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• 札幌医科大学   泌尿器科  

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• Incidence and risk factors for acute kidney injury after radical cystectomy

  Yoshinori Ikehata, Toshiaki Tanaka, Koji Ichihara, Ko Kobayashi, Hiroshi Kitamura, Satoshi Takahashi, Naoya Masumori

  INTERNATIONAL JOURNAL OF UROLOGY ( WILEY-BLACKWELL )  23 ( 7 ) 558 - 563  2016年07月  [査読有り]

  　概要を見る

  Objectives: To clarify the incidence, risk factors and clinical impact of acute kidney injury after radical cystectomy. Methods: A total of 210 patients who underwent radical cystectomy at Sapporo Medical University Hospital, Sapporo, Japan, from January 2006 through December 2012 were evaluated. The incidence of acute kidney injury was evaluated over the first 7 days postoperatively, during which time a ureteral catheter was inserted. Risk factors for postoperative acute kidney injury and its impacts on short-term clinical outcomes were evaluated. Results: Finally, 145 patients were eligible for this study. Postoperative acute kidney injury was observed in 48 patients (33.1%), with stages 1, 2, and 3 found in 33 (22.7%), 14 (9.6%) and 1 (0.7%), respectively. All patients with stage 1 and 2 acute kidney injury recovered by postoperative day 7, except for one with stage 1. Hypertension (P < 0.001), preoperative estimated glomerular filtration rate <60 mL/min/1.73 m(2) (P = 0.04) and neoadjuvant chemotherapy (P = 0.03) were independent risk factors for postoperative acute kidney injury. Furthermore, postoperative acute kidney injury was an independent risk factor for acute kidney injury after ureteral stent removal, but not of persistent elevated serum creatinine, prolonged hospital stay or the new onset of cardiovascular disorders during the hospital stay. Conclusions: The incidence of acute kidney injury after radical cystectomy is relatively high, although most cases are low grade and can be resolved. We should be aware of the risk for postoperative acute kidney injury, especially in patients who have comorbid hypertension, impaired renal function and received naoadjuvant chemotherapy.

  DOI PubMed

• Natural killer cells play a critical role in mediating inflammation and graft failure during antibody-mediated rejection of kidney allografts.

  Kohei N, Tanaka T, Tanabe K, Masumori N, Dvorina N, Valujskikh A, Baldwin WM, Fairchild RL

  Kidney international ( NATURE PUBLISHING GROUP )  89 ( 6 ) 1293 - 1306  2016年06月  [査読有り]

  　概要を見る

  While the incidence of antibody-mediated kidney graft rejection has increased, the key cellular and molecular participants underlying this graft injury remain unclear. Rejection of kidney allografts in mice lacking the chemokine receptor CCR5 is dependent on production of donor-specific antibody. Here we determine if cells expressing cytotoxic function contributed to antibody-mediated kidney allograft rejection in these recipients. Wild-type C57BL/6, B6. CCR5(-/-), and B6.CD8(-/-)/CCR5(-/-) mice were transplanted with complete MHC-mismatched A/J kidney grafts, and intragraft inflammatory components were followed to rejection. B6.CCR5(-/-) and B6.CD8(-/-)/CCR5(-/-) recipients rejected kidney allografts by day 35, whereas 65% of allografts in wild-type recipients survived past day 80 post-transplant. Rejected allografts in wild-type C57BL/6, B6.CCR5(-/-), and B6.CD8(-/-)/CCR5(-/-) recipients expressed high levels of VCAM-1 and MMP7 mRNA that was associated with high serum titers of donor-specific antibody. High levels of perforin and granzyme B mRNA expression peaked on day 6 post-transplant in allografts in all recipients, but were absent in isografts. Depletion of natural killer cells in B6.CD8(-/-)/CCR5(-/-) recipients reduced this expression to background levels and promoted the long-term survival of 40% of the kidney allografts. Thus, natural killer cells have a role in increased inflammation during antibody-mediated kidney allograft injury and in rejection of the grafts.

  DOI PubMed

• Editorial Comment to Implication of aortic calcification on persistent hypertension after laparoscopic adrenalectomy in patients with primary aldosteronism

  Toshiaki Tanaka

  INTERNATIONAL JOURNAL OF UROLOGY ( WILEY-BLACKWELL )  23 ( 5 ) 418 - 418  2016年05月  [査読有り]

  DOI PubMed

• IL-1 Receptor Signaling on Graft Parenchymal Cells Regulates Memory and De Novo Donor-Reactive CD8 T Cell Responses to Cardiac Allografts

  Shoichi Iida, Hidetoshi Tsuda, Toshiaki Tanaka, Danielle D. Kish, Toyofumi Abe, Charles A. Su, Ryo Abe, Kazunari Tanabe, Anna Valujskikh, William M. Baldwin, Robert L. Fairchild

  JOURNAL OF IMMUNOLOGY ( AMER ASSOC IMMUNOLOGISTS )  196 ( 6 ) 2827 - 2837  2016年03月  [査読有り]

  　概要を見る

  Reperfusion of organ allografts induces a potent inflammatory response that directs rapid memory T cell, neutrophil, and macrophage graft infiltration and their activation to express functions mediating graft tissue injury. The role of cardiac allograft IL-1 receptor (IL-1R) signaling in this early inflammation and the downstream primary alloimmune response was investigated. When compared with complete MHC-mismatched wild-type cardiac allografts, IL-1R(-/-) allografts had marked decreases in endogenous memory CD8 T cell and neutrophil infiltration and expression of proinflammatory mediators at early times after transplant, whereas endogenous memory CD4 T cell and macrophage infiltration was not decreased. IL-1R(-/-) allograft recipients also had marked decreases in de novo donor-reactive CD8, but not CD4, T cell development to IFN-gamma-producing cells. CD8 T cell-mediated rejection of IL-1R(-/-) cardiac allografts took 3 wk longer than wild-type allografts. Cardiac allografts from reciprocal bone marrow reconstituted IL-1R(-/-)/wild-type chimeric donors indicated that IL-1R signaling on graft nonhematopoietic-derived, but not bone marrow-derived, cells is required for the potent donor-reactive memory and primary CD8 T cell alloimmune responses observed in response to wild-type allografts. These studies implicate IL-1R-mediated signals by allograft parenchymal cells in generating the stimuli-provoking development and elicitation of optimal alloimmune responses to the grafts.

  DOI PubMed

• Clinicopathological characteristics of Xp11.2 translocation renal cell carcinoma in adolescents and adults: Diagnosis using immunostaining of transcription factor E3 and fluorescence in situ hybridization analysis

  Megumi Hirobe, Naoya Masumori, Toshiaki Tanaka, Hiroshi Kitamura, Akiko Tonooka, Tadashi Hasegawa, Taiji Tsukamoto

  INTERNATIONAL JOURNAL OF UROLOGY ( WILEY-BLACKWELL )  23 ( 2 ) 140 - 145  2016年02月  [査読有り]

  　概要を見る

  ObjectivesTo determine the rate and clinicopathological features of Xp11.2 translocation carcinoma using immunostaining of transcription factor E3 and fluorescence in situ hybridization analysis. MethodsWe evaluated 638 patients with renal cell carcinoma treated at Sapporo Medical University Hospital, Sapporo, Japan, from 1990 to 2009 by reviewing all hematoxylin-eosin-stained sections and carrying out immunostaining of transcription factor E3 for all cases. Fluorescence in situ hybridization analysis was carried out for patients with positive immunostaining or with findings suspicious for Xp11.2 translocation carcinoma on hematoxylin-eosin-stained sections. In this analysis, we set a cut-off level for split signals of at least 10% of nuclei. ResultsOf the 631 patients, 20 (3.2%) were positive for immunostaining. Finally, five patients were diagnosed with Xp11.2 translocation carcinoma (0.8%). Four of these patients were female and aged less than 50 years, and three cases were diagnosed as stage IV with multiple regional lymph nodal or visceral metastases. The positive predictive value of immunostaining was 25%. ConclusionPatients with Xp11 translocation renal cell carcinoma tend to be younger, more frequently female and diagnosed at a more advanced stage. Immunostaining followed by fluorescence in situ hybridization analysis is an accurate and cost-effective approach for diagnosis of Xp11 translocation renal cell carcinoma.

  DOI PubMed

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