Updated on 2022/12/01

写真a

 
IINO Noriaki
 
Organization
University Medical and Dental Hospital Uonuma Institute of Community Medicine Specially Appointed Professor
Title
Specially Appointed Professor
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Degree

  • Doctor (Medicine) ( 2001.3   Niigata University )

Research Interests

  • 腎臓発生

  • 疫学

  • 透析医療

  • 腎臓内科

  • 内科学

Research Areas

  • Life Science / Medical management and medical sociology

  • Life Science / Nephrology

Research History (researchmap)

  • Uonuma institute of Community Medicine, Niigata University Medical and Dental Hospital   Department of Clinical Nephrology and Rheumatology   Specially Appointed Professor

    2015.4

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  • Niigata University   Medical and Dental Hospital   Assistant Professor

    2012.11 - 2015.3

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  • Niigata University   Assistant Professor

    2011.4 - 2012.11

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  • Niigata University   Specially Appointed Assistant Professor

    2010.4 - 2011.3

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  • Niigata University   Specially Appointed Assistant Professor

    2006.4 - 2009.3

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  • Niigata University   Medical and Dental Hospital, Internal Medicine II

    2005.7 - 2005.11

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  • University of California, San Diego

    2003.7 - 2005.6

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  • 新潟県立がんセンター新潟病院   医長

    2001.7 - 2003.6

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  • Niigata University   Medical and Dental Hospital, Internal Medicine II

    1999.9 - 2001.6

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  • 新潟県立中央病院   内科医

    1997.1 - 1997.6

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  • 両津市民病院   内科医

    1996.7 - 1996.12

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  • Niigata University   Medical and Dental Hospital, Internal Medicine II

    1996.4 - 1996.6

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  • Toranomon Hospital

    1994.4 - 1996.3

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Research History

  • Niigata University   University Medical and Dental Hospital UONUMA CHIIKI IRYO KYOIKU CENTER JUNBISHITU   Specially Appointed Professor

    2015.4

  • Niigata University   University Medical and Dental Hospital Nephrology and Rheumatology   Assistant Professor

    2012.11 - 2015.3

  • Niigata University   Graduate School of Medical and Dental Sciences   Assistant Professor

    2011.4 - 2012.11

  • Niigata University   Graduate School of Medical and Dental Sciences   Specially Appointed Assistant Professor

    2010.4 - 2011.3

  • Niigata University   Graduate School of Medical and Dental Sciences   Specially Appointed Assistant Professor

    2006.4 - 2009.3

Education

  • Niigata University   Graduate School of Medical and Dental Sciences   Department of Medicine II

    1997.4 - 2001.3

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  • Niigata University   Department of Medicine

    1988.4 - 1994.3

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Professional Memberships

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Papers

  • Rationale and study design of a clinical trial to assess the effects of LDL apheresis on proteinuria in diabetic patients with severe proteinuria and dyslipidemia Reviewed

    Takashi Wada, Eri Muso, Shoichi Maruyama, Akinori Hara, Kengo Furuichi, Kenichi Yoshimura, Mariko Miyazaki, Eiichi Sato, Masanori Abe, Yugo Shibagaki, Ichiei Narita, Hitoshi Yokoyama, Noriko Mori, Yukio Yuzawa, Takeshi Matsubara, Tatsuo Tsukamoto, Jun Wada, Takafumi Ito, Kosuke Masutani, Kazuhiko Tsuruya, Shoichi Fujimoto, Akihiro Tsuda, Hitoshi Suzuki, Kenji Kasuno, Yoshio Terada, Takeshi Nakata, Noriaki Iino, Shuzo Kobayashi

    Clinical and Experimental Nephrology   22 ( 3 )   591 - 596   2018.6

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:Springer Tokyo  

    Background: Diabetic nephropathy is a leading cause of end-stage kidney disease in the world. Although various types of treatment for diabetes, hypertension and dyslipidemia have improved prognosis and quality of life in patients with diabetic nephropathy, there still exist some diabetic patients with severe proteinuria showing poor prognosis. This clinical trial, LICENSE, aims to confirm the impact of LDL apheresis on proteinuria exhibiting hyporesponsiveness to treatment. Methods: This ongoing trial is a multicenter, prospective study of diabetic patients with severe proteinuria. The objective is to examine the impact of LDL apheresis on proteinuria in patients with diabetic nephropathy. The other subject is to investigate safety of LDL apheresis in these patients. Results: The subjects consist of diabetic patients with serum creatinine (Cr) levels below 2 mg/dL who present severe proteinuria above 3 g/g Cr or 3 g/day and LDL cholesterol above 120 mg/dL. The target number of registered patients will be 35 patients. Urinary protein excretion and renal function will be observed for 24 weeks after the treatment of LDL apheresis. Conclusion: This study will determine the effectiveness and safety of LDL apheresis for diabetic nephropathy patients with severe proteinuria and dyslipidemia.

    DOI: 10.1007/s10157-017-1488-4

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  • Immune checkpoint inhibitor (nivolumab)-associated kidney injury and the importance of recognizing concomitant medications known to cause acute tubulointerstitial nephritis: A case report Reviewed

    Ryo Koda, Hirofumi Watanabe, Masafumi Tsuchida, Noriaki Iino, Kazuo Suzuki, Go Hasegawa, Naofumi Imai, Ichiei Narita

    BMC Nephrology   19 ( 1 )   2018.2

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:BioMed Central Ltd.  

    Background: Acute tubulointerstitial nephritis (ATIN) has been increasingly recognized as an important manifestation of kidney injury associated with the use of immune checkpoint inhibitors (anti-PD-1 and anti-CTLA-4). While the exact pathophysiology remains unknown, corticosteroids are the mainstay of management. Case presentation: We describe a 67-year-old man with stage IV non-small-cell lung cancer who developed kidney injury during treatment with the anti-PD-1 antibody nivolumab. A kidney biopsy showed ATIN without granuloma formation. Considering their mechanism of action, immune checkpoint inhibitors can alter immunological tolerance to concomitant drugs that have been safely used for a long time. For more than 4 years before the initiation of nivolumab therapy, the patient had been receiving the proton pump inhibitor lansoprazole, known to cause drug-induced ATIN, without significant adverse events including kidney injury. He showed rapid improvement in kidney function in 3 days (creatinine decreased from 2.74 to 1.82 mg/dl) on discontinuation of lansoprazole. He then received 500 mg intravenous methylprednisolone for 3 days followed by 1 mg/kg/day oral prednisolone and his creatinine levels eventually stabilized around 1.7 mg/dl. Drug-induced lymphocyte stimulation test (DLST) for lansoprazole was positive. Conclusions: The rapid improvement of kidney function after discontinuation and DLST positivity indicate that lansoprazole contributed to the development of ATIN during nivolumab therapy. Considering the time course, it is plausible that nivolumab altered the long-lasting immunological tolerance against lansoprazole in this patient. To the best of our knowledge, this is the first case report of DLST positivity for a drug that had been used safely before the initiation of an immune checkpoint inhibitor. Although corticosteroid therapy is recommended, the recognition and discontinuation of concomitant drugs, especially those known to induce ATIN, is necessary for the management of kidney injury associated with anti-PD-1 therapy.

    DOI: 10.1186/s12882-018-0848-y

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  • Legionella Pneumonia Complicated with Acquired Fanconi Syndrome Reviewed

    Koda Ryo, Itoh Ryo, Tsuchida Masafumi, Ohashi Kazumasa, Iino Noriaki, Takada Toshinori, Narita Ichiei

    INTERNAL MEDICINE   57 ( 20 )   2975 - 2980   2018

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    Publishing type:Research paper (scientific journal)   Publisher:Japanese Society of Internal Medicine  

    DOI: 10.2169/internalmedicine.0942-18

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  • The endocytic adaptor protein ARH associates with motor and centrosomal proteins and is involved in centrosome assembly and cytokinesis Reviewed

    Sanna Lehtonen, Mehul Shah, Rikke Nielsen, Noriaki Iino, Jennifer J. Ryan, Huilin Zhou, Marilyn G. Farquhar

    MOLECULAR BIOLOGY OF THE CELL   19 ( 7 )   2949 - 2961   2008.7

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:AMER SOC CELL BIOLOGY  

    Numerous proteins involved in endocytosis at the plasma membrane have been shown to be present at novel intracellular locations and to have previously unrecognized functions. ARH ( autosomal recessive hypercholesterolemia) is an endocytic clathrin-associated adaptor protein that sorts members of the LDL receptor superfamily ( LDLR, megalin, LRP). We report here that ARH also associates with centrosomes in several cell types. ARH interacts with centrosomal (gamma-tubulin and GPC2 and GPC3) and motor ( dynein heavy and intermediate chains) proteins. ARH cofractionates with gamma-tubulin on isolated centrosomes, and gamma-tubulin and ARH interact on isolated membrane vesicles. During mitosis, ARH sequentially localizes to the nuclear membrane, kinetochores, spindle poles and the midbody. Arh(-/-) embryonic fibroblasts (MEFs) show smaller or absent centrosomes suggesting ARH plays a role in centrosome assembly. Rat-1 fibroblasts depleted of ARH by siRNA and Arh(-/-) MEFs exhibit a slower rate of growth and prolonged cytokinesis. Taken together the data suggest that the defects in centrosome assembly in ARH depleted cells may give rise to cell cycle and mitotic/cytokinesis defects. We propose that ARH participates in centrosomal and mitotic dynamics by interacting with centrosomal proteins. Whether the centrosomal and mitotic functions of ARH are related to its endocytic role remains to be established.

    DOI: 10.1091/mbc.E07-05-0521

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  • Anemia is a predictive factor for the development of CKD only in man, but not in woman, of general Japanese population Reviewed

    Noriaki Iino, Ichiei Narita, Akihiko Saito, Fumitake Gejyo

    NEPHROLOGY   13   A34 - A34   2008.5

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  • Alterations in serum phosphate levels predict the long-term response to intravenous calcitriol therapy in dialysis patients with secondary hyperparathyroidism Reviewed

    Kiyoko Hosaka, Junichiro James Kazama, Suguru Yamamoto, Yumi Ito, Noriaki Iino, Hiroki Maruyama, Akihiko Saito, Ichiei Narita, Fumitake Gejyo

    JOURNAL OF BONE AND MINERAL METABOLISM   26 ( 2 )   185 - 190   2008.3

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:SPRINGER TOKYO  

    Calcitriol therapy is a central strategy for the treatment of uremic secondary hyperparathyroidism. Although indiscriminate use of calcitriol may lead to worse outcomes, it is difficult to make a decision to discontinue calcitriol therapy when its parathyroid suppression effect remains unsatisfactory. In this study, intravenous calcitriol was administered to 120 chronic hemodialysis patients. Therapy continued for 48 weeks or until plasma intact parathyroid hormone (iPTH) levels decreased to below 300 pg/ml or until the development of any significant adverse effect. Of the 120 patients, the treatment goal was achieved in 47 patients during the first 4 weeks, in 10 during the next 4 weeks, and in 22 patients thereafter. Logistic regression analysis and stepwise regression analysis revealed that iPTH levels were the only significant predictor of the response to calcitriol therapy at weeks 0 and 4. Besides iPTH, the inorganic phosphate (P) levels were another significant predictor of the ultimate response to calcitriol therapy at week 8. The point of best discrimination for successful treatment was P = 6.0 mg/dl at week 8, or P level at week 8/pretreatment P level = 1.0. In conclusion, the P level at week 8 is a predictor of the response to calcitriol therapy for uremic secondary hyperparathyroidism. Changes in treatment are recommended if patients show unsatisfactory parathyroid suppression with a hyperphosphatemic tendency.

    DOI: 10.1007/s00774-007-0809-1

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  • Longitudinal change in renal function in patients with idiopathic dilated cardiomyopathy without renal insufficiency at initial diagnosis Reviewed

    Komei Tanaka, Masahiro Ito, Makoto Kodama, Hiroki Maruyama, Makoto Hoyano, Wataru Mitsuma, Noriaki Iino, Satoru Hirono, Yuji Okura, Fumitake Gejyo, Naohito Tanabe, Yoshifusa Aizawa

    CIRCULATION JOURNAL   71 ( 12 )   1927 - 1931   2007.12

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:JAPANESE CIRCULATION SOC  

    Background Impaired renal function is associated with poor outcomes among patients with chronic heart failure (CHF). However, the long-term changes in renal function in CHF patients without renal insufficiency at initial diagnosis remain unclear.
    Methods and Results Retrospective analysis of patients presenting with idiopathic dilated cardiomyopathy (IDCM) from 1984 to 2003 and who had normal renal function defined as estimated creatinine clearance (eCcr) >= 60ml/min at the first diagnosis. Cumulative event proportions and renal insufficiency defined as eCcr < 60ml/min were calculated by the Kaplan-Meier method. The predictors of renal insufficiency were evaluated by logistic regression analysis. Impaired renal function developed in 20% during an 8-year follow-up and in 50% during a 20-year follow-up. Advanced age at the first diagnosis, high frequency of admissions, and hypotension during the clinical course were associated with the occurrence of impaired renal function. Beta-blocker therapy was a negative predictor of renal insufficiency.
    Conclusions In patients with IDCM without renal insufficiency at initial diagnosis, worsening renal function occurred during the follow-up period. Frequent admissions, hypotension, and lacking ss-blocker therapy were associated with a poor prognosis in renal function.

    DOI: 10.1253/circj.71.1927

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  • Role of megalin, a proximal tubular endocytic receptor, in calcium and phosphate homeostasis Reviewed

    Akihiko Saito, Noriaki Iino, Tetsuro Takeda, Fumitake Gejyo

    THERAPEUTIC APHERESIS AND DIALYSIS   11   S23 - S26   2007.10

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:WILEY-BLACKWELL  

    Megalin is expressed at the apical membranes of proximal tubule cells, acting as an endocytic receptor for a variety of ligands filtered by glomeruli. Megalin, also known as a Ca(2+)-binding receptor, is thought to be involved in systemic and intrarenal calcium and phosphate homeostasis. The complex of 25( OH) D(3) and vitamin D-binding protein is endocytosed via megalin into proximal tubule cells, leading to the activation of 25( OH) D3 to 1, 25( OH) D3 in the cells. Megalin knockout mice revealed impaired osteogenesis due to vitamin D deficiency. Megalin is also involved in the metabolism of parathyroid hormone and the regulation of the sodium phosphate cotransporter NaPi-IIa. Decreased expression of megalin may be associated with the pathogenesis of hyperphosphaturia observed in patients with Dent's disease. Further studies will elucidate more detailed roles of megalin in pathological states and the mechanisms for interacting with other molecules for the endocytic functions.

    DOI: 10.1111/j.1744-9987.2007.00514.x

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  • Megalin-mediated endocytosis of cystatin C in proximal tubule cells Reviewed

    Ryohei Kaseda, Noriaki Iino, Michihiro Hosojima, Tetsuro Takeda, Kiyoko Hosaka, Asako Kobayashi, Keiko Yamamoto, Akiyo Suzuki, Ayaka Kasai, Yoshiki Suzuki, Fumitake Gejyo, Akihiko Saito

    BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS   357 ( 4 )   1130 - 1134   2007.6

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:ACADEMIC PRESS INC ELSEVIER SCIENCE  

    Serum levels of cystatin C, an endogenous cysteine protemase inhibitor, are often used as an indicator of glomerular filtration rate. Although it is known that cystatin C is filtered by glomeruli and metabolized in proximal tubule cells (PTC), the precise molecular mechanism underlying this process is undetermined. Using quartz-crystal microbalance analyses, we demonstrate that cystatin C binds directly to megalin, an endocytic receptor in PTC, in a Ca(+)-dependent manner. We also find that cystatin C is endocytosed specifically via megalin in rat yolk sac epithelium-derived L2 cells which share a variety of characteristics with PTC. Finally, it? vivo studies using kidney-specific megalin knockout mice provide evidence that megalin mediates proximal tubular uptake of cystatin C. We conclude that megalin is an endocytic receptor of cystatin C in PTC. (c) 2007 Elsevier Inc. All rights reserved.

    DOI: 10.1016/j.bbrc.2007.04.072

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  • Functional characterization of a novel missense CLCN5 mutation causing alterations in proximal tubular endocytic machinery in Dent's disease Reviewed

    Atsuhito Tanuma, Hiroyoshi Sato, Tetsuro Takeda, Michihiro Hosojima, Hiroaki Obayashi, Hitomi Hama, Noriaki Iino, Kiyoko Hosaka, Ryohei Kaseda, Naofumi Imai, Mitsuhiro Ueno, Maya Yamazaki, Kenji Sakimura, Fumitake Gejyo, Akihiko Saito

    NEPHRON PHYSIOLOGY   107 ( 4 )   P87 - P97   2007

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

    Background/Aims: Mutations of the endosomal chloride/ proton exchanger gene, CLCN5, cause Dent's disease, an X-linked recessive proximal tubular disorder. The renal endocytic system was found to be affected in clcn5 knockout mice. However, the impaired endocytic machinery of Dent's disease patients has not been thoroughly investigated. Methods: The CLCN5 gene was sequenced in a Japanese patient with Dent's disease and his family. The loss-of-function phenotype of the missense CLCN5 mutation was investigated by gene expression in Xenopus oocytes and CHO cells. Immunohistochemical analysis was performed on kidney biopsy specimens for endocytic machinery proteins, megalin, cubilin, and disabled-2 (Dab2) in proximal tubules. Results: Genomic analysis revealed a novel G-to-A transition at the first nucleotide of the 333rd codon of CLCN5, causing a substitution of glycine with arginine. Inefficient expression of the mutant gene in Xenopus oocytes resulted in abolished chloride currents. Impaired N-glycosylation of the mutant protein was evident in the DNA-transfected CHO cells. Proximal tubular expression of megalin, cubilin, and Dab2 was markedly reduced and irregular staining in some portions was observed in the patient compared with controls. Conclusions: A novel G333R CLCN5 mutation caused defective expression of megalin, cubilin, and Dab2 in a patient with Dent's disease. Copyright (c) 2007 S. Karger AG, Basel.

    DOI: 10.1159/000111253

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  • Bioengineered implantation of megalin-expressing cells: A potential intracorporeal therapeutic model for uremic toxin protein clearance in renal failure Reviewed

    A Saito, JJ Kazama, N Iino, KJ Cho, N Sato, H Yamazaki, Y Oyama, T Takeda, RA Orlando, F Shimizu, Y Tabata, F Gejyo

    JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY   14 ( 8 )   2025 - 2032   2003.8

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:LIPPINCOTT WILLIAMS & WILKINS  

    Patients who have renal failure and are on dialysis therapy experience serious complications caused by low-molecular-weight uremic toxin proteins normally filtered by glomeruli and metabolized by proximal tubule cells (PTC). Dialysis-related amyloidosis is one such complication induced by systemic deposition of amyloid proteins derived from 12-kD beta(2)-microglobulin (beta(2)-M). Despite the use of high-flux membrane hemodialysis devices and direct absorbent columns, the removal of beta(2)-M is suboptimal, because the effects are transient and insufficient. Megalin is expressed in the apical membranes of PTC and recognized as a multiligand endocytic receptor that binds numerous low-molecular-weight proteins, including, beta(2)-M. This study tested the feasibility of an intra corporeal therapeutic model of continuous beta(2)-m removal using megalin-expressing cell implantation. By cell association and degradation assays, rat yolk sac-derived L2 cells were identified to internalize and degrade beta(2)-M via megalin. The cells were effectively implanted within the subcutaneous tissues of nude mice using a type I collagen scaffold and a method inducing local angiogenesis. After nephrectomy and intraperitoneal injection with I-125-beta(2)-m, it was found that the implanted cells took up the labeled ligand, efficiently removing it from the blood. Bioengineered implantation of megalin-expressing cells may represent a new supportive therapy for dialysis patients to compensate for the loss of renal protein metabolism and remove uremic toxin proteins.

    DOI: 10.1097/01.ASN.0000078804.98322.4A

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  • Adult onset anaphylactoid purpura with severe gastrointestinal involvement. Reviewed

    Oshima K, Iino N, Sasaki N, Takahashi N, Tanabe Y, Ito S, Ueno M, Nishi S, Tsukada H, Narita I, Hasegawa G, Suzuki E, Gejyo F

    Internal medicine (Tokyo, Japan)   42 ( 5 )   436 - 442   2003.5

  • [Swallow syncope]. Reviewed

    Iino N, Kojima A, Motoyama H, Akiyama N, Okada Y

    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine   91 ( 12 )   3494 - 3496   2002.12

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    Language:Japanese   Publisher:The Japanese Society of Internal Medicine  

    DOI: 10.2169/naika.91.3494

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    Other Link: https://jlc.jst.go.jp/DN/JALC/00162769883?from=CiNii

  • [Acquired coagulation abnormality due to factor V inhibitor]. Reviewed

    Iino N, Maruyama H, Gejyo F

    Nihon Naika Gakkai zasshi. The Journal of the Japanese Society of Internal Medicine   91 ( 11 )   3295 - 3297   2002.11

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  • Kidney-targeted naked DNA transfer by retrograde renal vein injection in rats Reviewed

    H Maruyama, N Higuchi, Y Nishikawa, H Hirahara, N Iino, S Kameda, H Kawachi, E Yaoita, F Gejyo, JI Miyazaki

    HUMAN GENE THERAPY   13 ( 3 )   455 - 468   2002.2

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    Language:English   Publishing type:Research paper (scientific journal)   Publisher:MARY ANN LIEBERT INC PUBL  

    Kidney-targeted gene transfer is expected to revolutionize the treatment of renal diseases. Previous gene transfer methods using nonviral vectors administered via renal arterial, pelvic, or ureteric routes into the glomerulus, tubules, or interstitial fibroblasts have resulted in low-level expression for <1 month. The peritubular capillaries (PTC) network is one of the main targets of kidney transplant rejection and of progressive tubulointerstitial fibrosis, which typifies all progressive renal diseases. To access the PTC, we retrogradely injected a lacZ expression plasmid in Ringer's solution into the renal vein of rats. We detected lacZ expression exclusively in the interstitial fibroblasts near the PTC of the injected kidney by immunoelectron microscopic analysis. Nephrotoxicity attributable to gene transfer was not apparent. We then used a rat erythropoietin (Epo) expression plasmid vector, pCAGGS-Epo, in a reporter assay. We obtained maximal Epo expression when the DNA solution was injected within 5 sec, and with a volume of 1.0 ml. We observed a dose-response relationship between serum Epo levels and the amount of injected DNA up to 100 μg. We detected the transgene-derived Epo mRNA by reverse transcription polymerase chain reaction only in the kidneys injected with pCAGGS-Epo. After an injection of 100 mg of pCAGGS-Epo, the serum Epo levels peaked at 208.3 +/- 71.8 mU/ml at week 5, and gradually decreased to 116.2 +/- 38.7 mU/ml at week 24. A similar pattern was obtained using smaller doses of plasmid, 2 μg or 30 μg of pCAGGS-Epo. Transgene-derived Epo secretion resulted in significant erythropoiesis. This novel technique is simple and safe, allowing high-level and long-term stable gene expression specific to the fibroblasts near the PTC, and should have therapeutic value for future applications in humans.

    DOI: 10.1089/10430340252792585

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MISC

  • 【透析食の調理者と透析患者】 全国各地の透析患者の食事事情 過疎地域に住む左半身麻痺のある50歳代男性患者

    篠原 未希, 恩田 佳代子, 飯野 則昭

    臨床透析   34 ( 11 )   1353 - 1358   2018.10

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    Language:Japanese   Publisher:(株)日本メディカルセンター  

    <文献概要>魚沼医療圏は買い物,通院などに車が不可欠である.家事全般を担当している透析患者が,大腿骨転子部骨折をし,車いす生活となった.骨折前はカリウム制限やリン制限,塩分制限に対する食事の問題点があっても,本人のみへ栄養指導を行うことで検査データの改善ができていた.骨折後は家事に関して家族の協力は得られず,食事内容の偏り,摂取エネルギー・栄養素不足となり,低栄養が問題となりONS(経口的栄養補助)が処方されている.都市部に比べ,社会サービスの選択肢が少ない過疎地では,透析患者を取り巻く状況が深刻である.本人のみへの栄養指導では解決に至らず,家族を巻き込んだ指導が必要と考える.

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  • 一側の下腿浮腫を契機とし,前立腺生検で組織診断したIgG4関連動脈周囲炎の一例

    土田 雅史, 乾 幸平, 甲田 亮, 中川 由紀, 飯野 則昭, 西山 勉, 小熊 文昭, 成田 一衛

    日本腎臓学会誌   60 ( 6 )   929 - 929   2018.8

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  • 肝細胞癌術前の腎機能障害精査でアデホビルによるFanconi症候群と診断された糖尿病合併腎臓病患者の一例

    甲田 亮, 上田 雅史, 渡辺 博文, 飯野 則昭, 成田 一衛

    日本腎臓学会誌   60 ( 6 )   889 - 889   2018.8

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  • 当院のシャント管理について

    今井 宗次郎, 笛木 真理子, 服部 高志, 本田 広貴, 上村 真由美, 草本 里美, 井口 かおる, 桐生 智, 和田 典子, 伊藤 聖学, 飯野 則昭, 田部井 薫

    日本透析医学会雑誌   51 ( Suppl.1 )   833 - 833   2018.5

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    Language:Japanese   Publisher:(一社)日本透析医学会  

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  • 魚沼地域医療再編後の腹膜透析診療の現状

    甲田 亮, 土田 雅史, 飯野 則昭, 渡辺 博文, 成田 一衛

    日本透析医学会雑誌   51 ( Suppl.1 )   660 - 660   2018.5

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  • 魚沼地域医療再編後に開設された新潟県立十日町病院腎臓外来から見たCKD医療連携の現状

    甲田 亮, 土田 雅史, 渡辺 博文, 飯野 則昭, 吉嶺 文俊, 成田 一衛

    日本腎臓学会誌   60 ( 3 )   400 - 400   2018.4

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  • 糖尿病腎症と非糖尿病腎症の血液透析導入期でのSwept source OCTによる脈絡膜評価

    中野 英之, 長谷部 日, 村上 健治, 張 大行, 近藤 大介, 飯野 則昭, 福地 健郎

    日本眼科学会雑誌   122 ( 臨増 )   235 - 235   2018.3

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    Language:Japanese   Publisher:(公財)日本眼科学会  

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  • 一目瞭然!目で診る症例

    渡辺 博文, 甲田 亮, 飯野 則昭, 成田 一衛

    日本内科学会雑誌   107 ( 2 )   315 - 317   2018.2

  • 腹膜透析に関連した非結核性抗酸菌感染症7例の検討

    酒巻 裕一, 川村 和子, 山本 卓, 忰田 亮平, 飯野 則昭, 田邊 嘉也, 成田 一衛, 丸山 弘樹

    腎と透析   83 ( 別冊 腹膜透析2017 )   194 - 195   2017.11

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  • ニボルマブ加療中の急性尿細管間質性腎炎発症にプロトンポンプ阻害薬の関与が考えられた進行期肺癌の1例

    甲田 亮, 土田 雅史, 渡辺 博文, 飯野 則昭, 鈴木 和夫, 今井 直史, 長谷川 剛, 成田 一衛

    日本腎臓学会誌   59 ( 6 )   890 - 890   2017.9

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  • 12 当院初の膵腎同時移植例における血糖コントロールについて(Ⅰ.一般演題, 第41回新潟糖尿病談話会)

    細島 康宏, 飯野 則昭, 山本 智, 大矢 洋, 佐藤 好信, 齋藤 和英, 高橋 公太, 鈴木 芳樹, 成田 一衛, 斎藤 亮彦

    新潟医学会雑誌   129 ( 8 )   479 - 479   2015.8

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  • アジルサルタンによる非糖尿病高血圧患者におけるインスリン抵抗性および尿中アルブミン排泄量に及ぼす影響

    細島康宏, 河野恵美子, 飯野則昭, 斎藤亮彦, 鈴木芳樹, 成田一衛

    血圧   20 ( 11 )   1138 - 1142   2013.11

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  • 保存期慢性腎臓病患者におけるダルベポエチンアルファおよびエポエチンベータペゴルの腎性貧血改善効果について

    飯野則昭, 後藤眞, 風間順一郎, 成田一衛

    腎と透析   75 ( 4 )   599 - 603   2013.10

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  • 肝性脳症による意識障害が血液透析濾過により改善しえたバッド・キアリ症候群合併透析患者の一例

    若松拓也, 矢田雄介, 山本卓, 中枝武司, 飯野則昭, 後藤眞, 風間順一郎, 成田一衛

    日本腎臓学会誌   55 ( 6 )   1045   2013.8

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  • 新潟県における腹膜透析医療の実際

    飯野則昭, 山本卓, 川村和子, 後藤眞, 風間順一郎, 丸山弘樹, 成田一衛

    日本透析医学会雑誌   46 ( Supplement 1 )   769   2013.5

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  • 腹膜透析患者におけるESA切替用量の検討,新潟県内多施設共同研究

    飯野則昭, 川村和子, 山本卓, 後藤眞, 丸山弘樹, 風間順一郎, 成田一衛

    日本透析医学会雑誌   46 ( Supplement 1 )   913   2013.5

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  • 血液透析患者におけるDPPIV阻害薬の血糖調節効果の検討

    佐藤隆之, 細島康宏, 飯野則昭, 斎藤亮彦, 鈴木芳樹, 成田一衛

    日本透析医学会雑誌   46 ( Supplement 1 )   671   2013.5

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  • 血液透析患者に合併した進行期胸腺癌に対し全身化学療法を施行した1例

    片桐隆幸, 三浦理, 山崎美穂子, 山本卓, 坂井勇仁, 飯野則昭, 後藤眞, 各務博, 風間順一郎, 成田一衛

    日本透析医学会雑誌   46 ( Supplement 1 )   547   2013.5

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  • 持続型ESA製剤を長期使用したCKD患者の透析導入時Hb値について

    青柳竜治, 三浦隆義, 飯野則昭, 成田一衛

    日本腎臓学会誌   55 ( 3 )   359   2013.4

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  • 保存期腎不全患者に対するダルベポエチンアルファを用いた腎性貧血治療の新潟県内多施設共同研究(第三報)

    飯野則昭, 風間順一郎, 成田一衛

    日本腎臓学会誌   55 ( 3 )   359   2013.4

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  • 保存期腎不全患者に対するエポエチンベータペゴルを用いた腎性貧血治療の多施設共同研究(第二報)

    飯野則昭, 風間順一郎, 成田一衛

    日本腎臓学会誌   55 ( 3 )   359   2013.4

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  • 14 著しい低ナトリウム血症を呈した陳旧性肺結核症の1例(一般演題,第50回下越内科集談会)

    田中 雅人, 照喜名 重朋, 小嶋 智子, 才田 優, 梶原 大季, 大森 健太郎, 飯野 則昭, 寺田 正樹, 高田 俊範, 成田 一衛, 阿部 英里

    新潟医学会雑誌   124 ( 6 )   353 - 354   2010.6

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  • A case of congenital renal arteriovenous fistula with high output heart failure

    Okada Yoshinobu, Sakaino Shinjirou, Iino Noriaki, Saitou Toshihiro

    Shinzo   37 ( 8 )   672 - 677   2005

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    われわれは,先天性aneurysmal typeの右腎動静脈瘻のため,高拍出性心不全を発症した1例を経験したので報告する.症例は70歳の女性で,息切れと全身性浮腫のため当院に入院した.精査の結果,先天性と考えられたaneurysmal typeの巨大右腎動静脈瘻が認められた.心臓カテーテル検査では,肺動脈楔入圧28/7(14)mmHg,肺動脈圧43/17(26)mmHg,右心房圧19/7(11)mmHg,心係数8.5L/min/m2,左右シャント率73.7%と高拍出性心不全状態であった.右腎摘出術を施行し,治癒した.高拍出性心不全を伴った腎動静脈瘻はまれである.

    DOI: 10.11281/shinzo1969.37.8_672

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  • 4)Bartter症候群の1例とPseudo Bartter症候群の2例(I. 一般演題, 第23回新潟高血圧談話会)

    林 浩司, 飯野 則昭, 佐藤 健比呂, 丸山 雄一郎

    新潟医学会雑誌   111 ( 9 )   605 - 605   1997.9

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Research Projects

  • メガリンの細胞内輸送を調節する分子学的機序の解明

    2006.4 - 2008.3

    文部科学省  科学研究費補助金若手研究(B) 

    飯野 則昭

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    Authorship:Principal investigator  Grant type:Competitive

    メガリンの細胞質領域と蛋白複合体を形成する新規蛋白non-muscle myosin heavy chain IIA(NMHCII-A)を培養細胞(IRPTC)からimmunoprecipitation 法と質量分析の手法で同定した。NMHCII-A はDab2 を介してメガリンの細胞質領域と結合することが明らかになった。NMHCII-A の機能阻害するblebbistatin を培養細胞に添加すると、メガリンのリガンドであるlactoferrin の細胞内への取り込みが抑制されることが明らかになった。さらに、blebbistatin 投与下でのメガリン受容体の動きを可視化すると、メガリンはリガンド結合後も細胞表面に留まっているように見えた。このことからNMHCII-A はメガリンのエンドサイトーシスにおいて、機能的に重要な働きを有していることが明らかになった。Sucrose gradientと超遠心を組み合わせて細胞内の各コンポーネントを分画したところ、メガリン、Dab2、NMHCII-A は同一のendosomal fraction に存在することも明らかになった。以上よりIn vivoにおいてもこれらの三者は協調しながらメガリンのエンドサイトーシスを調節している可能性が示唆された。今後、さらに知見が蓄積されることで、複雑なエンドサイトーシスの分子学的機序が明らかにされることが期待される。

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