Details of a Researcher - Hashiguchi, Akinori

Papers - Hashiguchi, Akinori

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免疫チェックポイント阻害薬投与後に抗GBM抗体型糸球体腎炎と尿細管間質性腎炎を併発した1例

杉浦康平, 大島洋一, 中村彰良, 堤遼太郎, 圓谷泰章, 杉原晋之介, 加藤亜唯, 緒方大, 橋口明典, 小松素明

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 6-E ) 575 - 575 2023.09

Joint Work, ISSN 0385-2385

免疫チェックポイント阻害薬(ICI)投与後に抗GBM抗体型糸球体腎炎と尿細管間質性腎炎を併発したRPGNの1例

杉浦康平, 大島洋一, 中村彰良, 堤遼太郎, 圓谷泰章, 杉原晋之介, 加藤亜唯, 緒方大, 橋口明典, 小松素明

神奈川腎炎研究会抄録集 (神奈川腎炎研究会) 81回 np1 - np20 2023.09

Joint Work

一次性膜性腎症の経過中に腎静脈血栓症と肺血栓塞栓症を来した一例

中野朋香, 小松素明, 長澤瑞恵, 杉渉, 加藤亜唯, 藤井健太郎, 吉藤歩, 橋口明典, 竜崎崇和

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 6-E ) 625 - 625 2023.09

Joint Work, ISSN 0385-2385

リンパ系腫瘍に細線維状沈着物を伴うネフローゼ症候群を発症した一例

丸木友美, 吉本憲史, 中山尭振, 橋口明典, 山口慎太郎, 林香

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 6-E ) 583 - 583 2023.09

Joint Work, ISSN 0385-2385

ステロイド治療不応IgA優位沈着性糸球体腎炎に対し感染コントロールで透析離脱できた一例

伊藤敬, 川口隆久, 三崎美佳, 橋口明典, 尾田高志, 安藤孝

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 6-E ) 624 - 624 2023.09

Joint Work, ISSN 0385-2385

ステロイド治療が有効であったFSGS型C3腎症の一例

菊地隆之, 深澤佑介, 山中真理子, 大久保泰宏, 橋口明典

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 6-E ) 635 - 635 2023.09

Joint Work, ISSN 0385-2385

ステロイドが著効したイムノタクトイド腎症の2例

殿村駿, 吉本憲史, 満野竜ノ介, 橋口明典, 山口慎太郎, 林香

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 6-E ) 639 - 639 2023.09

Joint Work, ISSN 0385-2385

SARS-CoV-2ワクチン接種後に発熱,蛋白尿,血尿を認め,腎生検でC3腎症と診断した1例

中村共生, 井田真規子, 黄田宗明, 重原理宏, 神戸香織, 荒木崇志, 森永正二郎, 橋口明典

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 6-E ) 638 - 638 2023.09

Joint Work, ISSN 0385-2385

IgA血管炎と鑑別を要した本態性クリオグロブリン血症性糸球体腎炎の一例

堤遼太郎, 大島洋一, 中村彰良, 杉浦康平, 圓谷泰章, 杉原晋之介, 加藤亜唯, 橋口明典, 小松素明

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 6-E ) 607 - 607 2023.09

Joint Work, ISSN 0385-2385

Hepatitis B Virus-related Membranous Nephropathy with Crescentic Formation in an Inactive Carrier of Positive Hepatitis B Surface Antigen with Undetectable DNA under Anti-viral Treatment: A Case Report.

Kounoue N., Oguchi H., Mikami T., Yamaguchi Y., Hashiguchi A., Nagai H., Watanabe K., Furukawa S., Hisamatsu K., Sakai K.

Internal medicine (Tokyo, Japan) 63 ( 1 ) 101 - 106 2023.05

Joint Work, ISSN 0918-2918

A man who was an inactive hepatitis B virus (HBV) carrier with positive hepatitis B surface antigen (HBs antigen) and undetectable HBV-DNA under anti-viral treatment developed nephrotic syndrome at 52 years old, and a renal biopsy revealed advanced membranous nephropathy (MN) with focal cellular crescents, interstitial hemorrhaging, and peritubular capillaritis. Immunofluorescence studies demonstrated granular IgG deposition and HBs antigen-positivity along the capillaries. Glomeruli were negative for phospholipase A2 receptor 1. There were no clinical findings of systemic vasculitis. We considered MN combined with small-vessel vasculitis due to HBV infection. These results suggest that HBV-related kidney disease should be considered even in patients with an inactive HBV carrier status under treatment.

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IgA腎症におけるステロイド療法,扁摘と腎予後の関連性

平野景太, 川村哲也, 小池健太郎, 西川正子, 清水章, 城謙輔, 片渕律子, 橋口明典, 松崎慶一, 丸山彰一, 坪井伸夫, 成田一衛, 矢野裕一朗, 横尾隆, 鈴木祐介

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 3 ) 272 - 272 2023.05

Joint Work, ISSN 0385-2385

J-IGACSを用いたIgA腎症Oxford分類を構成する病変の組み合わせと治療反応性との関連の検討

坂口涼子, 城謙輔, 小此木英男, 中里毅, 橋口明典, 片渕律子, 清水章, 小池健太郎, 平野景太, 坪井伸夫, 川村哲也, 横尾隆, 成田一衛, 鈴木祐介

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 3 ) 320 - 320 2023.05

Joint Work, ISSN 0385-2385

J-IGACSを用いたIgA腎症Oxford分類を構成する病変の組み合わせと治療反応性との関連の検討

坂口涼子, 城謙輔, 小此木英男, 中里毅, 橋口明典, 片渕律子, 清水章, 小池健太郎, 平野景太, 坪井伸夫, 川村哲也, 横尾隆, 成田一衛, 鈴木祐介

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 3 ) 320 - 320 2023.05

Joint Work, ISSN 0385-2385

IgA腎症におけるステロイド療法,扁摘と腎予後の関連性

日本腎臓学会誌 ((一社)日本腎臓学会) 65 ( 3 ) 272 - 272 2023.05

Joint Work, ISSN 0385-2385

短腸症候群による二次性オキサローシスが腎機能障害の原因と考えられた1例

熊谷聡佑, 川口隆久, 有馬功一郎, 橋口明典, 高木英恵, 野崎博之, 安藤孝

日本内科学会関東地方会 (日本内科学会-関東地方会) 686回 48 - 48 2023.05

Joint Work

Immunohistochemistry May Not Replace Immunofluorescence in Paraffin-embedded Tissue for Detecting Masked Monoclonal Immunoglobulin Deposits: A Case Report.

Oda Y, Ikeda Y, Abe H, Hashiguchi A, Hatanaka K, Sawai T, Ushiku T, Nangaku M

Internal medicine (Tokyo, Japan) 62 ( 24 ) 3657 - 3661 2023.04

Joint Work, ISSN 0918-2918

An 84-year-old man developed a membranoproliferative glomerulonephritis pattern of injury, and the most likely cause detected during a workup was monoclonal IgG-λ in the urine and serum. Predominant IgG and λ light chain deposition was confirmed only by immunofluorescence using formalin-fixed, paraffin-embedded tissue and not by immunohistochemistry. A smaller and non-linear dynamic range of immunohistochemistry makes it less quantitative than immunofluorescence staining and may explain why immunohistochemistry failed to detect the light chain restriction. This case suggests that immunohistochemistry may not serve as a substitute for immunofluorescence on formalin-fixed, paraffin-embedded tissue in detecting masked monoclonal immunoglobulin deposits, although further research is warranted.

Access to Document (DOI)

DNA-damaged podocyte-CD8 T cell crosstalk exacerbates kidney injury by altering DNA methylation

Nakamichi R, Hishikawa A, Chikuma S, Yoshimura A, Sasaki T, Hashiguchi A, Abe T, Tokuhara T, Yoshimoto N, Nishimura E.S, Hama E.Y, Azegami T, Nakayama T, Hayashi K, Itoh H

Cell Reports (Cell Reports) 42 ( 4 ) 112302 - 112302 2023.04

Joint Work

Recent epigenome-wide studies suggest an association between blood DNA methylation and kidney function. However, the pathological importance remains unclear. Here, we show that the homing endonuclease I-PpoI-induced DNA double-strand breaks in kidney glomerular podocytes cause proteinuria, glomerulosclerosis, and tubulointerstitial fibrosis with DNA methylation changes in blood cells as well as in podocytes. Single-cell RNA-sequencing analysis reveals an increase in cytotoxic CD8+ T cells with the activating/costimulatory receptor NKG2D in the kidneys, which exhibit a memory precursor effector cell phenotype, and the CD44high memory CD8+ T cells are also increased in the peripheral circulation. NKG2D blockade attenuates the renal phenotype caused by podocyte DNA damage. Blood methylome shows increased DNA methylation in binding sites for STAT1, a transcription factor contributing to CD8+ T cell homeostasis. Collectively, podocyte DNA damage alters the blood methylome, leading to changes in CD8+ T cells, which contribute to sustained renal injury in chronic kidney disease.

Access to Document (DOI)

Significance of podocyte DNA damage and glomerular DNA methylation in CKD patients with proteinuria

Yoshimoto N, Hayashi K, Hishikawa A, Hashiguchi A, Nakamichi R, Sugita-Nishimura E, Yoshida-Hama E, Azegami T, Nakayama T, Itoh H

Hypertension Research (Hypertension Research) 46 ( 4 ) 1000 - 1008 2023.04

Joint Work, ISSN 09169636

The number of chronic kidney disease (CKD) patients is increasing worldwide, and it is necessary to diagnose CKD patients in earlier stages to improve their prognosis. Previously, in a study using human samples, we reported that DNA methylation and DNA damage in podocytes are potential markers for kidney function decline in IgA nephropathy; however, these candidate markers have not been adequately investigated in other glomerular diseases. Here, we report that the association of podocyte DNA damage and DNA methylation with eGFR decline and proteinuria differs depending on the type of glomerular disease. Patients diagnosed with minor glomerular abnormality (MGA, n = 33), membranous nephropathy (MN, n = 9) or diabetic nephropathy (DN, n = 10) following kidney biopsy at Keio University Hospital from 2015 to 2017 were included. In MGA patients, both podocyte DNA damage and glomerular DNA methylation were associated with the severity of proteinuria. In DN patients, podocyte DNA double-strand breaks (DSBs) and glomerular DNA methylation were associated with an eGFR decline. When patients with urinary protein levels of more than 1 g/gCr were examined, fewer podocyte DNA DSBs were detected in MN patients than in MGA patients, and the level of glomerular DNA methylation was lower in MN patients than in MGA or DN patients. These results indicate that investigating podocyte DNA DSBs and DNA methylation changes may be useful for understanding the pathogenesis of CKD with proteinuria in humans. [Figure not available: see fulltext.].

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Case report: Importance of early and continuous tocilizumab therapy in nephrotic syndrome associated with idiopathic multicentric Castleman disease: A case series.

Daiki Kojima, Shintaro Yamaguchi, Akinori Hashiguchi, Kaori Hayashi, Kiyotaka Uchiyama, Norifumi Yoshimoto, Keika Adachi, Takashin Nakayama, Ken Nishioka, Takaya Tajima, Kohkichi Morimoto, Jun Yoshino, Tadashi Yoshida, Toshiaki Monkawa, Takeshi Kanda, Hiroshi Itoh

Frontiers in medicine (Frontiers in Medicine) 9 1037032 - 1037032 2023.01

Joint Work, ISSN 2296-858X

Idiopathic multicentric Castleman disease (iMCD) is a systemic and polyclonal lymphoproliferative disease involving multiple organs, including the kidneys, due to the overproduction of interleukin-6 (IL-6). Recently, several reports have suggested that excessive IL-6 actions in iMCD could have a causal relationship with the development of diverse histopathological renal manifestations that cause nephrotic syndrome. However, the treatment for such cases remains unclear. We report a series of three cases of nephrotic syndrome due to iMCD that helps to delineate the importance of early and continuous therapy with the anti-interleukin-6 receptor antibody tocilizumab. First, treatment was suspended for infectious control, and the patient presented with nephrotic syndrome due to diffuse mesangial and endocapillary hypercellularity without immune deposits complicating acute kidney injury. Second, iMCD was treated with prednisolone alone. The patient suddenly developed nephrotic syndrome due to immune-complex glomerulonephritis, not otherwise specified, complicated with acute kidney injury. In the third case, nephrotic syndrome secondary to membranous glomerulonephritis was diagnosed, with a skin rash and IgE antibodies to tocilizumab, and was therefore treated with prednisolone alone. In contrast to the first two cases, the third progressed to end-stage renal disease on hemodialysis. Taken together, this series suggests that clinicians should maintain clinical vigilance for iMCD as a possible underlying component of nephrotic syndrome, since iMCD presents with a variety of renal pathologies. Prompt initiation and continuous administration of tocilizumab are likely key determinants of renal outcomes in such cases. In particular, when tocilizumab is suspended due to infection or in the perioperative period, consideration of its expeditious resumption should be made, taking into account both the withdrawal period and systemic conditions.

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Antineutrophil cytoplasmic antibody-associated vasculitis predominantly manifesting tubulointerstitial nephritis: A case report.

Ken Nishioka, Shintaro Yamaguchi, Akinori Hashiguchi, Norifumi Yoshimoto, Takaya Tajima, Itaru Yasuda, Kiyotaka Uchiyama, Kenji Kaneko, Mitsuhiro Aso, Jun Yoshino, Toshiaki Monkawa, Takeshi Kanda, Kaori Hayashi, Hiroshi Itoh

SAGE open medical case reports (SAGE Open Medical Case Reports) 11 2050313X231197324 2023.01

Joint Work, ISSN 2050-313X

The common histopathology of antineutrophil cytoplasmic antibody-associated vasculitis comprises pauci-immune crescentic glomerulonephritis with concomitant tubulointerstitial nephritis. Tubulointerstitial nephritis in the absence of glomerular involvement in patients with antineutrophil cytoplasmic antibody-associated vasculitis is uncommon. We report a case of antineutrophil cytoplasmic antibody-associated vasculitis-associated acute kidney injury manifesting as tubulointerstitial nephritis without glomerulonephritis. A 75-year-old woman with fever, cough, and myalgia developed kidney dysfunction with inflammatory reactions and tubular-type proteinuria, without glomerular hematuria. A kidney biopsy revealed tubulointerstitial nephritis with arteritis. We ruled out important underlying etiologies of tubulointerstitial nephritis, including infection, drug reactions, and autoimmune diseases. Since chest high-resolution computed tomography demonstrated mild interstitial pneumonia in bilateral lower lung fields, myeloperoxidase antineutrophil cytoplasmic antibody was measured and found to be positive. Therefore, we diagnosed the patient with antineutrophil cytoplasmic antibody-associated vasculitis-associated tubulointerstitial nephritis but not glomerulonephritis, and interstitial pneumonia. The patient's kidney function and symptoms markedly improved with prednisolone treatment. Clinicians should maintain high-level vigilance for antineutrophil cytoplasmic antibody-associated vasculitis as a possible underlying component of tubulointerstitial nephritis, particularly when kidney function deteriorates with tubulointerstitial injuries without glomerular features.

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