasmapheresis. Outcomes included graft survival, biopsy-proven acute rejection, de novo donor-specific antibody (DSA) formation, infection, severe neutropenia, and PLS.&lt;br&gt;
Results 1-year graft survival was 100% in both groups. 5-year death-censored graft survival was 95.8% (Rit) vs 95.9% (Non-Rit), respectively (log-rank P&#8201;=&#8201;0.43). Biopsy-proven acute rejection (7.5% vs 3.7%, P&#8201;=&#8201;0.50) and de novo DSA production were equivalent (Class I: 5.5% vs 2.2%; Class II: 6.6% vs 8.7%; both P&#8201;=&#8201;1.00), with lower mean fluorescent intensity (MFI) in the Rit group. Cytomegalovirus disease, urinary tract infection and fungal infection rates were comparable between both groups. Grade 4 neutropenia was not associated with Rit (OR 2.65; 95% CI 0.63&#8211;11.0; P&#8201;=&#8201;0.18). Blood transfusion for hemoglobin declines occurred in 5.6% vs 7.4%, with preserved haptoglobin in all cases, indicating no PLS.&lt;br&gt;
Conclusions Low-dose Rit induction achieves excellent graft survival and effective PLS prevention, without increasing toxicity, supporting its adoption as an optimal desensitization strategy.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">Kidney transplantation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">ABO-mismatch</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Low-dose rituximab</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Graft survival</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Passenger lymphocyte syndrome</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Springer Science and Business Media LLC</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2192-4449</Issn>
      <Volume>15</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2026</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>A case of tubulointerstitial nephritis with infiltration of neutrophils and interleukin-17-positive cells associated with Beh&#231;etfs disease</ArticleTitle>
    <FirstPage LZero="delete">35</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Naruhiko</FirstName>
        <LastName>Uchida</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiko</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Natsuki</FirstName>
        <LastName>Kubota</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takayuki</FirstName>
        <LastName>Katsuyama</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Haruhito A.</FirstName>
        <LastName>Uchida</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Beh&#231;etfs disease (BD) is a non-infectious inflammatory condition characterized by neutrophilic infiltration. In addition to primary symptoms, including oral and genital ulcers, ocular involvement, and skin lesions, BD can also affect various organs. However, renal involvement, particularly in tubulointerstitial nephritis, has rarely been described. Herein, a rare case of acute tubulointerstitial nephritis in a patient clinically diagnosed with BD is reported. The renal lesion presented with other symptoms of BD and fever, and was considered to be BD-related due to the presence of neutrophilic infiltration and its responsiveness to BD-directed therapy. Alterations in T-helper (Th) 1, Th2, and Th17 cytokine profiles are associated with BD activity. Interleukin (IL)-17 plays a central role in neutrophil activation, and recent studies have demonstrated a strong correlation between IL-17A levels and BD activity. In the present case, elevated serum IL-17A levels and infiltration of IL-17A-positive cells into the renal tissue reflected an active phase of BD and a BD-associated renal lesion.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">Tubulointerstitial nephritis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Beh&#231;etfs disease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Neutrophils</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Interleukin-17</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">T-helper (Th) 1/Th2/Th17  cytokines</Param>
      </Object>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Japanese Society of Internal Medicine</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-2918</Issn>
      <Volume>63</Volume>
      <Issue>23</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2024</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Successful Treatment for Life Threatening Recurrent Non-traumatic Rectus Sheath Hematoma in a Case with Microscopic Polyangiitis with Rapidly Progressive Glomerulonephritis</ArticleTitle>
    <FirstPage LZero="delete">3243</FirstPage>
    <LastPage>3248</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Nakanoh</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hidemi</FirstName>
        <LastName>Takeuchi</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shiho</FirstName>
        <LastName>Morimoto</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuya</FirstName>
        <LastName>Terajima</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shugo</FirstName>
        <LastName>Okamoto</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuhiro</FirstName>
        <LastName>Onishi</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiko</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takayuki</FirstName>
        <LastName>Katsuyama</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Tsuji</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshinori</FirstName>
        <LastName>Matsumoto</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Morinaga</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mayu</FirstName>
        <LastName>Uka</LastName>
        <Affiliation>Department of Radiology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koji</FirstName>
        <LastName>Tomita</LastName>
        <Affiliation>Department of Radiology, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Haruhito A.</FirstName>
        <LastName>Uchida</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takao</FirstName>
        <LastName>Hiraki</LastName>
        <Affiliation>Department of Radiology, Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Faculty of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>A 68-year-old woman was admitted to our hospital because of a rapid progression of renal dysfunction with positive myeloperoxidase antineutrophil cytoplasmic antibody and was diagnosed with rapidly progressive glomerulonephritis associated with microscopic polyangiitis (MPA). Severe right rectus sheath hematoma (RSH) bleeding from the inferior epigastric artery developed after starting hemodialysis, which required 4 transarterial embolizations due to recurrent bleeding. After additional treatment with methylprednisolone pulse therapy and rituximab, no rebleeding occurred. Although the giant hematoma reached the pelvis, it shrank spontaneously without any intervention. Nontraumatic RSH should therefore be considered when treating patients with multiple risk factors.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">rectus sheath hematoma</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">microscopic polyangiitis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">hemodialysis</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier BV</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2468-0249</Issn>
      <Volume>10</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Dotinurad Treatment for Patients With Hyperuricemia Complicating CKD</ArticleTitle>
    <FirstPage LZero="delete">1711</FirstPage>
    <LastPage>1720</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomokazu</FirstName>
        <LastName>Nunoue</LastName>
        <Affiliation>Nunoue Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Itabashi</LastName>
        <Affiliation>Itabashi Diabetes and Dermatology Medical Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akihiro</FirstName>
        <LastName>Katayama</LastName>
        <Affiliation>NHO Okayama Medical Center</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akihiko</FirstName>
        <LastName>Nakamura</LastName>
        <Affiliation>Osafune Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Ohbayashi</LastName>
        <Affiliation>Tohno Chuo Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuhiro</FirstName>
        <LastName>Onishi</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kyoko</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Japanese Red Cross Okayama Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keisuke</FirstName>
        <LastName>Maruyama</LastName>
        <Affiliation>Okayama Saiseikai Outpatient Center Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takeshi</FirstName>
        <LastName>Hosoya</LastName>
        <Affiliation>Hosoya Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shinichi</FirstName>
        <LastName>Okada</LastName>
        <Affiliation>Okada Medical Clinic</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Introduction: The management of hyperuricemia is important to reduce cardiovascular risk and the progression of renal injury in chronic kidney disease (CKD). This study aimed to assess the efficacy and safety of dotinurad, a novel urate transporter-1 inhibitor, in patients with hyperuricemia and CKD.&lt;br&gt;
Methods: In a nonrandomized, parallel interventional study, patients were grouped based on their estimated glomerular filtration rate (eGFR) at baseline. The starting dotinurad dose was 0.5 mg/d and titrated to a final dose of 2 mg/d to 4 mg/d. The primary end point was the noninferiority of the change in serum uric acid (UA) levels between the G1/G2 and G3/G4 groups at week 24. The main secondary end points were changes in eGFR and UA clearance-to-creatinine clearance ratio (CUA/CCr). Reported adverse events were also investigated.&lt;br&gt;
Results: Ninety-eight patients continued the dose titration. The mean percentage reduction in serum UA level at week 24 were 47.2% and 42.8% for the G1/G2 and G3/G4 groups, respectively; the between-group difference was |4.3% (95% confidence interval [CI], |9.5% to 0.9%, noninferiority P = 0.0321), validating the noninferiority of treatment in the G3/G4 group to the G1/G2 group. eGFR tended to increase slightly through to week 24, suggesting that spontaneous eGFR decline was counteracted. Mean CUA/CCr generally increased over time from week 4 to week 24. No new safety issues of particular concern were identified; and there were no marked changes in urinary pH.&lt;br&gt;
Conclusion: Dotinurad therapy may be well-tolerated in patients with hyperuricemia and may have efficacy comparable with existing standard treatment in patients with CKD stages G3/G4. Randomized controlled trials in larger patient groups are needed.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">chronic kidney disease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">dotinurad</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">efficacy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">hyperuricemia</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">safety</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">serum uric acid</Param>
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    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Public Library of Science</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1932-6203</Issn>
      <Volume>20</Volume>
      <Issue>3</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2025</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Serum uric acid level is associated with renal arteriolar hyalinosis and predicts post-donation renal function in living kidney donors</ArticleTitle>
    <FirstPage LZero="delete">e0320482</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yuzuki</FirstName>
        <LastName>Kano</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masashi</FirstName>
        <LastName>Kitagawa</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Medicine, Kawasaki Medical School General Medical Center and Department of Medical Care Work, Kawasaki College of Health Professions</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoaki</FirstName>
        <LastName>Yamanoi</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kasumi</FirstName>
        <LastName>Yoshinaga</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kensuke</FirstName>
        <LastName>Bekku</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shingo</FirstName>
        <LastName>Nishimura</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Motoo</FirstName>
        <LastName>Araki</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Major guidelines for living-donor kidney transplantation underscore the need for pre-donation evaluation of renal function, hypertension, obesity, diabetes mellitus, and albuminuria to minimize the risk of donation from marginal donors. However, validity is yet to be established. We retrospectively investigated the relationship between clinical characteristics and histological indices in baseline renal biopsies (0-h biopsies) and whether these parameters could predict renal function in living kidney donors one year post-donation. Seventy-six living kidney donors were recruited for this study. In histological analyses, glomerulosclerosis, arteriosclerosis, arteriolosclerosis, arteriolar hyalinosis, and interstitial fibrosis and tubular atrophy scores/indices were evaluated. Post-donation serum creatinine levels in kidney donors with arteriolar hyalinosis were significantly higher than those in individuals without arteriolar hyalinosis. There was a significant correlation between baseline serum uric acid levels and the arteriolar hyalinosis index, with baseline uric acid level identified as an independent factor for hyalinosis in multiple regression analysis. Additionally, the serum uric acid level was a significant prognostic factor for post-donation serum creatinine after adjustment for baseline clinical parameters. These data demonstrate that pre-donation serum uric acid levels are associated with arteriolar hyalinosis in the kidney and could predict a decline in renal function during the first year after donation in living kidney donors.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>American Physiological Society</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1931-857X</Issn>
      <Volume>326</Volume>
      <Issue>6</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2024</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Preventive effects of vasohibin-2-targeting peptide vaccine for diabetic nephropathy</ArticleTitle>
    <FirstPage LZero="delete">F1054</FirstPage>
    <LastPage>F1065</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yuri</FirstName>
        <LastName>Nakashima</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoyo</FirstName>
        <LastName>Mifune</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takato</FirstName>
        <LastName>Nakadoi</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroki</FirstName>
        <LastName>Hayashi</LastName>
        <Affiliation>Department of Health Development and Medicine, Osaka University Graduate School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hironori</FirstName>
        <LastName>Nakagami</LastName>
        <Affiliation>Department of Health Development and Medicine, Osaka University Graduate School of Medicine</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasufumi</FirstName>
        <LastName>Sato</LastName>
        <Affiliation>New Industry Creation Hatchery Center, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Diabetic nephropathy remains the leading cause of end-stage kidney disease in many countries, and additional therapeutic targets are needed to prevent its development and progression. Some angiogenic factors are involved in the pathogenesis of diabetic nephropathy. Vasohibin-2 (VASH2) is a novel proangiogenic factor, and our previous study showed that glomerular damage is inhibited in diabetic Vash2 homozygous knockout mice. Therefore, we established a VASH2-targeting peptide vaccine as a tool for anti-VASH2 therapy in diabetic nephropathy. In this study, the preventive effects of the VASH2-targeting peptide vaccine against glomerular injury were examined in a streptozotocin (STZ)-induced diabetic mouse model. The mice were subcutaneously injected with the vaccine at two doses 2 wk apart and then intraperitoneally injected with 50 mg/kg STZ for 5 consecutive days. Glomerular injury was evaluated 20 wk after the first vaccination. Treatment with the VASH2-targeting peptide vaccine successfully induced circulating anti-VASH2 antibody without inflammation in major organs. Although the vaccination did not affect blood glucose levels, it significantly prevented hyperglycemia-induced increases in urinary albumin excretion and glomerular volume. The vaccination did not affect increased VASH2 expression but significantly inhibited renal angiopoietin-2 (Angpt2) expression in the diabetic mice. Furthermore, it significantly prevented glomerular macrophage infiltration. The preventive effects of vaccination on glomerular injury were also confirmed in db/db mice. Taken together, the results of this study suggest that the VASH2-targeting peptide vaccine may prevent diabetic glomerular injury in mice by inhibiting Angpt2-mediated microinflammation.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">albuminuria</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">diabetic nephropathy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">macrophages</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">peptide vaccine</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">vasohibin-2</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Frontiers Media</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2296-858X</Issn>
      <Volume>11</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2024</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Late-onset renal variant Fabry disease with R112H mutation and mild increase in plasma globotriaosylsphingosine: a case report</ArticleTitle>
    <FirstPage LZero="delete">1383309</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Keiko</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation>Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Department of Nephrology,  Rheumatology, Endocrinology and Metabolism, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Department of Nephrology,  Rheumatology, Endocrinology and Metabolism, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Morinaga</LastName>
        <Affiliation>Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Department of Nephrology,  Rheumatology, Endocrinology and Metabolism, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Akifumi</FirstName>
        <LastName>Onishi</LastName>
        <Affiliation>Department of Nephrology, Fukuyama City  Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Department of Nephrology,  Rheumatology, Endocrinology and Metabolism, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Haruhito A.</FirstName>
        <LastName>Uchida</LastName>
        <Affiliation>Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Department of Nephrology,  Rheumatology, Endocrinology and Metabolism, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroki</FirstName>
        <LastName>Maruyama</LastName>
        <Affiliation>Department of Clinical Nephroscience, Niigata University Graduate  School of Medical and Dental Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Faculty of Medicine, Dentistry and Pharmaceutical Sciences, Department of Nephrology,  Rheumatology, Endocrinology and Metabolism, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Fabry disease (FD) is an X-linked disorder resulting in a deficiency of alpha-galactosidase A (GLA) activity. The R112H mutation of GLA is relatively common in Japanese FD patients, characterized by a late-onset phenotype, almost normal to mild lyso-Gb3 elevation, and mild clinical symptoms, despite low GLA activity. This is due to the structural features of the R112H GLA protein. We herein report the case of a 42-year-old male patient with late-onset FD with a R112H mutation. The patient exhibited only renal involvement with no other organ damage and was successfully treated with galactosidase beta and subsequent migalastat for approximately 10 years. Especially, migalastat was clinically effective in normalizing plasma lyso-Gb3 levels and inhibiting the progression of renal damage associated with FD. Therefore, the use of migalastat in the FD patients with R112H mutation is highly recommended based on this case report.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Fabry disease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">R112H mutation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">migalastat</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">proteinuria</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">chronic kidney disease</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Lippincott Williams &amp; Wilkins</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0025-7974</Issn>
      <Volume>101</Volume>
      <Issue>7</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2022</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Silica-associated systemic lupus erythematosus with lupus nephritis and lupus pneumonitis A case report and a systematic review of the literature</ArticleTitle>
    <FirstPage LZero="delete">e28872</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kazuhiko</FirstName>
        <LastName>Fukushima</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Haruhito A.</FirstName>
        <LastName>Uchida</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuko</FirstName>
        <LastName>Fuchimoto</LastName>
        <Affiliation>Department of Respiratory Medicine, Okayama Rosai Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoyo</FirstName>
        <LastName>Mifune</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Mayu</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kenji</FirstName>
        <LastName>Tsuji</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masaru</FirstName>
        <LastName>Kinomura</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shinji</FirstName>
        <LastName>Kitamura</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yosuke</FirstName>
        <LastName>Miyamoto</LastName>
        <Affiliation>Department of Respiratory Medicine, Okayama Rosai Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sae</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Respiratory Medicine, Okayama Rosai Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Taisaku</FirstName>
        <LastName>Koyanagi</LastName>
        <Affiliation>Department of Respiratory Medicine, Okayama Rosai Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takumi</FirstName>
        <LastName>Kishimoto</LastName>
        <Affiliation>Department of Respiratory Medicine, Okayama Rosai Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">lupus nephritis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">lupus pneumonitis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">silicosis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">SLE</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier BV</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0006-291X</Issn>
      <Volume>599</Volume>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2022</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Vasohibin-1 has ƒ¿-tubulin detyrosinating activity in glomerular podocytes</ArticleTitle>
    <FirstPage LZero="delete">93</FirstPage>
    <LastPage>99</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Tomoyo</FirstName>
        <LastName>Mifune</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuri</FirstName>
        <LastName>Nakashima</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Tanimura</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences,</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasufumi</FirstName>
        <LastName>Sato</LastName>
        <Affiliation>New Industry Creation Hatchery Center, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>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 ƒ¿-tubulin. We aimed to examine the role of VASH1 in regulating ƒ¿-tubulin detyrosination in podocytes and the potential involvement of VASH1 deficiency in renal morphology. In normal mouse kidneys, detyrosinated ƒ¿-tubulin was mainly identified in glomeruli, especially in podocytes; meanwhile, in cultured immortalized podocytes, ƒ¿-tubulin detyrosination was promoted with cell differentiation. Notably, ƒ¿-tubulin detyrosination in glomeruli was diminished in Vash1 homozygous knockout (Vash1|/|) mice, and knockdown of VASH1 in cultured podocytes prevented ƒ¿-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 ƒ¿-tubulin detyrosination in podocytes was mainly regulated by VASH1 and that VASH1 deficiency-mediated decreases in ƒ¿-tubulin detyrosination led to minor alterations in podocyte morphology and predisposition to albuminuria. VASH1 expression and ƒ¿-tubulin detyrosination may be novel targets for maintaining glomerular filtration barrier integrity.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">Vasohibin-1</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Microtubules</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Detyrosination</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Podocytes</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Lippincott Williams • Wilkins</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0025-7974</Issn>
      <Volume>100</Volume>
      <Issue>50</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Management of corticosteroid-dependent eosinophilic interstitial nephritis A case report</ArticleTitle>
    <FirstPage LZero="delete">e28252</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Natsumi</FirstName>
        <LastName>Matsuoka-Uchiyama</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoyo</FirstName>
        <LastName>Mifune</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Chieko</FirstName>
        <LastName>Kawakita</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>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. &lt;br&gt;
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. &lt;br&gt;
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.&lt;br&gt; 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). &lt;br&gt;
Outcomes: MMF was well tolerated and PSL was successfully tapered to 5 mg/d; renal function stabilized over a 20-month period. &lt;br&gt;
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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">corticosteroid</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">drug-induced interstitial nephritis</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">eosinophils</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">mycophenolate mofetil</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">polypharmacy</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Elsevier BV</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0041-1345</Issn>
      <Volume>53</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>ABO Blood Incompatibility Positively Affects Early Graft Function: Single-Center Retrospective Cohort Study</ArticleTitle>
    <FirstPage LZero="delete">1494</FirstPage>
    <LastPage>1500</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Shogo</FirstName>
        <LastName>Watari</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Motoo</FirstName>
        <LastName>Araki</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koichiro</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kasumi</FirstName>
        <LastName>Yoshinaga</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuki</FirstName>
        <LastName>Maruyama</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yosuke</FirstName>
        <LastName>Mitsui</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takuya</FirstName>
        <LastName>Sadahira</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Risa</FirstName>
        <LastName>Kubota</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shingo</FirstName>
        <LastName>Nishimura</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuyuki</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hidemi</FirstName>
        <LastName>Takeuchi</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masashi</FirstName>
        <LastName>Kitagawa</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Morinaga</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shinji</FirstName>
        <LastName>Kitamura</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology, and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masami</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toyohiko</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasutomo</FirstName>
        <LastName>Nasu</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Science</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Background&lt;br&gt;
We investigated the association between ABO-incompatible (ABO-I) kidney transplantation and early graft function.&lt;br&gt;
&lt;br&gt;
Methods&lt;br&gt;
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 &gt;3 mg/dL and estimated glomerular filtration rate (eGFR) &lt;20 mL/min/1.73 m2. Logistic regression analysis was performed to analyze the effect of ABO-I on the incidence of SGF.&lt;br&gt;
&lt;br&gt;
Results&lt;br&gt;
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 &gt;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.&lt;br&gt;
&lt;br&gt;
Conclusion&lt;br&gt;
ABO-I reduces the incidence of SGF, which is associated with an inferior graft function up to 6 months.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Wiley</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>2050-4527</Issn>
      <Volume/>
      <Issue/>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Feasible kidney donation with living marginal donors, including diabetes mellitus</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Kasumi</FirstName>
        <LastName>Yoshinaga</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Motoo</FirstName>
        <LastName>Araki</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koichiro</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takanori</FirstName>
        <LastName>Sekito</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shogo</FirstName>
        <LastName>Watari</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuki</FirstName>
        <LastName>Maruyama</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yosuke</FirstName>
        <LastName>Mitsui</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takuya</FirstName>
        <LastName>Sadahira</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Risa</FirstName>
        <LastName>Kubota</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shingo</FirstName>
        <LastName>Nishimura</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kohei</FirstName>
        <LastName>Edamura</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuyuki</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hidemi</FirstName>
        <LastName>Takeuchi</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masashi</FirstName>
        <LastName>Kitagawa</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shinji</FirstName>
        <LastName>Kitamura</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masami</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toyohiko</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasutomo</FirstName>
        <LastName>Nasu</LastName>
        <Affiliation>Department of Urology, Graduate School of Medicine, Dentistry and Pharmaceutical Science, Okayama University</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>Objectives: To compare the donor outcomes of living donor kidney transplantation between standard donors (SDs) and marginal donors (MDs) including diabetic patients (MD + DM). &lt;br&gt;
Methods: MDs were defined according to Japanese guideline criteria: (a) age &gt;70-years, (b) blood pressure &lt;= 130/80 mmHg on hypertension medicine, (c) body mass index &gt;25 to &lt;= 32 kg/m(2), (d) 24-h creatinine clearance &gt;= 70 to &lt;80 ml/min/1.73 m(2), and (e) hemoglobin A1c &gt; 6.2 or &lt;= 6.5 with oral diabetic medicine. Fifty-three of 114 donors were MDs. We compared donor kidney functions until 60 months postoperatively. &lt;br&gt;
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 &lt; .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 &lt; .01), 63 vs. 57 (2, p &lt; .01), 64 vs. 56 (12, p &lt; .01), 63 vs. 57 (24, p &lt; .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 &gt;= 2 risk factors. &lt;br&gt;
Conclusions: Although long-term observation of donor kidney function is necessary, careful MD + DM selection had the potential to expand the donor pool.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">diabetes mellitus</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">kidney function</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">kidney transplantation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">marginal donor</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Japanese Society of Internal Medicine</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0918-2918</Issn>
      <Volume>60</Volume>
      <Issue>7</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2021</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Acute Kidney Injury Caused by Evans Syndrome with Systemic Lupus Erythematosus and Systemic Sclerosis</ArticleTitle>
    <FirstPage LZero="delete">1055</FirstPage>
    <LastPage>1060</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Natsumi</FirstName>
        <LastName>Matsuoka</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Haruki</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoko</FirstName>
        <LastName>Kurooka</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Sumari</FirstName>
        <LastName>Kato</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Chika</FirstName>
        <LastName>Higashi</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Division of Hemodialysis and Apheresis, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masaru</FirstName>
        <LastName>Kinomura</LastName>
        <Affiliation>Division of Hemodialysis and Apheresis, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nobuharu</FirstName>
        <LastName>Fujii</LastName>
        <Affiliation>Department of Transfusion Medicine, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Ken-Ei</FirstName>
        <LastName>Sada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry, and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      <Object Type="keyword">
        <Param Name="value">acute kidney injury</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Evans syndrome</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">autoimmune hemolytic anemia</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Lippincott, Williams &amp; Wilkins</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0025-7974</Issn>
      <Volume>99</Volume>
      <Issue>21</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Nivolumab-induced IgA nephropathy in a patient with advanced gastric cancer A case report</ArticleTitle>
    <FirstPage LZero="delete">e20464</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiromitsu</FirstName>
        <LastName>Kanzaki</LastName>
        <Affiliation>Department of Gastroenterology and Hepatology</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takahira</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuri</FirstName>
        <LastName>Nakashima</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Okada</LastName>
        <Affiliation>Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
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      </Object>
      <Object Type="keyword">
        <Param Name="value">gastric cancer</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">IgA nephropathy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">nivolumab</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">steroid</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>MDPI</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1422-0067</Issn>
      <Volume>21</Volume>
      <Issue>12</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Genetic Deletion of Vasohibin-2 Exacerbates Ischemia-Reperfusion-Induced Acute Kidney Injury</ArticleTitle>
    <FirstPage LZero="delete">4545</FirstPage>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hiromasa</FirstName>
        <LastName>Miyake</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Satoshi</FirstName>
        <LastName>Tanimura</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuri</FirstName>
        <LastName>Nakashima</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoyo</FirstName>
        <LastName>Morioka</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kana</FirstName>
        <LastName>Masuda</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasufumi</FirstName>
        <LastName>Sato</LastName>
        <Affiliation>New Industry Creation Hatchery Center, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>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) andVash2homozygous 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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">acute kidney injury</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">ischemia-reperfusion</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">oxidative stress</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">vasohibin-2</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">peritubular capillaries</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Public Library of Science</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>1932-6203</Issn>
      <Volume>15</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Podocyte autophagy is associated with foot process effacement and proteinuria in patients with minimal change nephrotic syndrome</ArticleTitle>
    <FirstPage LZero="delete"/>
    <LastPage/>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Ayu</FirstName>
        <LastName>Ogawa-Akiyama</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masashi</FirstName>
        <LastName>Kitagawa</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Keiko</FirstName>
        <LastName>Tanaka</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuzuki</FirstName>
        <LastName>Kano</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koki</FirstName>
        <LastName>Mise</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Nozomu</FirstName>
        <LastName>Otaka</LastName>
        <Affiliation>Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Morinaga</LastName>
        <Affiliation>Division of Medical Informatics,Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masaru</FirstName>
        <LastName>Kinomura</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Haruhito A.</FirstName>
        <LastName>Uchida</LastName>
        <Affiliation>Department of Chronic Kidney Disease and Cardiovascular Disease, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType/>
    <ArticleIdList>
      <ArticleId IdType="doi"/>
    </ArticleIdList>
    <Abstract>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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList/>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>74</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2020</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Robotic Renal Autotransplantation: A Feasibility Study in a Porcine Model</ArticleTitle>
    <FirstPage LZero="delete">53</FirstPage>
    <LastPage>58</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Risa</FirstName>
        <LastName>Kubota</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Motoo</FirstName>
        <LastName>Araki</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koichiro</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kasumi</FirstName>
        <LastName>Kawamura</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuki</FirstName>
        <LastName>Maruyama</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yosuke</FirstName>
        <LastName>Mitsui</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takuya</FirstName>
        <LastName>Sadahira</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuichi</FirstName>
        <LastName>Ariyoshi</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takehiro</FirstName>
        <LastName>Iwata</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Shingo</FirstName>
        <LastName>Nishimura</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Atsushi</FirstName>
        <LastName>Takamoto</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tomoko</FirstName>
        <LastName>Sako</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Kohei</FirstName>
        <LastName>Edamura</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuyuki</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuzuki</FirstName>
        <LastName>Kano</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masashi</FirstName>
        <LastName>Kitagawa</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masami</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toyohiko</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasutomo</FirstName>
        <LastName>Nasu</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/57953</ArticleId>
    </ArticleIdList>
    <Abstract> 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&#174; 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&#174; and irrigated on ice with Ringerfs 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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">renal autotransplantation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">robotic</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">porcine model</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">transplantation</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>71</Volume>
      <Issue>5</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2017</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Immunohistochemistry of Vasohibin-2 in Human Kidney Disease : Implications in Impaired Glucose Tolerance and Reduced Renal Function</ArticleTitle>
    <FirstPage LZero="delete">369</FirstPage>
    <LastPage>380</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Yuka</FirstName>
        <LastName>Arata</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medical, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medical, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norikazu</FirstName>
        <LastName>Hinamoto</LastName>
        <Affiliation>Pharmaceuticals and Medical Devices Agencies</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroko</FirstName>
        <LastName>Yamasaki</LastName>
        <Affiliation>Takahashi Central Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Human Resource Development of Dialysis Therapy for Kidney Disease, Okayama University Graduate School of Medical, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yohei</FirstName>
        <LastName>Maeshima</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medical, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Kanomata</LastName>
        <Affiliation>Department of Pathology 2, Kawasaki Medical School</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasufumi</FirstName>
        <LastName>Sato</LastName>
        <Affiliation>Department of Vascular Biology, Institute of Development, Aging, and Cancer, Tohoku University</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medical, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/55434</ArticleId>
    </ArticleIdList>
    <Abstract> 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 patientsf 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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">vasohibin-2</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">kidney disease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">vasa recta</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">medullary tubules</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>70</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2016</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>The Efficacy of Rituximab in High-risk Renal Transplant Recipients</ArticleTitle>
    <FirstPage LZero="delete">295</FirstPage>
    <LastPage>297</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Motoo</FirstName>
        <LastName>Araki</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Koichiro</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yosuke</FirstName>
        <LastName>Mitsui</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Risa</FirstName>
        <LastName>Kubota</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Takashi</FirstName>
        <LastName>Yoshioka</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yuichi</FirstName>
        <LastName>Ariyoshi</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasuyuki</FirstName>
        <LastName>Kobayashi</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masashi</FirstName>
        <LastName>Kitagawa</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Jun</FirstName>
        <LastName>Wada</LastName>
        <Affiliation>Department of Nephrology, Rheumatology, Endocrinology and Metabolism, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masami</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Center for Innovative Clinical Medicine, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Toyohiko</FirstName>
        <LastName>Watanabe</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Hotta</LastName>
        <Affiliation>Center for Innovative Clinical Medicine, Okayama University Hospital</Affiliation>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasutomo</FirstName>
        <LastName>Nasu</LastName>
        <Affiliation>Department of Urology, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences</Affiliation>
      </Author>
    </AuthorList>
    <PublicationType>Clinical Study Protocols</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/54507</ArticleId>
    </ArticleIdList>
    <Abstract>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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">end-stage renal disease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">immunosuppression</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">kidney transplantation</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>69</Volume>
      <Issue>1</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2015</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>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</ArticleTitle>
    <FirstPage LZero="delete">1</FirstPage>
    <LastPage>15</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Watatani</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroko</FirstName>
        <LastName>Yamasaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yohei</FirstName>
        <LastName>Maeshima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tatsuyo</FirstName>
        <LastName>Nasu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Norikazu</FirstName>
        <LastName>Hinamoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Haruyo</FirstName>
        <LastName>Ujike</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yoshiki</FirstName>
        <LastName>Sakai</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hirofumi</FirstName>
        <LastName>Makino</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/53117</ArticleId>
    </ArticleIdList>
    <Abstract>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 A2 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-ƒÀ1, ƒ¿-smooth muscle actin (ƒ¿-SMA) and MCP-1 compared to vehicle treatment. In cultured mouse mesangial cells, ONO-1301 concentration-dependently suppressed the increases in TGF-ƒÀ, type IV collagen, ƒ¿-SMA, MCP-1 and fibronectin induced by high ambient glucose, at least partly through prostacyclin (PGI2) 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.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">prostacyclin</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">ONO-1301</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">diabetic nephropathy</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">TGF-ƒÀ1</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">diabetes mellitus</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
  <Article>
    <Journal>
      <PublisherName>Okayama University Medical School</PublisherName>
      <JournalTitle>Acta Medica Okayama</JournalTitle>
      <Issn>0386-300X</Issn>
      <Volume>68</Volume>
      <Issue>4</Issue>
      <PubDate PubStatus="ppublish">
        <Year>2014</Year>
        <Month/>
      </PubDate>
    </Journal>
    <ArticleTitle>Renal Distribution of Vasohibin-1 in Patients with Chronic Kidney Disease</ArticleTitle>
    <FirstPage LZero="delete">219</FirstPage>
    <LastPage>233</LastPage>
    <Language>EN</Language>
    <AuthorList>
      <Author>
        <FirstName EmptyYN="N">Norikazu</FirstName>
        <LastName>Hinamoto</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yohei</FirstName>
        <LastName>Maeshima</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Daisuke</FirstName>
        <LastName>Saito</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroko</FirstName>
        <LastName>Yamasaki</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Katsuyuki</FirstName>
        <LastName>Tanabe</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Tatsuyo</FirstName>
        <LastName>Nasu</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hiroyuki</FirstName>
        <LastName>Watatani</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Haruyo</FirstName>
        <LastName>Ujike</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Masaru</FirstName>
        <LastName>Kinomura</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hitoshi</FirstName>
        <LastName>Sugiyama</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hikaru</FirstName>
        <LastName>Sonoda</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Naoki</FirstName>
        <LastName>Kanomata</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Yasufumi</FirstName>
        <LastName>Sato</LastName>
        <Affiliation/>
      </Author>
      <Author>
        <FirstName EmptyYN="N">Hirofumi</FirstName>
        <LastName>Makino</LastName>
        <Affiliation/>
      </Author>
    </AuthorList>
    <PublicationType>Original Article</PublicationType>
    <ArticleIdList>
      <ArticleId IdType="doi">10.18926/AMO/52788</ArticleId>
    </ArticleIdList>
    <Abstract>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
(r0.48, p0.001) or cortex (r0.64, pƒ0.0001), 2) interstitial cell infiltration and the number of VASH-1+ cells in the cortex (r0.34, p0.02), 3) the glomerular VEGFR-2+ area and the number of VASH-1+ cells in the glomerulus (r0.44, p0.01) or medulla (r0.63, p0.01). These results suggest that the renal levels of VASH-1 may be affected by local inflammation, crescentic lesions and VEGFR-2.</Abstract>
    <CoiStatement>No potential conflict of interest relevant to this article was reported.</CoiStatement>
    <ObjectList>
      <Object Type="keyword">
        <Param Name="value">chronic kidney disease</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">inflammation</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">Vasohibin-1</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">VEGF-A</Param>
      </Object>
      <Object Type="keyword">
        <Param Name="value">VEGFR-2</Param>
      </Object>
    </ObjectList>
    <ReferenceList/>
  </Article>
</ArticleSet>
