Koziolek, Michael Johann

[["dc.bibliographiccitation.firstpage","384"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","388"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.contributor.author","Zipfel, Peter F."],["dc.contributor.author","Skerka, Christine"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Groene, Elisabeth F."],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Strutz, Frank M."],["dc.date.accessioned","2018-11-07T11:12:37Z"],["dc.date.available","2018-11-07T11:12:37Z"],["dc.date.issued","2008"],["dc.description.abstract","A 36-year-old patient complained of progressing fatigue, lack of appetite, and weakness for a few weeks, for which he had been using paracetamol (acetaminophen) intermittently. He was referred to our center from another hospital with hemolysis, thrombocytopenia, and acute renal failure (ARF). On admission, the patient did not complain of any specific additional symptoms. Besides paracetamol, he had not received any other medication. The patient reported flu-like symptoms 3 months before admission. The family history was unremarkable. Physical examination revealed a pale-looking patient (180 cm; 81 kg) with icteric sclerae. He was tachycardic (110 heart beats per min) and had elevated blood pressure (155/90mmHg). No other physical abnormalities were detectable. Laboratory investigations are depicted in Table 1. Specific analyses: von Willebrand factor cleavage protease activity 31% (40-120%), von Willebrand Factor Multimere negative, antibodies to von Willebrand Factor cleavage protease negative, factor H 614 mgl(-1) (345-590 mgl(-1)). Western blot analyses with patient's serum revealed the presence of complement factor H (CFH) and complement factor H-like protein 1 (CFHL1), but no detectable levels of complement factor H-related proteins 1 and 3 (CFHR1 and CFHR3) (Figure 1a). Antibodies to CFHR1 were negative. Genetic analyses 1 showed no CFH mutation, but revealed homozygous deletion of a 83 kb genomic fragment representing CFHR3 and CFHR1 (Figure 1b). Kidneys were of normal size with increased density by ultrasound examination. Electrocardiography revealed ischemic changes posteroseptally, and hypertrophy of the left ventricle was diagnosed by echocardiography."],["dc.identifier.doi","10.1038/ki.2008.133"],["dc.identifier.isi","000257622900018"],["dc.identifier.pmid","18449173"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6184"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53705"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0085-2538"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Chronic course of a hemolytic uremic syndrome caused by a deficiency of factor H-related proteins (CFHR1 and CFHR3)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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 prüfen"],["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"]]

[["dc.bibliographiccitation.firstpage","563"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Clinical and Experimental Nephrology"],["dc.bibliographiccitation.lastpage","568"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Vasko, Radovan"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Ratliff, Brian B."],["dc.contributor.author","Jung, Klaus"],["dc.contributor.author","Gauczinski, Sarah"],["dc.contributor.author","Koziolek, Michael Johann"],["dc.date.accessioned","2018-11-07T09:21:45Z"],["dc.date.available","2018-11-07T09:21:45Z"],["dc.date.issued","2013"],["dc.description.abstract","The assessment of hydration status remains a challenging task in hemodialysis (HD) management. There are only limited data available on the relevance of clinical decisions in the estimation of dialysis overhydration (OH). The objective of this study was to examine the significance of clinical judgment in the assessment of pre-dialysis OH. We compared the performance of three methods of OH assessment: (1) clinical judgment guided by a single clinical examination with (2) multifrequency bioimpedance analysis (BIA) and (3) complex systematic clinical approach. We additionally studied the associations of these methods with selected laboratory and imaging parameters. Any of the single parameters alone reached a sufficient level of accuracy for reliable prediction of OH. Clinical judgment was the single most important factor in OH estimation, and also had the highest contribution when in combination with other parameters. BIA reliably measured extracellular fluid, but the automatically calculated OHBIA exhibited a substantial degree of inaccuracy that precludes the use of BIA as a standard at present. The combination of clinical judgment with additional clinical parameters had the highest prediction accuracy for OH. Among the parameters studied, vena cava collapsibility index and calf circumference showed the strongest association with OH. Echocardiography, cardiothoracic index, atrial natriuretic peptide levels and spirometry did not have acceptable sensitivity. The systematic clinical approach combining physician and patient inputs, laboratory and imaging data enables an individualized decision and a superior accuracy in OH assessment."],["dc.identifier.doi","10.1007/s10157-012-0745-9"],["dc.identifier.isi","000323511000012"],["dc.identifier.pmid","23192771"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10331"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29183"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","1342-1751"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Clinical judgment is the most important element in overhydration assessment of chronic hemodialysis patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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 prüfen"],["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"]]

[["dc.bibliographiccitation.artnumber","31"],["dc.bibliographiccitation.journal","BMC Nephrology"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Bramlage, Carsten Paul"],["dc.contributor.author","Tampe, Bjoern"],["dc.contributor.author","Koziolek, Michael"],["dc.contributor.author","Maatouk, Imad"],["dc.contributor.author","Bevanda, Jelena"],["dc.contributor.author","Bramlage, Peter"],["dc.contributor.author","Ahrens, Katharina"],["dc.contributor.author","Lange, Katharina"],["dc.contributor.author","Schmid, Holger"],["dc.contributor.author","Cohen, Clemens D."],["dc.contributor.author","Kretzler, Matthias"],["dc.contributor.author","Mueller, Georg Anton"],["dc.date.accessioned","2018-11-07T08:36:49Z"],["dc.date.available","2018-11-07T08:36:49Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Bone Morphogenetic Protein (BMP)-7 is protective in different animal models of acute and chronic kidney disease. Its role in human kidneys, and in particular hypertensive nephrosclerosis, has thus far not been described. Methods: BMP-7 mRNA was quantified using real-time PCR and localised by immunostaining in tissue samples from normal and nephrosclerotic human kidneys. The impact of angiotensin (AT)-II and the AT-II receptor antagonist telmisartan on BMP-7 mRNA levels and phosphorylated Smad 1/5/8 (pSmad 1/5/8) expression was quantified in proximal tubular cells (HK-2). Functional characteristics of BMP-7 were evaluated by testing its influence on TGF-beta induced epithelial-to-mesenchymal transition (EMT), expression of TGF-beta receptor type I (TGF-beta RI) and phosphorylated Smad 2 (pSmad 2) as well as on TNF-alpha induced apoptosis of proximal tubular cells. Results: BMP-7 was predominantly found in the epithelia of the distal tubule and the collecting duct and was less abundant in proximal tubular cells. In sclerotic kidneys, BMP-7 was significantly decreased as demonstrated by real-time PCR and immunostaining. AT-II stimulation in HK-2 cells led to a significant decrease of BMP-7 and pSmad 1/5/8, which was partially ameliorated upon co-incubation with telmisartan. Only high concentrations of BMP-7 (100 ng/ml) were able to reverse TNF-alpha-induced apoptosis and TGF-beta-induced EMT in human proximal tubule cells possibly due to a decreased expression of TGF-beta RI. In addition, BMP-7 was able to reverse TGF-beta-induced phosphorylation of Smad 2. Conclusions: The findings suggest a protective role for BMP-7 by counteracting the TGF-beta and TNF-alpha-induced negative effects. The reduced expression of BMP-7 in patients with hypertensive nephrosclerosis may imply loss of protection and regenerative potential necessary to counter the disease."],["dc.identifier.doi","10.1186/1471-2369-11-31"],["dc.identifier.isi","000208334700001"],["dc.identifier.pmid","21080950"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5802"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18396"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2369"],["dc.rights","CC BY 2.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/2.0"],["dc.title","Bone Morphogenetic Protein (BMP)-7 expression is decreased in human hypertensive nephrosclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]