Options
Korsten, Peter
Loading...
Preferred name
Korsten, Peter
Official Name
Korsten, Peter
Alternative Name
Korsten, P.
Main Affiliation
Now showing 1 - 10 of 10
2015Journal Article [["dc.bibliographiccitation.firstpage","290"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Zeitschrift fĂĽr Rheumatologie"],["dc.bibliographiccitation.lastpage","299"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T09:57:36Z"],["dc.date.available","2018-11-07T09:57:36Z"],["dc.date.issued","2015"],["dc.description.abstract","Interstitial nephritis is responsible for about 12% of end-stage renal disease in Germany. It comprises an etiologically heterogenous group of inflammatory renal disorders which primarily affect the renal interstitium and tubuli. Drugs, predominantly antibiotics, nonsteroidal anti-inflammatory drugs and proton pump inhibitors are causative in the majority of cases. Rheumatic diseases frequently affect the kidneys, either the glomeruli or the interstitial tissues. Inflammatory interstitial processes can be accompanied by complex functional tubular disorders. This review gives an overview about clinical and laboratory findings of interstitial nephritis in the context of rheumatic diseases. Sarcoidosis, tubulointerstitial nephritis and uveitis (TINU) syndrome, primary Sjogren's syndrome, and IgG4-related disease often show an interstitial nephritis when the kidneys are affected. Other diseases, such as systemic lupus erythematosus, systemic sclerosis, drug reaction with eosinophilia and systemic symptoms (DRESS) syndrome, and granulomatosis with polyangiitis are more rarely associated with predominant interstitial nephritis. Glucocorticoids are the mainstay of therapy for most cases; in refractory cases or when side effects occur, second-line immunosuppressants such as mycophenolate mofetil, azathioprine and others, rarely biologics, can be used."],["dc.identifier.doi","10.1007/s00393-014-1482-0"],["dc.identifier.isi","000355606600004"],["dc.identifier.pmid","25962450"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37197"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1435-1250"],["dc.relation.issn","0340-1855"],["dc.title","Interstitial nephritis in rheumatic diseases"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2011Journal Article [["dc.bibliographiccitation.artnumber","R94"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Critical Care"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Johanna, Temme"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Wessels, Johannes Theodor"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T09:01:04Z"],["dc.date.available","2018-11-07T09:01:04Z"],["dc.date.issued","2011"],["dc.description.abstract","Introduction: Sepsis is characterized by systemic microvascular dysfunction. Endothelial progenitor cells (EPCs) are critically involved in maintaining vascular homeostasis under both physiological and pathological conditions. The aim of the present study was to analyze the endothelial progenitor cell system in patients suffering from sepsis with acute renal dysfunction. Methods: Patients with newly diagnosed sepsis were recruited from the ICU in a nonrandomized prospective manner. Blood samples were obtained within the first 12 hours after the diagnosis of sepsis. For quantifying endothelial progenitor cells (EPCs), CD133(+)/Flk-1(+) cells were enumerated by cytometric analysis. Analysis of EPC proliferation was performed by a colony-forming units (CFU) assay. Blood concentrations of proangiogenic mediators were measured by ELISA. Acute renal dysfunction was diagnosed according to the Acute Kidney Injury Network (AKIN) criteria. Depending on the overall mean creatinine concentration during the stay at the ICU, patients were either assigned to a 'normal creatinine group' or to a 'high creatinine group'. Survival rates, frequency of dialysis, the simplified acute physiology score (SAPS) II scores, and different laboratory parameters were collected/used for further clinical characterization Results: Circulating EPCs were significantly higher in all sepsis patients included in the study as opposed to healthy controls. Patients within the 'high creatinine group' showed an even more pronounced EPC increase. In contrast, EPC proliferation was severely affected in sepsis. Neither total circulating EPCs nor EPC proliferation differed between patients requiring dialysis and patients without renal replacement therapy. Cell numbers and cell proliferation also did not differ between surviving patients and patients with sepsis-related death. Serum levels of vascular endothelial growth factor (VEGF), stromal derived factor-1 (SDF-1), and Angiopoietin-2 were higher in sepsis than in healthy controls. Sepsis patients within the 'high creatinine group' showed significantly higher mean serum levels of uric acid. Conclusions: Sepsis significantly affects the endothelial progenitor cell system, as reflected by increased EPC numbers, increased concentrations of proangiogenic mediators, and reduced proliferative capacity of the cells. This occurs independently from the frequency of dialysis and from patient survival. Increased serum levels of uric acid are possibly responsible for stronger EPC mobilization in sepsis patients with higher average creatinine levels."],["dc.identifier.doi","10.1186/cc10100"],["dc.identifier.isi","000292506000018"],["dc.identifier.pmid","21396100"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24323"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.intern","In goescholar not merged with http://resolver.sub.uni-goettingen.de/purl?gs-1/15283 but duplicate"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1466-609X"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.holder","Patschan et al.; licensee BioMed Central Ltd."],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Endothelial progenitor cells (EPC) in sepsis with acute renal dysfunction (ARD)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2016Journal Article [["dc.bibliographiccitation.firstpage","1173"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Arthritis Care & Research"],["dc.bibliographiccitation.lastpage","1179"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Konig, Maximilian F."],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Barrantes-Freer, Alonso"],["dc.contributor.author","Sweiss, Nadera J."],["dc.contributor.author","Vasko, Radovan"],["dc.date.accessioned","2018-11-07T10:10:47Z"],["dc.date.available","2018-11-07T10:10:47Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1002/acr.22781"],["dc.identifier.isi","000383501900015"],["dc.identifier.pmid","26555558"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39927"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","2151-4658"],["dc.relation.issn","2151-464X"],["dc.title","Respiratory Distress and Nephropathy in a Young Male With Small-Joint Polyarthritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2013Journal Article [["dc.bibliographiccitation.firstpage","1523"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Lupus"],["dc.bibliographiccitation.lastpage","1525"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Fliesser, E. E."],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Niewold, T. B."],["dc.contributor.author","Patschan, Daniel"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Patschan, Susann Andrea"],["dc.date.accessioned","2018-11-07T09:16:51Z"],["dc.date.available","2018-11-07T09:16:51Z"],["dc.date.issued","2013"],["dc.description.abstract","We report the case of a 19-year-old woman with progressive proliferative lupus nephritis (LN) class III after induction and maintenance therapy with mycophenolate mofetil (MMF). Despite a satisfying clinical improvement proteinuria progressed under this medication. We treated the patient with additional belimumab after discussing other options. Following treatment with belimumab, proteinuria rapidly improved to almost normal levels and clinical remission lasted. Belimumab might hold promise for this indication."],["dc.description.sponsorship","GlaxoSmithKline"],["dc.identifier.doi","10.1177/0961203313504145"],["dc.identifier.isi","000329545400012"],["dc.identifier.pmid","24014569"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13039"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28030"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.relation.eissn","0961-2033"],["dc.relation.issn","1477-0962"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Successful treatment of a mycophenolate mofetil-refractory proliferative lupus nephritis with Belimumab in a 19-year-old woman"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2011Journal Article [["dc.bibliographiccitation.firstpage","507"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Therapeutic Apheresis and Dialysis"],["dc.bibliographiccitation.lastpage","509"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Groenewold, Frauke"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Koziolek, Michael"],["dc.date.accessioned","2018-11-07T08:51:21Z"],["dc.date.available","2018-11-07T08:51:21Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1111/j.1744-9987.2011.00978.x"],["dc.identifier.isi","000295138900015"],["dc.identifier.pmid","21974708"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21915"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1744-9979"],["dc.title","Plasmapheresis-Refractory Thrombotic Microangiopathy in a Hematopoietic Stem Cell Transplant Recipient"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2016Journal Article [["dc.bibliographiccitation.firstpage","1625"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Lupus"],["dc.bibliographiccitation.lastpage","1626"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Wallbach, Manuel"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Hoffmann, S."],["dc.contributor.author","Niewold, T. B."],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Korsten, Peter"],["dc.date.accessioned","2018-11-07T10:05:33Z"],["dc.date.available","2018-11-07T10:05:33Z"],["dc.date.issued","2016"],["dc.identifier.doi","10.1177/0961203316651746"],["dc.identifier.isi","000387447700015"],["dc.identifier.pmid","27216419"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/38918"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1477-0962"],["dc.relation.issn","0961-2033"],["dc.title","Elevated procalcitonin levels in a severe lupus flare without infection"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2016Journal Article [["dc.bibliographiccitation.firstpage","513"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","CLINICAL AND EXPERIMENTAL RHEUMATOLOGY"],["dc.bibliographiccitation.lastpage","520"],["dc.bibliographiccitation.volume","34"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Streich, J.-H."],["dc.contributor.author","Blaschke, S."],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Mai, Burkhard"],["dc.contributor.author","Kostrzewa, Markus"],["dc.contributor.author","Sparbier, Katrin"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Bohr, Stefan"],["dc.contributor.author","Dihazi, Hassan"],["dc.date.accessioned","2018-11-07T10:14:47Z"],["dc.date.available","2018-11-07T10:14:47Z"],["dc.date.issued","2016"],["dc.description.abstract","Objective To study the protein expression differences between primary fibroblasts explanted from synovial membranes of patients with rheumatoid arthritis (RA) and osteoarthritis (OA). Methods Fibroblast cultures were obtained from 10 patients with RA and 5 patients with OA. After two-dimensional gel electrophoresis, proteins were excised and identified using peptide mass fingerprint. Expression of selected proteins was subsequently examined by immunoblot. Furthermore, we examined the cellular lysates for the presence of citrullinated proteins. Results The study was designed to compare expression changes of the common proteins detected in all studied fibroblast cultures (i.e. detected in all patients samples). We totally identified 191 shared proteins between RA and OA fibroblasts. A significant difference was defined as at least 2-fold upregulation or 0.6-fold downregulation of protein expression. The most obvious alteration observed in RA was the appearance of several vimentin fragments not present in OA. We did not detect citrullinated proteins in lysates from RA fibroblasts. This corroborates the current assumption that fibroblasts are not able to citrullinate proteins by themselves and that invading macrophages play a central role in this process. Conclusion We demonstrated that fibroblasts from patients with RA, despite being grown under identical conditions, preserve a particular feature and generate vimentin fragments not present in fibroblasts from OA. Elevated levels of different vimentin fragments have been recently reported in several rheumatic conditions. Further studies are needed to elucidate the pathogenic mechanisms induced by vimentin fragments in RA."],["dc.identifier.isi","000376977900019"],["dc.identifier.pmid","27049516"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40684"],["dc.language.iso","en"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1593-098X"],["dc.relation.issn","0392-856X"],["dc.title","Vimentin fragments are potential markers of rheumatoid synovial fibroblasts"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details PMID PMC WOS2014Journal Article [["dc.bibliographiccitation.firstpage","98"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Journal of Emergency Medicine"],["dc.bibliographiccitation.lastpage","104"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Sliwa, Bodo"],["dc.contributor.author","Kuehn, Matthias"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Blaschke, Sabine"],["dc.date.accessioned","2018-11-07T09:41:57Z"],["dc.date.available","2018-11-07T09:41:57Z"],["dc.date.issued","2014"],["dc.description.abstract","Objectives In emergency departments (EDs), overcrowding, workload complexity, and cost containment represent current operational problems. In this retrospective observational study, we analyzed the effects of a professional quality management (QM) system on patient flow, diagnostic validity, and hospital costs. Materials and methods In 2005/2006, the main ED at the University Medical Center Goettingen was reorganized. A professional QM system according to DIN EN ISO 9001:2008 was introduced in 2008. In a retrospective observational study, we compared the number of cases, the spectrum of clinical diagnoses, the validity of diagnoses, and hospital costs in the ED before (2005) and 2 years after the introduction of the QM system (2010). Results In the ED at the University Medical Center Goettingen, the number of cases increased by 22.7% between 2005 and 2010. After the introduction of the QM system, a significant reduction in patients' length of stay within the ED was achieved (P < 0.001). Furthermore, the rate of diagnostic errors for patients assigned for admission within the ED could be reduced significantly (P=0.002). A reduction of patient-related hospital costs of 8.9% was achieved by restriction of diagnostic tests according to standard operating procedures for each emergency diagnosis. Conclusion The introduction of a professional QM system in EDs improves patient flow as well as quality of medical care and results in a significant reduction in hospital costs. Further analyses should evaluate the effects of QM on quality indicators in a prospective multicenter study. Validation of results has to be performed in a dynamic model for process simulation."],["dc.identifier.doi","10.1097/MEJ.0b013e3283613e8d"],["dc.identifier.isi","000332210100004"],["dc.identifier.pmid","24573191"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33847"],["dc.language.iso","en"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.relation.eissn","0969-9546"],["dc.relation.issn","1473-5695"],["dc.title","Impact of professional quality management on interdisciplinary emergency care units"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2014Journal Article [["dc.bibliographiccitation.firstpage","722"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Der Internist"],["dc.bibliographiccitation.lastpage","725"],["dc.bibliographiccitation.volume","55"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Schrempf, L. E."],["dc.contributor.author","Zimmermann, Ortrud"],["dc.contributor.author","Schulze, Marco H."],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T09:39:43Z"],["dc.date.available","2018-11-07T09:39:43Z"],["dc.date.issued","2014"],["dc.description.abstract","We present the case of a 48-year-old Vietnamese man with endophthalmitis, liver abscess, and pulmonary and cerebral septic emboli. Klebsiella pneumoniae was isolated as the causative organism; there were no laboratory findings suggestive of invasive fungal infection. Klebsiella pneumoniae invasive syndrome is a rare disease in Germany. This case report exemplifies the necessity of a dedicated diagnostic approach that takes into consideration factors such as ethnic origin and accompanying diseases of the patient."],["dc.identifier.doi","10.1007/s00108-014-3484-z"],["dc.identifier.isi","000336451400009"],["dc.identifier.pmid","24682317"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33350"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1432-1289"],["dc.relation.issn","0020-9554"],["dc.title","Endophthalmitis, liver abscess, and cerebral and pulmonary emboli in a 48-year-old Vietnamese man"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2010Journal Article [["dc.bibliographiccitation.firstpage","E17"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","American Journal of Kidney Diseases"],["dc.bibliographiccitation.lastpage","E21"],["dc.bibliographiccitation.volume","56"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Sweiss, Nadera J."],["dc.contributor.author","Nagorsnik, Ulf"],["dc.contributor.author","Niewold, Timothy B."],["dc.contributor.author","Groene, Hermann-Josef"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T08:35:56Z"],["dc.date.available","2018-11-07T08:35:56Z"],["dc.date.issued","2010"],["dc.description.abstract","Tumor necrosis factor alpha (TNF-alpha) inhibitors are used in the treatment of rheumatoid arthritis, psoriasis, psoriatic arthritis, Crohn disease, ankylosing spondylitis, and juvenile idiopathic arthritis. Use of TNF inhibitors is associated with the induction of autoimmunity (systemic lupus erythematosus, vasculitis, psoriasis, and sarcoidosis/sarcoid-like granulomas). We report a case of interstitial granulomatous nephritis in a patient with ankylosing spondylitis after 18 months of treatment with adalimumab. Previously reported cases of sarcoid-like reactions secondary to the use of TNF-alpha inhibitors involved the liver, lung, lymph nodes, central nervous system, and skin. Granulomatous nephritis after adalimumab treatment has not been described. Close observation of patients undergoing treatment with TNF inhibitors for evolving signs and symptoms of autoimmunity is required. Organ involvement is unpredictable, which makes correct diagnosis and management extremely challenging. Am J Kidney Dis 56:e17-e21. (C) 2010 by the National Kidney Foundation, Inc."],["dc.identifier.doi","10.1053/j.ajkd.2010.08.019"],["dc.identifier.isi","000284401800001"],["dc.identifier.pmid","20974510"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18197"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","W B Saunders Co-elsevier Inc"],["dc.relation.issn","0272-6386"],["dc.title","Drug-Induced Granulomatous Interstitial Nephritis in a Patient With Ankylosing Spondylitis During Therapy With Adalimumab"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS