Nephron Experimental Nephrology最新文献

{"title":"Inhalation of Hydrogen Gas Is Beneficial for Preventing Contrast-Induced Acute Kidney Injury in Rats.","authors":"Koichiro Homma, Tadashi Yoshida, Maho Yamashita, Kei Hayashida, Matsuhiko Hayashi, Shingo Hori","doi":"10.1159/000369068","DOIUrl":"10.1159/000369068","url":null,"abstract":"<p><p>Background: The present study aimed at investigating the effect of a novel antioxidant, hydrogen (H₂) gas, on the severity of contrast-induced acute kidney injury (CIAKI) in a rat model. Methods: CIAKI was induced in rats by intravenous injection of a contrast medium, Ioversol, in addition to reagents inhibiting prostaglandin and nitric oxide synthesis. During the injection of these reagents, the rats inhaled H₂ gas or control gas. Results: One day after the injection, serum levels of urea nitrogen were significantly lower in H₂ gas-inhaling CIAKI rats (17.6 ± 2.3 mg/dl) than those in control gas-treated CIAKI rats (36.0 ± 7.3 mg/dl), although they both were elevated as compared to untreated rats (14.9 ± 0.9 mg/dl). Consistently, creatinine clearance in H₂ gas-treated CIAKI rats was higher than that in control gas-treated counterparts. Renal histological analysis revealed that the formation of proteinaceous casts and tubular necrosis was improved by H₂ gas inhalation. Mechanistic analyses showed that inhalation of H₂ gas significantly reduced renal cell apoptosis, expression of cleaved caspase 3, and expression of an oxidative stress marker, 8-hydroxydeoxyguanosine, in injured kidneys. Conclusion: Results suggest that H₂ gas inhalation is effective in ameliorating the severity of CIAKI in rats by reducing renal cell apoptosis and oxidative stress. © 2015 S. Karger AG, Basel.</p>","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":" ","pages":"None"},"PeriodicalIF":0.0,"publicationDate":"2015-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32978007","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contents Vol. 128, 2014","authors":"J. Latus, S. Segerer, N. Braun, D. Kitterer, J. Dippon, Simon Müller, F. Artunc, M. Alscher, Anne-Émilie Declèves, K. Sharma, J. Satriano, M. Ullian, L. Luttrell, Mi‐Hye Lee, T. Morinelli, K. Homma, Tadashi Yoshida, Maho Yamashita, K. Hayashida, M. Hayashi, S. Hori, Satz Mengensatzproduktion, Druckerei Stückle","doi":"10.1159/000375518","DOIUrl":"https://doi.org/10.1159/000375518","url":null,"abstract":" Chronic Kidney Disease and Hypertension A. Levin, Vancouver, B.C. R. Gansevoort, Groningen  Acute Kidney Injury R. Mehta, San Diego, Calif. N. Kolhe, Derby  Dialysis J. Daugirdas, Chicago, Ill. C. Hutchison, Hawkes Bay C. Fraansen, Groningen  Patient Subjective Experience, Healthcare Delivery and Innovation in Practice R. Fluck, Derby E. Brown, London  Crossover States with Non-Renal Organ Systems C. Chan, Toronto, Ont. T. Breidthardt, Basel N. Selby, Derby  Transplantation A. Chandraker, Boston, Mass. A. Salama, London Editor-in-Chief","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":"128 1","pages":"I - VI"},"PeriodicalIF":0.0,"publicationDate":"2015-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000375518","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64772455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stimulation of Cyclooxygenase 2 Expression in Rat Peritoneal Mesothelial Cells.","authors":"Michael E Ullian, Louis M Luttrell, Mi-Hye Lee, Thomas A Morinelli","doi":"10.1159/000368673","DOIUrl":"10.1159/000368673","url":null,"abstract":"<p><p>Objective: Since peritoneal dialysis causes peritoneal fibrosis, we examined how glucose (osmotic factor), mannitol (osmotic control), and angiotensin II (AngII) regulate proinflammatory cyclooxygenase 2 (COX-2) in primary rat peritoneal mesothelial cells. Materials and Methods: For this study, we used the following material (n = 4-8 cell lines): cells, passages 1-2; ¹²⁵I-AngII receptor surface binding (AT1R antagonist losartan, AT2R antagonist PD123319; both 10 µM); intracellular calcium probe calcium-5; COX-2 immunoblotting (β-actin normalized); real-time PCR of COX-2 gene PTGS2, and NF-κB inhibitor Ro-1069920 (5 µM). Results: AngII surface receptors were predominantly AT1R (minimally AT2R). AngII and glucose increased COX-2 protein expression concentration dependently; mannitol also increased COX-2 expression. Maximal COX-2 protein expression was observed after 6 h (AngII) and 24 h (glucose, mannitol). The time course of increases in PTGS2 mRNA levels reflected that of COX-2 protein expression. At optimal exposure conditions (time/concentration), glucose was 5-fold more efficacious in stimulating COX-2 protein expression than AngII or mannitol. Losartan fully inhibited COX-2 protein responses to AngII and mannitol, but minimally inhibited responses to glucose. Ro-1069920 fully inhibited COX-2 protein responses to each effector. Conclusion: AngII, glucose, and osmotic stress (mannitol) activate COX-2; NF-κB may be an ideal site for COX-2 blockade, and COX-2 activation by osmotic stress requires AT1R, but activation by glucose is more robust and mechanistically complex. © 2014 S. Karger AG, Basel.</p>","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":" ","pages":"None"},"PeriodicalIF":0.0,"publicationDate":"2014-12-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32928022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Polyuria in Hantavirus Infection Reflects Disease Severity and Is Associated with Prolonged Hospital Stay: A Systematic Analysis of 335 Patients from Southern Germany.","authors":"Joerg Latus, Daniel Kitterer, Juergen Dippon, Simon Müller, Ferruh Artunc, Stephan Segerer, M Dominik Alscher, Niko Braun","doi":"10.1159/000368934","DOIUrl":"10.1159/000368934","url":null,"abstract":"<p><p>Background/Aims: Puumala virus (PUUV) infection leads to nephropathia epidemica (NE), especially in endemic areas in Central Europe. The clinical course of NE is characterized by acute kidney injury (AKI) with thrombocytopenia followed by polyuria to a different degree. The prevalence of polyuria and its associated risk factors have not been reported in a large cohort of NE patients. Methods: Clinical and laboratory data during the acute phase of the disease were obtained from the medical reports and files of 335 patients who received in-hospital treatment during acute hantavirus infection. Comprehensive statistical models were developed to estimate the probability of polyuria. Results: The median age at diagnosis was 47 years (interquartile range, IQR 40-59) and 48% of the patients developed polyuria with a urinary output of 5,100 ml/day (IQR 4,200-7,300). The hospital stay was significantly longer in the polyuric group compared to the nonpolyuric group [8 days (IQR 6-10) vs. 6 days (IQR 5-8); p = 0.04]. Using logistic regression analysis, male gender (odds ratio, OR = 1.6; 95% confidence interval, CI 1.05-2.58; p = 0.03), oliguria/anuria during NE (OR = 2.56; 95% CI 1.65-4.01; p < 0.001), severe AKI (OR = 1.87; 95% CI 1.22-2.9; p < 0.001), and hematuria (OR = 1.78; 95% CI 1.02-3.15; p = 0.04) were significantly associated with the development of polyuria. In a multivariate model, the probability of polyuria was 0.19 (SEM ± 0.05) in female patients presenting with mild/moderate AKI without anuria/oliguria. Conclusions: Almost 50% of hospitalized NE patients developed polyuria, which was associated with a prolonged hospital stay. The probability of the development of polyuria was lowest in female patients with mild/moderate, non-oliguric/anuric AKI. © 2014 S. Karger AG, Basel.</p>","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":" ","pages":"None"},"PeriodicalIF":0.0,"publicationDate":"2014-12-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32926883","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Beneficial Effects of AMP-Activated Protein Kinase Agonists in Kidney Ischemia-Reperfusion: Autophagy and Cellular Stress Markers.","authors":"Anne-Emilie Declèves, Kumar Sharma, Joseph Satriano","doi":"10.1159/000368932","DOIUrl":"10.1159/000368932","url":null,"abstract":"<p><p>Background: Kidney ischemia-reperfusion is a form of acute kidney injury resulting in a cascade of cellular events prompting rapid cellular damage and suppression of kidney function. A cellular response to ischemic stress is the activation of AMP-activated protein kinase (AMPK), where AMPK induces a number of homeostatic and renoprotective mechanisms, including autophagy. However, whether autophagy is beneficial or detrimental in ischemia-reperfusion remains controversial. We investigated the effects of agonist induction of AMPK activity on autophagy and cell stress proteins in the model of kidney ischemia-reperfusion. Methods: AMPK agonists, AICAR (0.1 g/kg) and metformin (0.3 g/kg), were administered 24 h prior to ischemia, with kidneys harvested at 24 h of reperfusion. Results: We observed a paradoxical decrease in AMPK activity accompanied by increases in mammalian target of rapamycin (mTOR) C1 activity and p62/SQSTM1 expression. These results led us to propose that AMPK and autophagy are insufficient to properly counter the cellular insults in ischemia-reperfusion. Agonist induction of AMPK activity with AICAR or metformin increased macroautophagy protein LC3 and normalized p62/SQSTM1 expression and mTOR activity. Ischemia-reperfusion increases in Beclin-1 and PINK1 expressions, consistent with increased mitophagy, were also mitigated with AMPK agonists. Stress-responsive and apoptotic marker expressions increase in ischemia-reperfusion and are significantly attenuated with agonist administration, as are early indicators of fibrosis. Conclusions: Our data suggest that levels of renoprotective AMPK activity and canonical autophagy are insufficient to maintain cellular homeostasis, contributing to the progression of ischemia-reperfusion injury. We further demonstrate that induction of AMPK activity can provide beneficial cellular effects in containing injury in ischemia-reperfusion. © 2014 S. Karger AG, Basel.</p>","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":" ","pages":"None"},"PeriodicalIF":0.0,"publicationDate":"2014-12-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4458239/pdf/nihms637786.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"32904967","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Contents Vol. 126, 2014","authors":"S. O'Neill, E. Harrison, J. Ross, S. Wigmore, J. Hughes, Wanjun Zhu, Junichiro Kato, M. Nakayama, T. Yokoo, S. Ito, J. Kingma, Denys Simard, P. Voisine, J. Rouleau, B. Betz, B. Conway, Satz Mengensatzproduktion, Druckerei Stückle","doi":"10.1159/000366182","DOIUrl":"https://doi.org/10.1159/000366182","url":null,"abstract":"","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":"126 1","pages":"I - IV"},"PeriodicalIF":0.0,"publicationDate":"2014-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000366182","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64737675","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Front & Back Matter","authors":"C. McIntyre, S. Beesley","doi":"10.1159/000365338","DOIUrl":"https://doi.org/10.1159/000365338","url":null,"abstract":"Each paper needs an abstract of up to 250 words. It should be structured as follows: Background/Aims: What is the major problem that prompted the study? Methods: How was the study carried out? Results: Most important findings? Conclusion: Most important conclusion? Abstracts of Minireviews: Should be divided into the following subsections: Background, Summary and Key Messages. The Background should provide a brief clinical context for the review and is followed by the Summary, which should include a concise description of the main topics covered in the text. The Key Messages encapsulate the main conclusions of the review.s of Minireviews: Should be divided into the following subsections: Background, Summary and Key Messages. The Background should provide a brief clinical context for the review and is followed by the Summary, which should include a concise description of the main topics covered in the text. The Key Messages encapsulate the main conclusions of the review. Footnotes: Avoid footnotes. Tables and illustrations: Tables are part of the text. Place them at the end of the text file. Illustration data must be stored as separate files. Do not integrate figures into the text. Electronically submitted b/w half-tone and color illustrations must have a final resolution of 300 dpi after scaling, line drawings one of 800–1,200 dpi. Color illustrations Online edition: Color illustrations are reproduced free of charge. In the print version, the illustrations are reproduced in black and white. Please avoid referring to the colors in the text and figure legends. Print edition: Up to 6 color illustrations per page can be integrated within the text at CHF 800.00 per page. References: In the text identify references by Arabic numerals [in square brackets]. Material submitted for publication but not yet accepted should be noted as [unpublished data] and not be included in the reference list. The list of references should include only those publications which are cited in the text. Number references in the order in which they are first mentioned in the text; do not list alphabetically. The surnames of the authors followed by initials should be given. There should be no punctuation other than a comma to separate the authors. Preferably, please cite all authors. Abbreviate journal names according to the Index Medicus system. Also see International Committee of Medical Journal Editors: Uniform requirements for manuscripts submitted to biomedical journals (www. icmje.org). Examples (a) Papers published in periodicals: Tomson C: Vascular calcification in chronic renal failure. Nephron Clin Pract 2003;93:c124–c130. (b) Papers published only with DOI numbers: Theoharides TC, Boucher W, Spear K: Serum interleukin-6 reflects disease severity and osteoporosis in mastocytosis patients. Int Arch Allergy Immunol DOI: 10.1159/000063858. (c) Monographs: Matthews DE, Farewell VT: Using and Understanding Medical Statistics, ed 3, revised. Basel, Karger, 1996. (d) Edited b","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":"9 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000365338","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64728896","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Author and Subject Index Vol. 126, No. 2, 2014","authors":"","doi":"10.1159/000362773","DOIUrl":"https://doi.org/10.1159/000362773","url":null,"abstract":"","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":"126 1","pages":"125 - 125"},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000362773","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64719518","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Title Page / Table of Contents","authors":"","doi":"10.1159/000362772","DOIUrl":"https://doi.org/10.1159/000362772","url":null,"abstract":"","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":"126 1","pages":"I - IV"},"PeriodicalIF":0.0,"publicationDate":"2014-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000362772","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64719198","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Front & Back Matter","authors":"","doi":"10.1159/000362512","DOIUrl":"https://doi.org/10.1159/000362512","url":null,"abstract":"Each paper needs an abstract of up to 250 words. It should be structured as follows: Background/Aims: What is the major problem that prompted the study? Methods: How was the study carried out? Results: Most important findings? Conclusion: Most important conclusion? Abstracts of Minireviews: Should be divided into the following subsections: Background, Summary and Key Messages. The Background should provide a brief clinical context for the review and is followed by the Summary, which should include a concise description of the main topics covered in the text. The Key Messages encapsulate the main conclusions of the review.s of Minireviews: Should be divided into the following subsections: Background, Summary and Key Messages. The Background should provide a brief clinical context for the review and is followed by the Summary, which should include a concise description of the main topics covered in the text. The Key Messages encapsulate the main conclusions of the review. Footnotes: Avoid footnotes. Tables and illustrations: Tables are part of the text. Place them at the end of the text file. Illustration data must be stored as separate files. Do not integrate figures into the text. Electronically submitted b/w half-tone and color illustrations must have a final resolution of 300 dpi after scaling, line drawings one of 800–1,200 dpi. Color illustrations Online edition: Color illustrations are reproduced free of charge. In the print version, the illustrations are reproduced in black and white. Please avoid referring to the colors in the text and figure legends. Print edition: Up to 6 color illustrations per page can be integrated within the text at CHF 800.– per page. References: In the text identify references by Arabic numerals [in square brackets]. Material submitted for publication but not yet accepted should be noted as [unpublished data] and not be included in the reference list. The list of references should include only those publications which are cited in the text. Number references in the order in which they are first mentioned in the text; do not list alphabetically. The surnames of the authors followed by initials should be given. There should be no punctuation other than a comma to separate the authors. Preferably, please cite all authors. Abbreviate journal names according to the Index Medicus system. Also see International Committee of Medical Journal Editors: Uniform requirements for manuscripts submitted to biomedical journals (www. icmje.org). Examples (a) Papers published in periodicals: Tomson C: Vascular calcification in chronic renal failure. Nephron Clin Pract 2003;93:c124–c130. (b) Papers published only with DOI numbers: Theoharides TC, Boucher W, Spear K: Serum interleukin-6 reflects disease severity and osteoporosis in mastocytosis patients. Int Arch Allergy Immunol DOI: 10.1159/000063858. (c) Monographs: Matthews DE, Farewell VT: Using and Understanding Medical Statistics, ed 3, revised. Basel, Karger, 1996. (d) Edited bo","PeriodicalId":18993,"journal":{"name":"Nephron Experimental Nephrology","volume":"126 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2014-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000362512","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"64716459","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}