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Yokosuka, Japan

Stanton M.L.,University of Florida | Joy M.S.,Kidney Center | Frye R.F.,University of Florida
Journal of Chromatography B: Analytical Technologies in the Biomedical and Life Sciences

A rapid method to determine fexofenadine concentrations in human plasma using protein precipitation in 96-well plates and liquid chromatography-tandem mass spectrometry was validated. Plasma proteins were precipitated with acetonitrile containing the internal standard fexofenadine-d6, mixed briefly, and then filtered into a collection plate. The resulting filtrate was diluted and injected onto a Phenomenex Gemini C18 (50 mm × 2.0 mm, 5 μm) analytical column. The mobile phase consisted of 0.1% formic acid, 5 mM ammonium acetate in deionized water and methanol (35:65, v/v). The flow rate was 0.2 ml/min and the total run time was 2 min. Detection of the analytes was achieved using positive ion electrospray ionization and high resolution multiple reaction monitoring mode (H-SRM). The linear standard curve ranged from 1 to 500 ng/ml and the precision and accuracy (intra- and inter-run) were within 4.3% and 8.0%, respectively. The method has been applied successfully to determine fexofenadine concentrations in human plasma samples obtained from subjects administered a single oral dose of fexofenadine. The method is rapid, sensitive, selective and directly applicable to human pharmacokinetic studies involving fexofenadine. © 2009 Elsevier B.V. All rights reserved. Source

Nitta K.,Kidney Center | Ogawa T.,Tokyo Womens Medical University
Contributions to Nephrology

Vascular calcification is very common in patients with end-stage renal disease (ESRD) and has been found to be associated with mineral and bone disorders. There are two types of vascular calcification: intimal and medial calcification. The transformation of vascular smooth muscle cells into osteoblast-like cells seems to be a key element in the pathogenesis of medial calcification in the presence of calcium and phosphate deposition. Vascular calcification causes increased arterial stiffness by medial calcification, which leads to left ventricular hypertrophy and decreased coronary artery perfusion and causes myocardial ischemia by intimal calcification. Thus, vascular calcification is thought to be associated with increased cardiovascular morbidity and mortality. Although current treatment strategies focus on correcting abnormal calcium, phosphate, parathyroid hormone, or vitamin D levels in ESRD patients, a better understanding of the mechanisms of vascular calcification may lead to the development of new therapeutic strategies that are capable of reducing vascular calcification and improving the cardiovascular outcome of ESRD patients. This review summarizes the pathophysiology, diagnostic procedure and therapeutic implication of vascular calcification in ESRD patients. © 2015 S. Karger AG, Basel. Source

Fujimori A.,Kidney Center
Blood Purification

Super high-flux HD is quite popular in Japan. 90% of -dialysis patients are treated using dialyzers with a β2-microglobulin clearance of >50 ml/min. If the target is β2-microglobulin, HDF is not necessary. However, removal of uremic toxins with a higher molecular weight and stability of circulation status, which is expected of on-line HDF, would lead to better survival of the patients. Demonstration of the beneficial effect of on-line HDF on the outcome in patients is awaited. Copyright © 2013 S. Karger AG, Basel. Source

Haratake J.,Saiseikai Yahata General Hospital | Yasunaga C.,Kidney Center | Shimajiri S.,University of Occupational and Environmental Health Japan | Matsuyama A.,University of Occupational and Environmental Health Japan | Hisaoka M.,University of Occupational and Environmental Health Japan
American Journal of Surgical Pathology

Pathologic lesions caused by lanthanum carbonate (LC), a recently developed phosphate-binding agent, have not been recorded. A peculiar gastroduodenal histiocytic lesion associated with a mucosal lanthanum overload was reported. Our routine gastrointestinal biopsy series included 6 cases with heavy lanthanum burden in the gastroduodenal mucosa. In addition to routine histopathologic examinations, a series of immunohistochemical analysis and electron microscopic examinations associated with x-ray diffraction and elemental analysis were performed. Six cases, 3 of male and 3 of female individuals with ages from 59 to 69 years, were all patients of end-stage renal diseases managed under dialysis and treated with LC for >21 months. Endoscopic examinations demonstrated gastric erosions in 3, gastric polyps in 2, and duodenal ulcer in 1. In the mucosal layer, there were numerous non-Langerhans cell histiocytes, stained with CD68 but not S100 protein, engulfing a large amount of mineral-like materials. An electron microscopic and elemental analysis revealed a similar distribution of lanthanum and phosphorus in the histiocytes. Long-standing LC administration can cause massive mucosal accumulation of lanthanum in the tissue histiocytes associated with several forms of gastroduodenal lesions. A long-standing outcome is not clear at present; hence, careful follow-up studies of these patients may be needed. Copyright © 2015 Wolters Kluwer Health, Inc. All rights reserved. Source

Ciavatta D.,Kidney Center | Falk R.J.,Kidney Center | Falk R.J.,University of North Carolina at Chapel Hill
Clinical and Experimental Immunology

Although studies on the immunopathogenesis of anti-neutrophil cytoplasm antibody (ANCA) vasculitis have been directed at understanding the autoantibody, there is growing evidence that points to the importance of ANCA autoantigen genes and their regulation. Transcriptional analysis indicates that ANCA autoantigen genes are active in mature neutrophils of ANCA vasculitis patients compared to healthy controls. The unusual transcriptional state of neutrophils from ANCA vasculitis patients appears to be a consequence of failed or disrupted epigenetic silencing. Defective epigenetic silencing could have global effects, by altering the transcriptional and phenotypic state of neutrophils, or local effects by permitting transcription of autoantigen genes from both strands resulting in anti-sense transcripts. Although the role of anti-sense transcripts is currently unknown, there are two intriguing possibilities. Anti-sense transcripts could function (as described for other genes) in transcriptional silencing of autoantigen genes, which takes place in normal neutrophil progenitors. In the setting of failed epigenetic silencing, the fate of anti-sense transcripts may be pathological and serve as a template for production of complementary autoantigens. The observation that ANCA vasculitis patients have anti-sense transcripts and antibodies to complementary proteins is consistent with a role of anti-sense transcripts in complementary protein production. A better understanding of epigenetic silencing and complementary proteins in ANCA vasculitis may unlock the underlying pathology of this condition. © 2011 The Authors; Clinical and Experimental Immunology © 2011 British Society for Immunology. Source

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