Shuichi Kaneko

Kanazawa University, Kanazawa, Ishikawa, Japan

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Publications (529)2363.23 Total impact

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    ABSTRACT: Background: Apoptosis inhibitor of macrophage (AIM) expressed on macrophages prolongs inflammation by protecting macrophages from apoptosis. Most circulating AIM co-exists with immunoglobulin M (IgM). AIM's pathophysiological role in relation to IgM remains unclear. Here we evaluated the glomerular expression/deposition of AIM and IgM in the kidney using immunohistochemistry and its associations with clinical manifestations in 43 patients with biopsy-confirmed kidney diseases. Methods: Kidney biopsy tissue from all patients was immunostained for AIM and IgM. Staining patterns and percent stained areas within the glomeruli were determined. Cells expressing AIM were identified by co-staining with macrophage and endothelial cell surface markers. Correlations between staining results and clinical parameters were evaluated using univariate and multivariate analyses. Results: AIM was deposited in various areas, such as mesangial and capillary area. A part of AIM expression was localized to CD68-positive macrophages in the glomerulus. Amount of glomerular expression was positively correlated with urinary protein in patients with severe proteinuria (urinary protein ≥0.5 g/day) and kidney dysfunction [estimated glomerular filtration ratio (eGFR) <60 ml/min/1.73 m(2)]. Urinary protein was higher in patients exhibiting overlapping glomerular expression of AIM and IgM. Annual eGFR decline rate negatively correlated with AIM-positive area. AIM-positive area and initial serum creatinine were independently associated with decreased kidney function. Conclusion: AIM expression in the kidney was associated with urinary protein and decline in kidney function. Co-expression with IgM appeared to exacerbate AIM's deleterious effects on kidney function. Combined glomerular AIM and IgM expression is a candidate prognostic index for kidney disease.
    No preview · Article · Feb 2016 · Clinical and Experimental Nephrology
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    ABSTRACT: Objective We evaluated the relationships between the serum autotaxin (ATX) levels and the clinical and pathological parameters, as well as the long-term renal outcome, in type 2 diabetic patients with biopsy-proven diabetic nephropathy. Methods In this retrospective single-center cohort study, serum samples were collected from 38 Japanese type 2 diabetic patients with biopsy-proven diabetic nephropathy at the time of renal biopsy. The serum ATX levels were measured using a specific sandwich enzyme immunoassay. Results A multivariate linear regression analysis revealed the urinary protein excretion to be independently associated with the serum ATX levels. In addition, patients with serum ATX levels above the median showed more advanced diffuse lesions, nodular lesions and arteriolar hyalinosis compared to those with serum ATX levels below the median. However, high serum ATX levels were not associated with any increase in the number of renal composite events [a need for dialysis or a 50% decline in the estimated glomerular filtration rate (eGFR) from baseline]. Conclusion The serum ATX levels in type 2 diabetic patients with diabetic nephropathy were associated with proteinuria and diabetic kidney lesions, although the serum ATX levels were not identified to be a predictive indicator for the renal outcome.
    Preview · Article · Jan 2016 · Internal Medicine
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    ABSTRACT: The hepatitis B virus (HBV) is a kind of pandemic infectious disease. It is becoming a major health problem in Asian and African countries, however, less so in other areas around the world. There is a vast background for studying HBV. However, some problems still require further study. For example, when the patient is infected by HBV, how to arrange the treatment schedule? Using long term continuous treatment or others? Therefore, we wish to readdress the study of HBV. First, we propose a new hybrid model that contains both continuous and discrete variables. Second, we analyze its dynamical behavior. We hope that this study may provide some new insight for HBV disease and some new guidance for the therapy.
    Preview · Article · Dec 2015
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    ABSTRACT: Chronic hepatitis B (CHB), chronic hepatitis C (CHC), and associated hepatocellular carcinoma (HCC) are characterized by cholesterol imbalance and dyslipidemia; however, the key regulatory drivers of these phenotypes are incompletely understood. Using gene expression microarrays and high-throughput sequencing of small RNAs, we performed integrative analysis of microRNA (miRNA) and gene expression in nonmalignant and matched cancer tissue samples from human subjects with CHB or CHC and HCC. We also carried out follow-up functional studies of specific miRNAs in a cell-based system. These studies led to four major findings. First, pathways affecting cholesterol homeostasis were among the most significantly overrepresented among genes dysregulated in chronic viral hepatitis and especially in tumor tissue. Second, for each disease state, specific miRNA signatures that included miRNAs not previously associated with chronic viral hepatitis, such as miR-1307 in CHC, were identified. Notably, a few miRNAs, including miR-27 and miR-224, were components of the miRNA signatures of all four disease states: CHB, CHC, CHB-associated HCC, and CHC-associated HCC. Third, using a statistical simulation method (miRHub) applied to the gene expression data, we identified candidate master miRNA regulators of pathways controlling cholesterol homeostasis in chronic viral hepatitis and HCC, including miR-21, miR-27, and miR-33. Last, we validated in human hepatoma cells that both miR-21 and miR-27 significantly repress cholesterol synthesis and that miR-27 does so in part through regulation of the gene that codes for the rate-limiting enzyme 3-hydroxy-3-methyl-glutaryl-coenzyme A (HMG-CoA) reductase ( HMGCR ). IMPORTANCE Hepatitis B virus (HBV) and hepatitis C virus (HCV) are phylogenetically unrelated hepatotropic viruses that persistently infect hundreds of millions of people world-wide, often leading to chronic liver disease and hepatocellular carcinoma (HCC). Chronic hepatitis B (CHB), chronic hepatitis C (CHC), and associated HCC often lead to cholesterol imbalance and dyslipidemia. However, the regulatory mechanisms underlying the dysregulation of lipid pathways in these disease states are incompletely understood. MicroRNAs (miRNAs) have emerged as critical modulators of lipid homeostasis. Here we use a blend of genomic, molecular, and biochemical strategies to identify key miRNAs that drive the lipid phenotypes of chronic viral hepatitis and HCC. These findings provide a panoramic view of the miRNA landscape in chronic viral hepatitis, which could contribute to the development of novel and more-effective miRNA-based therapeutic strategies.
    Full-text · Article · Dec 2015 · mBio
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    ABSTRACT: Background: Although an increased epicardial adipose tissue (EAT) volume around the left atrium (LA) is related to the atrial fibrillation (AF) burden, the role of EAT inflammation in AF is unclear. We investigated the association between AF and inflammation of the EAT around the LA. Methods: We retrospectively identified regions of EAT around the LA and measured the density of these areas using computed tomography (CT). Results: A total of 32 patients who underwent their first catheter ablation for paroxysmal AF (PAF) were enrolled (mean age 62.5±11.1 years). Patients without a history of AF (n=32), but who underwent cardiac CT and were matched by age, sex, and metabolic risk factors, were enrolled in the control group (62.2±12.1 years). The mean EAT density around the LA was significantly higher in the PAF group than in the control group (-108.1±6.7 vs. -111.6±5.5 Hounsfield units; p=0.02), while the densities of subcutaneous adipose tissue (SAT) in the abdomen and thorax did not differ between the two groups. In a multiple logistic regression analysis, a higher EAT density was significantly associated with the presence of PAF after adjusting for other risk factors (odds ratio: 1.25; 95% confidence interval: 1.08-1.45, p=0.003). Conclusions: This study supports the hypothesis that inflammation of EAT around the LA, but not SAT, is related to the presence of PAF.
    No preview · Article · Dec 2015 · Journal of Cardiology
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    ABSTRACT: Backgrounds: Although nucleos(t)ide analog (NA) therapy effectively reduces hepatitis B virus (HBV)-DNA in serum in patients with chronic hepatitis B (CH-B), it does not completely reduce the incidence of hepatocellular carcinoma (HCC). Methods and results: 109 CH-B patients receiving NA were analyzed. Multivariate cox regression analysis showed age (>60 years, HR=2.66) and Fib-4 index (>2.1, HR=2.57) and the presence of hepatitis core-related antigen (HBcrAg; HR=3.53) during treatment were significantly associated with the development of HCC. The amount of HBV-DNA and pregenome (pg)RNA in liver were significantly higher in HBcrAg(+) patients (n=16) than HBcrAg(-) patents (n=12), suggesting the presence of active HBV replication in HBcrAg(+) liver. Hepatic gene expression profiling showed that HBV promoting transcriptional factors, HNF4á, PPARá and LRH1 etc. were up-regulated in HBcrAg(+) liver. HepAD38 cells overexpressing LRH1 increased HBV replication characterized by the higher HBV-DNA and pg RNA under the long-term exposure to entecavir. Conversely, overexpression of preC/C in HepG2 cells increased these transcriptional factors. Metformin efficiently repressed HBV replication in primary human hepatocytes. Conclusions: Modulating HBV transcriptional factors by Metformin in combination with NA therapy would potentiate anti HBV activity and reduce the incidence of HCC in HBcrAg(+) patients.
    No preview · Article · Nov 2015 · The Journal of Infectious Diseases
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    ABSTRACT: Hepatic insulin resistance and nonalcoholic steatohepatitis (NASH) could be caused by excessive hepatic lipid accumulation and peroxidation. Vitamin E has become a standard treatment for NASH. However, astaxanthin, an antioxidant carotenoid, inhibits lipid peroxidation more potently than vitamin E. Here, we compared the effects of astaxanthin and vitamin E in NASH. We first demonstrated that astaxanthin ameliorated hepatic steatosis in both genetically (ob/ob) and high-fat-diet-induced obese mice. In a lipotoxic model of NASH: mice fed a high-cholesterol and high-fat diet, astaxanthin alleviated excessive hepatic lipid accumulation and peroxidation, increased the proportion of M1-type macrophages/Kupffer cells, and activated stellate cells to improve hepatic inflammation and fibrosis. Moreover, astaxanthin caused an M2-dominant shift in macrophages/Kupffer cells and a subsequent reduction in CD4+ and CD8+ T cell recruitment in the liver, which contributed to improved insulin resistance and hepatic inflammation. Importantly, astaxanthin reversed insulin resistance, as well as hepatic inflammation and fibrosis, in pre-existing NASH. Overall, astaxanthin was more effective at both preventing and treating NASH compared with vitamin E in mice. Furthermore, astaxanthin improved hepatic steatosis and tended to ameliorate the progression of NASH in biopsy-proven human subjects. These results suggest that astaxanthin might be a novel and promising treatment for NASH.
    Preview · Article · Nov 2015 · Scientific Reports
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    ABSTRACT: Background: The prevention of relapse and infection complications during remission maintenance therapy is required to improve the prognosis of patients with microscopic polyangiitis (MPA) showing rapidly progressive glomerulonephritis (RPGN). The clinicopathological characteristics of patients with ANCA-positive MPA were examined to determine the risk factors for relapse or infectious complications after remission induction therapy. Patients and methods: The study population consisted of 52 patients diagnosed as ANCA-positive MPA showing RPGN from 2002 to 2012, after publication of the Japanese guideline for RPGN. The clinicopathological findings were examined between the presence and absence of relapse or infectious complications. Results: The value of vasculitis damage index (VDI) was high for the relapse group and VDI value was identified as the leading factor associated with relapse [hazard ratio (HR) 3.36, 95 % confidence interval (CI) 1.58-7.12, P < 0.01]. On the other hand, the values of Birmingham Vasculitis Activity Score, clinical grade category of RPGN at diagnosis, and VDI at remission were high in the infectious group. Furthermore, clinical grade category of RPGN was the leading factor associated with infectious complications (HR 5.30, 95 % CI 1.41-19.9, P = 0.01). Conclusion: The disease activity at diagnosis and severity of organ damage at remission were associated with relapse and infectious complications during remission maintenance therapy and infectious complication affected kidney survival and all-cause mortality in patients with ANCA-positive MPA exhibiting RPGN.
    No preview · Article · Nov 2015 · Clinical and Experimental Nephrology
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    ABSTRACT: Background: Renal coloboma syndrome (RCS) is characterized by renal anomalies and optic nerve colobomas. PAX2 mutations contribute to RCS. However, approximately half of the patients with RCS have no mutation in PAX2 gene. Methods: To investigate the incidence and effects of mutations of PAX2 and 25 candidate genes, patient genes were screened using next-generation sequence analysis, and candidate mutations were confirmed using Sanger sequencing. The correlation between mutations and clinical manifestation was evaluated. Result: Thirty patients, including 26 patients (two families of five and two, 19 sporadic cases) with RCS, and 4 optic nerve coloboma only control cases were evaluated in the present study. Six PAX2 mutations in 21 probands [28%; two in family cohorts (n = 5 and n = 2) and in 4 out of 19 patients with sporadic disease] including four novel mutations were confirmed using Sanger sequencing. Moreover, four other sequence variants (CHD7, SALL4, KIF26B, and SIX4) were also confirmed, including a potentially pathogenic novel KIF26B mutation. Kidney function and proteinuria were more severe in patients with PAX2 mutations than in those without the mutation. Moreover, the coloboma score was significantly higher in patients with PAX2 gene mutations. Three out of five patients with PAX2 mutations had focal segmental glomerulosclerosis (FSGS) diagnosed from kidney biopsies. Conclusion: The results of this study identify several new mutations of PAX2, and sequence variants in four additional genes, including a novel potentially pathogenic mutation in KIF26B, which may play a role in the pathogenesis of RCS.
    Preview · Article · Nov 2015 · PLoS ONE
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    ABSTRACT: Here, we report a fluorescent probe based on a macrocyclic peptide scaffold that specifically stains EpCAM-expressing MCF7 cells. The 14-mer macrocyclic peptide binding to the extracellular domain of EpCAM with a dissociation constant in the low nM range (1.7 nM) was discovered using the random non-standard peptide-integrated discovery system. Notably, this probe containing a fluorescence tag is less than 3000 Da in total and able to visualize nearly every live cell under high cell-density conditions, which was not achieved by the conventional mAb staining method. This suggests that the molecular probe based on the compact macrocyclic scaffold has great potentials as an imaging tool for the EpCAM biomarker as well as a delivery vehicle for drug conjugates.
    Full-text · Article · Nov 2015 · Journal of Molecular Evolution
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    ABSTRACT: A bent cannula tip and agglutination (arrow) in a 6-mm-long Quick-set® cannula.
    Preview · Article · Nov 2015 · Journal of Diabetes Investigation

  • No preview · Article · Nov 2015
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    ABSTRACT: Significant associations of HLA-DP alleles with chronic hepatitis B (CHB) infection are evident in Asian and Arabian populations, including Japanese, Han Chinese, Korean, and Saudi Arabian populations. Here, significant associations between CHB infection and five DPB1 alleles (two susceptibility alleles, DPB1(*) 05:01 and (*) 09:01, and three protective alleles, DPB1(*) 02:01, (*) 04:01, and (*) 04:02) were confirmed in a population comprising of 2582 Japanese individuals. Furthermore, odds ratios for CHB were higher for those with both DPB1 susceptibility alleles than for those with only one susceptibility allele; therefore, effects of susceptibility alleles were additive for risk of CHB infection. Similarly, protective alleles showed an additive effect on protection from CHB infection. Moreover, heterozygotes of any protective allele showed stronger association with CHB than did homozygotes, suggesting that heterozygotes may bind a greater variety of hepatitis B-derived peptides, and thus present these peptides more efficiently to T-cell receptors than homozygotes. Notably, compound heterozygote of the protective allele (any one of DPB1*02:01, *04:01, and *04:02) and the susceptible allele DPB1*05:01 was significantly associated with protection against CHB infection, which indicates that one protective HLA-DPB1 molecule can provide dominant protection. Identification of the HLA-DPB1 genotypes associated with susceptibility to and protection from CHB infection is essential for future analysis of the mechanisms responsible for immune recognition of hepatitis B virus antigens by HLA-DPB1 molecules.
    No preview · Article · Oct 2015 · Tissue Antigens
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    ABSTRACT: Background: In the current American Joint Committee on Cancer/International Union Against Cancer staging system (seventh edition) for intrahepatic cholangiocarcinoma (ICC), tumor size was excluded, and periductal invasion was added as a new tumor classification-defining factor. The objective of the current report was to propose a new staging system for ICC that would be better for stratifying the survival of patients based on data from the nationwide Liver Cancer Study Group of Japan database. Methods: Of 756 patients who underwent surgical resection for ICC between 2000 and 2005, multivariate analyses of the clinicopathologic factors of 419 patients who had complete data sets were performed to elucidate relevant factors for inclusion in a new tumor classification and staging system. Results: Overall survival data were best stratified using a cutoff value of 2 cm using a minimal P value approach to discriminate patient survival. The 5-year survival rate of 15 patients who had ICC measuring ≤2 cm in greatest dimension without lymph node metastasis or vascular invasion was 100%, and this cohort was defined as T1. Multivariate analysis of prognostic factors for 267 patients with lymph node-negative and metastasis-negative (N0M0) disease indicated that the number of tumors, the presence arterial invasion, and the presence major biliary invasion were independent and significant prognostic factors. The proposed new system, which included tumor number, tumor size, arterial invasion, and major biliary invasion for tumor classification, provided good stratification of overall patient survival according to disease stage. Macroscopic periductal invasion was associated with major biliary invasion and an inferior prognosis. Conclusions: The proposed new staging system, which includes a tumor cutoff size of 2 cm and major biliary invasion, may be useful for assigning patients to surgery. Cancer 2015. © 2015 American Cancer Society.
    No preview · Article · Oct 2015 · Cancer
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    ABSTRACT: Aim: Although sorafenib is a standard drug for advanced hepatocellular carcinoma (HCC), little is known about a patient's clinical course after treatment. We investigated the effect of post-progression survival (PPS) and progression-free survival (PFS) on overall survival (OS) in patients whose advanced HCC was treated by sorafenib. Methods: We searched in the PubMed database for reports with survival data of patients with HCC treated with sorafenib monotherapy, and selected reports with ≥ 20 patients each that provided data for both OS and PFS or time to progression (TTP). Median PPS (mPPS) was defined as the period obtained by subtracting median PFS or TTP (mPFS/TTP) from median OS (mOS). We identified 56 reports with 5803 patients. We investigated the correlation of mOS and either mPPS or mPFS/TTP using weighted linear regression. Results: Median PPS correlated with mOS (r = 0.834) very strongly, whereas mPFS/TTP did not correlate with mOS as highly as PPS did (r = 0.546). When we stratified survival data by Child-Pugh classification, a significantly greater average percentage of mPPS to mOS was seen in Child-Pugh class A (54.4 ± 17.6 %) than in Child-Pugh class B (32.0 ± 11.6 %) (P = 0.015). Conclusions: PPS highly correlated with OS, and its importance should be more emphasized for advanced HCC patients treated after sorafenib therapy, whereas we need to take more care in interpreting the results of PFS to evaluate treatment efficacy in clinical trial of advanced HCC. This article is protected by copyright. All rights reserved.
    No preview · Article · Oct 2015 · Hepatology Research
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    ABSTRACT: Background: Various sleep abnormalities, such as delayed sleep onset, frequent awakening and daytime sleepiness, deteriorate the quality of life in patients with chronic kidney disease (CKD), including those on haemodialysis (HD). Although there are some candidate causative molecules in the central nervous system, the contribution of peripheral blood cells (PBCs) remains unclear. In this study, we performed polysomnographic analysis in CKD patients and used PBCs to examine the expression of genes related to sleep and wakefulness states. Methods: Polysomnographic analysis was performed in 9 CKD patients and 6 controls. Genes related to sleep and wakefulness were evaluated by RNA microarray in 19 subjects, including CKD patients and control subjects. Results: Polysomnographic analysis revealed that the duration of the rapid eye movement (REM)/non-REM phases during total sleep time was different between CKD patients and healthy controls. In mRNA microarray evaluation, hierarchical clustering analysis showed different patterns of sleep-related gene expression in HD patients. mRNA expression levels of GABA receptor (GABBR2), noradrenaline receptor (ADRA1A), dopamine receptor (DRD1) and histamine receptor (HRH1) showed an inverse correlation with renal function. Moreover, the mRNA expression of orexin and its receptor (HCRTR1 and HCRTR2) was also inversely correlated with renal function. Conclusion: These data indicate that the expression of sleep-related genes in PBCs of CKD patients may be associated with sleep abnormalities.
    No preview · Article · Sep 2015 · Clinical and Experimental Nephrology
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    ABSTRACT: Background: Some observational studies have shown the relationships between hyperuricemia and chronic kidney disease (CKD); however, the threshold of serum uric acid (SUA) for deterioration of kidney function and the association between SUA and kidney injury by baseline kidney function remains unclear. This study aimed to clarify the relationships between SUA and reduced kidney function. Methods: We analyzed a historical cohort of male Japanese individuals who underwent medical checkup between 1998 and 2007. Participants with baseline data and who were followed up for at least one year were included and stratified according to baseline kidney function. Kidney function was classified as normal [estimated glomerular filtration rate (eGFR) ≥ 90 ml/min/1.73 m2] or mildly reduced (eGFR 60-89 ml/min/1.73 m2). The outcome measured was kidney impairment defined as a decrease in eGFR to < 60 ml/min/1.73 m2. Associations between SUA and risk for outcome and eGFR slopes were assessed. Results: A total of 41632 subjects with mean age 45.4 years were included. During a mean follow-up of four years, 3186 (7.6%) subjects developed kidney dysfunction. Subjects with SUA ≥ 6.0 mg/dL had a significantly increased risk for kidney impairment compared with subjects with SUA of 4-4.9 mg/dL. SUA threshold levels were different according to baseline kidney function; SUA ≥ 7.0 and ≥ 6.0 mg/dL for normal and mildly reduced kidney function, respectively. Approximately the same trends were observed for eGFR slopes. Conclusion: In the general population, hyperuricemia appears to be a risk factor for kidney impairment in males. For participants with mild kidney dysfunction, even a slight elevation of SUA can be a risk factor.
    Preview · Article · Sep 2015 · PLoS ONE
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    ABSTRACT: Multidrug resistance-associated protein 3 (MRP3) is a carrier-type transport protein belonging to the ABC transporters. In this study, we investigated the safety and immunogenicity of a MRP3-derived peptide (MRP3765) as a vaccine and characterized the MRP3-specific T cell responses induced. Twelve hepatocellular carcinoma (HCC) patients treated with hepatic arterial infusion chemotherapy (HAIC) were enrolled. The MRP3-derived peptide was emulsified in incomplete Freund's adjuvant and administered via subcutaneous immunization three times weekly. No serious adverse drug reactions to the peptide vaccine were observed, and the vaccination was well tolerated. The vaccination induced MRP3-specific immunity in 72.7% of the patients. In a phenotypic analysis, the largest post-vaccinated increase in MRP3-specific T cells was due to an increase in cells with the effector memory phenotype. Among the 12 patients, one patient showed a partial response, nine showed a stable disease, and two showed a progressive disease. The median overall survival time was 14.0 months. In conclusion, the safety, effects of immune boosting, and possible prolongation of overall survival by the MRP3-derived peptide demonstrate the potential of the peptide to provide clinical benefit in HCC patients. Copyright © 2015. Published by Elsevier Ireland Ltd.
    No preview · Article · Sep 2015 · Cancer letters
  • Y. Sakai · M. Nagashimada · N. Nagata · Y. Ni · S. Kaneko · T. Ota

    No preview · Conference Paper · Sep 2015
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    ABSTRACT: A 60-year-old male with end-stage kidney disease due to autosomal polycystic kidney disease began maintenance hemodialysis in 2005. A brain CT scan showed dilatation of left vertebral artery, basilar artery, bilateral post cerebral artery, and middle cerebral artery. At the time, he was diagnosed as vertebrobasilar dolichoectasia. He was once admitted to our hospital for ischemic stroke. After discharge, he was treated with anticoagulant agent from 2010 to 2012 without any new stroke events. In March, 2012, he was admitted to our hospital for an evaluation of diplopia and left hemiplegia. Brain MRI showed acute ischemia of bilateral pons and right temporal lobe. He was once recovered with urokinase and argatroban, but 3 months after admission, he died with sudden hypotension and impaired consciousness. Autopsy revealed that subarachnoid hemorrhage due to the rupture of basilar artery aneurysm was responsible for this event.
    Preview · Article · Aug 2015

Publication Stats

11k Citations
2,363.23 Total Impact Points

Institutions

  • 1985-2015
    • Kanazawa University
      • • Department of Gastroenterology
      • • Department of Disease Control and Homeostasis
      • • Department of Internal Medicine
      • • Department of Laboratory Medicine
      • • School of Medicine
      • • Division of Immunology and Molecular Biology
      Kanazawa, Ishikawa, Japan
  • 1997-2014
    • Kanazawa Medical University
      • • Department of Gastroenterology
      • • Department of Internal Medicine (III)
      Kanazawa, Ishikawa, Japan
  • 2002-2006
    • The University of Tokyo
      • • Department of Chemistry
      • • School of Medicine
      Tōkyō, Japan
  • 1994
    • Nippon Kayaku Co., Ltd.
      Edo, Tōkyō, Japan
  • 1989
    • National Institute of Allergy and Infectious Diseases
      • Laboratory of Immunoregulation
      베서스다, Maryland, United States