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| 1.
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Hara, Akinori ; Furuichi, Kengo ; Koshino, Akihiko ; Yasuda, Haruka ; Tran, Trang Thi Thu ; Iwata, Yasunori ; Sakai, Norihiko ; Shimizu, Miho ; Kaneko, Shuichi ; Nakamura, Hiroyuki ; Wada, Takashi ; 原, 章規 ; 古市, 賢吾 ; 岩田, 恭宜 ; 坂井, 宣彦 ; 清水, 美保 ; 金子, 周一 ; 中村, 裕之 ; 和田, 隆志
概要:
金沢大学医薬保健研究域医学系<br />Introduction: We examined the impact of autoantibodies on the erythropoietin receptor (EPOR) in type
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2 diabetic patients with chronic kidney disease (CKD). Methods: A total of 112 Japanese patients with type 2 diabetes who had CKD were enrolled in this study and followed for a mean of 45 months. Sera from these patients were screened for anti-EPOR antibodies using enzyme-linked immunosorbent assays. Results: Anti-EPOR antibodies were detected in 26 patients (23%). Anti-EPOR antibodies were associated with low hemoglobin concentrations and decreased renal function. In patients with biopsy-proven diabetic nephropathy, anti-EPOR antibodies were associated with increased levels of interstitial inflammation. A decrease in renal function was observed more frequently in patients with antibodies than in those without antibodies, and the presence of the antibodies together with well-known clinical parameters, including proteinuria and low glomerular filtration rate, was a significant risk factor for end-stage renal disease. In human tubular epithelial HK-2 cells, IgG fractions containing anti-EPOR antibodies upregulated the expression of monocyte chemoattractant protein-1 mRNA under a high concentration of glucose. Conclusion: Anti-EPOR antibodies might be involved in the progression of renal lesions and in the impaired erythropoiesis in type 2 diabetic patients with CKD. Furthermore, the presence of anti-EPOR antibodies may be an additional predictor for end-stage renal disease in type 2 diabetes. © 2017 International Society of Nephrology<br />Embargo Period 12 months
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| 2.
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岩田, 恭宜 ; Iwata, Yasunori
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取得学位 : 博士（医学）, 学位授与番号 : 医博甲第1555号, 学位授与年月日 : 平成14年12月31日, 学位授与大学 : 金沢大学
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| 3.
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Iwata, Yasunori ; Wada, Takashi ; Yokoyama, Hitoshi ; Toyama, Tadashi ; Kitajima, Shinji ; Okumura, Toshiya ; Hara, Akinori ; Yamahana, Junya ; Nakaya, Izaya ; Kobayashi, Motoo ; Kitagawa, Kiyoki ; Kokubo, Satoshi ; Yoshimoto, Keiichi ; Shimizu, Kazuaki ; Sakai, Norihiko ; Furuichi, Kengo ; Koshino, Yoshitaka ; Takaeda, Chikako ; Takeda, Shinichi ; Takasawa, Kazuya ; Ohta, Satoshi ; Takaeda, Masayoshi ; Kaneko, Shuichi
概要:
金沢大学保健管理センター<br />金沢大学大学院医学系研究科<br />金沢大学附属病院<br />Background: In hemodialysis patients, adynamic bone disease has been
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reported to be closely associated with low levels of parathyroid hormone (PTH) due to exposure to high levels of serum calcium following the administration of calcium carbonate (CaCO3) or vitamin D agents. This study was conducted to clarify the therapeutic effect of a non-calcemic phosphate binder, sevelamer hydrochloride (sevelamer), for hypoparathyroidism in hemodialysis patients with or without diabetes mellitus. Methods: Based on entry criteria, 40 Japanese chronic hemodialysis patients (22 males and 18 females with a mean age of 60.6, 14 diabetic patients and 26 non-diabetic patients) were switched from CaCO3 to sevelamer for 48 weeks. Serum calcium, phosphate, intact (i) PTH and PTH-(1-84) were analyzed. Bone remodeling activity was evaluated by determining intact osteocalcine (iOC), bone-specific alkaline phosphatase (BAP). Results: The switch from CaCO3 to sevelamer significantly decreased the serum levels of calcium, resulting in the elevation of iPTH levels from 31±18 pg/mL to 95±96 pg/mL by 48 weeks. In contrast, serum phosphate levels remained similar to those in patients with CaCO3 treatment. Concomitantly, the levels of BAP and iOC were elevated. Further, these beneficial effects on bone turnover were observed in both diabetic and non-diabetic patients. Conclusion: Sevelamer reduced the calcium concentration and thereby increased PTH levels, resulting in the improvement of markers of bone turnover. The administration of sevelamer is of therapeutic benefit for the improvement of bone remodeling activity even in hemodialysis patients with diabetes. © 2007 The Japanese Society of Internal Medicine.
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| 4.
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Iwata, Yasunori ; Wada, Takashi ; Furuichi, Kengo ; Kitagawa, Kiyoki ; Kokubo, Satoshi ; Kobayashi, Motoo ; Sakai, Norihiko ; Yoshimoto, Keiichi ; Shimizu, Miho ; Kobayashi, Kenichi ; Yokoyama, Hitoshi
概要:
金沢大学医薬保健研究域医学系<br />Objective. KL-6 is reported to be excreted from the lung alveolar and bronchial epithelial cells and
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may be a good marker for monitoring disease activity of interstitial pneumonia. This study was designed to ascertain the clinical significance of serum KL-6 levels in interstitial pneumonia associated with anti-neutrophil cytoplasmic antibody (ANCA)-related vasculitis. Methods. Serum KL-6 levels were determined by an enzyme-linked immunosorbent assay. Patients. We examined 20 healthy subjects, 13 patients with perinuclear (myeloperoxidase, MPO) ANCA-related vasculitis and 12 dermatomyositis (DM)/polymyositis (PM) patients as disease controls in this study. Six out of 13 patients with ANCA-related vasculitis had interstitial pneumonia. Results. Serum levels of KL-6 in ANCA-positive patients with interstitial pneumonia were significantly elevated, while they remained as low as those of healthy subjects in ANCA- positive patients without interstitial pneumonia. Similarly, KL-6 levels in sera were higher in 12 dermatomyositis/polymyositis patients with interstitial pneumonia, while they remained low in DM/PM patients without interstitial pneumonia. Moreover, the elevated serum KL-6 level was reduced during the convalescence induced by glucocorticoid therapy and reflected the disease activity of interstitial pneumonia associated with ANCA-related vasculitis. Conclusion. These data suggest that the measurement of serum KL-6 levels may be a good monitoring system for the diagnosis and follow-up of interstitial pneumonia of patients with ANCA-related vasculitis.
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| 5.
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Menke, Julia ; Iwata, Yasunori ; Rabacal, Whitney A. ; Basu, Ranu ; Yeung, Yee G. ; Humphreys, Benjamin D. ; Wada, Takashi ; Schwarting, Andreas ; Stanley, E. Richard ; Kelley, Vicki R.
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金沢大学医薬保健研究域医学系<br />Tubular damage following ischemic renal injury is often reversible, and tubular epithelial cell (TEC
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) proliferation is a hallmark of tubular repair. Macrophages have been implicated in tissue repair, and CSF-1, the principal macrophage growth factor, is expressed by TECs. We therefore tested the hypothesis that CSF-1 is central to tubular repair using an acute renal injury and repair model, ischemia/reperfusion (I/R). Mice injected with CSF-1 following I/R exhibited hastened healing, as evidenced by decreased tubular pathology, reduced fibrosis, and improved renal function. Notably, CSF-1 treatment increased TEC proliferation and reduced TEC apoptosis. Moreover, administration of a CSF-1 receptor-specific (CSF-1R-specific) antibody after I/R increased tubular pathology and fibrosis, suppressed TEC proliferation, and heightened TEC apoptosis. To determine the contribution of macrophages to CSF-1-dependent renal repair, we assessed the effect of CSF-1 on I/R in mice in which CD11b + cells were genetically ablated and determined that macrophages only partially accounted for CSF-1-dependent tubular repair. We found that TECs expressed the CSF-1R and that this receptor was upregulated and coexpressed with CSF-1 in TECs following renal injury in mice and humans. Furthermore, signaling via the CSF-1R stimulated proliferation and reduced apoptosis in human and mouse TECs. Taken together, these data suggest that CSF-1 mediates renal repair by both a macrophage-dependent mechanism and direct autocrine/paracrine action on TECs.
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| 6.
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Nakaya, Izaya ; Iwata, Yasunori ; Abe, Toshio ; Yokoyama, Hitoshi ; Oda, Yoshio ; Nomura, Gakuji
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金沢大学医薬保健研究域医学系<br />A 69-year-old man was admitted with a large elastic mass in the upper abdomen. Computed tomography r
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evealed a massive tumor in contact with the liver and gastrointestinal endoscopy revealed a gastric adenocarcinoma. He developed acute renal failure with massive proteinuria and died with a marked enlargement of the tumor. Autopsy revealed a tumor located in the lesser omentum. The tumor was considered to be a Gastrointestinal Stromal Tumor (GIST) because it was positive for c-kit. In addition, crescent formations and immune complexes in glomeruli were observed. We report the first case of GIST complicated by rapidly progressive glomerulonephritis and gastric carcinoma.
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| 7.
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Iwata, Yasunori ; Wada, Takashi ; Uchiyama, Akio ; Miwa, Atsuo ; Nakaya, Izaya ; Tohyama, Tadashi ; Yamada, Yuhji ; Kurokawa, Toshiro ; Yoshida, Takashi ; Ohta, Satoshi ; Yokoyama, Hitoshi ; Iida, Hiroyuki
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金沢大学医薬保健研究域医学系<br />We report a case with immunoglobulin A (IgA) nephropathy, showing IgA deposition which disappeared a
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fter peripheral blood stem cell transplantation (PBSCT) for acute lymphocytic leukemia (ALL). In 1996, a 28-year-old man was diagnosed with IgA nephropathy by renal biopsy. Steroid therapy improved proteinuria from 3 g/day to 1 g/day. In 2003, he received PBSCT following the initial therapy for ALL. After complete remission, urinary protein and hematuria remained at between (-) and (±). In 2004, the second renal biopsy specimen revealed no deposit of IgA or C3. These findings suggested that immune reconstruction with PBSCT following immunosuppression therapy was of benefit to IgA nephropathy. © 2006 The Japanese Society of Internal Medicine.
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| 8.
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Iwata, Yasunori ; Furuichi, Kengo ; Kitagawa, Kiyoki ; Hara, Akinori ; Okumura, Toshiya ; Kokubo, Satoshi ; Shimizu, Kazuaki ; Sakai, Norihiko ; Sagara, Akihiro ; Kurokawa, Yukie ; Ueha, Satoshi ; Matsushima, Satoshi ; Kaneko, Shuichi ; Wada, Takashi
概要:
金沢大学医薬保健研究域医学系<br />Objective: Myeloid-derived suppressor cells (MDSCs) have been identified as immunosuppressive cells
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in tumor-related inflammation. However, the pathogenesis of MDSCs for autoimmune disease has not been investigated as yet. The aim of this study was to address whether MDSCs contribute to autoimmune organ injury in lupus-prone mice. Methods: MDSCs were analyzed by flow cytometric staining of CD11b+ GR-1+ in MRL-Faslpr mice. CD4+ T-cell proliferation assay was performed by coculture with CD11b+ GR-1+ splenocytes. The percentage of immunosuppressive cells was examined during disease progression. Expression of chemokine receptor on immunosuppressive cells was analyzed, and chemotaxis assay was performed. Results: CD11b+ GR-1low cells had a suppressive effect on CD4+ T-cell proliferation, which was restored by an arginase-1 inhibitor. CD11b+ GR-1low cells increased in percentage during disease progression in kidney and blood. The number of migrated CD11b+ GR-1low cells increased in the presence of monocyte chemoattractant protein-1/CCL2. Conclusion: We assessed the involvement of CD11b+ GR-1low cells in autoimmune disorder in MRL-Faslpr mice. These cells regulate immunological responses via CCL2/CCR2 signaling. The regulation of immunosuppressive monocytes may provide novel therapeutic strategy for organ damage in autoimmune diseases. © 2010 Japanese Society of Nephrology..
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| 9.
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Oshima, Megumi ; Kitajima, Shinji ; Toyama, Tadashi ; Hara, Akinori ; Kitagawa, Kiyoki ; Iwata, Yasunori ; Shimizu, Miho ; Nishio, Saori ; Imura, Junko ; Yokoyama, Hitoshi ; Furuichi, Kengo ; Kaneko, Shuichi ; Wada, Takashi
概要:
We herein report a case of spontaneous pregnancy and preterm delivery in a 29-year-old patient with myeloperoxidase-anti
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neutrophil cytoplasmic antibody (ANCA)-associated glomerulonephritis. Her basal serum creatinine level before pregnancy was 1.4 mg/dL and her urinary protein level was approximately 2 g/day. The proteinuria and hematuria increased during pregnancy, and the patient was admitted to our hospital and treated with prednisolone (PSL). At 27 weeks of gestation, she delivered a live infant weighing 848 g via cesarean section. No relapse of ANCA-associated glomerulonephritis occurred. © 2013 The Japanese Society of Internal Medicine.
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| 10.
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Iwata, Yasunori ; Furuichi, Kengo ; Kaneko, Shuichi ; Wada, Takashi
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Lupus nephritis (LN) is a major clinical manifestation of systemic lupus erythematosus (SLE). Although numerous abnormal
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ities of immune system have been proposed, cytokine overexpression plays an essential role in the pathogenesis of LN. In the initial phase of the disease, the immune deposits and/or autoantibodies induce cytokine production in renal resident cells, leading to further inflammatory cytokine/chemokine expression and leukocyte infiltration and activation. Then, infiltrate leukocytes, such as macrophages (Mψ) and dendritic cells (DCs), secrete a variety of cytokines and activate nave T cells, leading the cytokine profile towards T helper (Th)1, Th2, and/or Th17. Recent studies revealed these inflammatory processes in experimental animal models as well as human LN. The cytokine targeted intervention may have the therapeutic potentials for LN. This paper focuses on the expression of cytokine and its functional role in the pathogenesis of LN. © 2011 Yasunori Iwata et al.
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