Tampe, Désirée

[["dc.bibliographiccitation.firstpage","2682"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-08-12T07:45:59Z"],["dc.date.available","2021-08-12T07:45:59Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a small vessel vasculitis, most frequently presenting as microscopic polyangiitis (MPA) or granulomatosis with polyangiitis (GPA). Acute tubular injury with the presence of tubulitis was previously reported to be of prognostic value in ANCA glomerulonephritis (GN). In particular, distinct tubular injury lesions were associated with the deterioration of kidney function at AAV disease onset, as well as renal resistance to treatment, and higher risk of progression to composite outcome in patients with AAV. To expand our knowledge regarding distinct tubular lesions in AAV, we aimed to describe acute tubular injury patterns in association with glomerular lesions in ANCA GN by systematic histological scoring. Methods: A total number of 48 renal biopsies with confirmed renal involvement of AAV admitted to the University Medical Center Göttingen from 2015 to 2020 were retrospectively examined. By systematic scoring of tubular injury lesions, the association between clinical parameters, laboratory markers, and histopathological findings was explored. Results: We have shown that cellular casts in renal biopsies were frequently observed in the majority of cases with ANCA GN. Furthermore, we showed that tubular epithelial simplification with dilatation correlated with MPA and MPO subtypes, C3c hypocomplementemia, severe renal involvement, and uACR. Red blood cell (RBC) casts were associated with increased levels of C-reactive protein (CRP), leukocyturia, and hematuria. Finally, we found that hyaline casts were associated with an increased fraction of glomeruli with global glomerular sclerosis. Conclusions: Acute tubular injury patterns were correlated with active ANCA GN, whereas tubular injury lesions reflecting the later stages of kidney disease correlated with chronic glomerular lesions. These results suggest an interplay between different renal compartments."],["dc.description.abstract","Background: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a small vessel vasculitis, most frequently presenting as microscopic polyangiitis (MPA) or granulomatosis with polyangiitis (GPA). Acute tubular injury with the presence of tubulitis was previously reported to be of prognostic value in ANCA glomerulonephritis (GN). In particular, distinct tubular injury lesions were associated with the deterioration of kidney function at AAV disease onset, as well as renal resistance to treatment, and higher risk of progression to composite outcome in patients with AAV. To expand our knowledge regarding distinct tubular lesions in AAV, we aimed to describe acute tubular injury patterns in association with glomerular lesions in ANCA GN by systematic histological scoring. Methods: A total number of 48 renal biopsies with confirmed renal involvement of AAV admitted to the University Medical Center Göttingen from 2015 to 2020 were retrospectively examined. By systematic scoring of tubular injury lesions, the association between clinical parameters, laboratory markers, and histopathological findings was explored. Results: We have shown that cellular casts in renal biopsies were frequently observed in the majority of cases with ANCA GN. Furthermore, we showed that tubular epithelial simplification with dilatation correlated with MPA and MPO subtypes, C3c hypocomplementemia, severe renal involvement, and uACR. Red blood cell (RBC) casts were associated with increased levels of C-reactive protein (CRP), leukocyturia, and hematuria. Finally, we found that hyaline casts were associated with an increased fraction of glomeruli with global glomerular sclerosis. Conclusions: Acute tubular injury patterns were correlated with active ANCA GN, whereas tubular injury lesions reflecting the later stages of kidney disease correlated with chronic glomerular lesions. These results suggest an interplay between different renal compartments."],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.3390/jcm10122682"],["dc.identifier.pii","jcm10122682"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88590"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Systematic Scoring of Tubular Injury Patterns Reveals Interplay between Distinct Tubular and Glomerular Lesions in ANCA-Associated Glomerulonephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Pharmacology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Plüß, Marlene; \r\n1\r\nDepartment of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Tampe, Désirée; \r\n1\r\nDepartment of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Schwörer, Harald; \r\n2\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Bremer, Sebastian Christopher Benjamin; \r\n2\r\nDepartment of Gastroenterology, Gastrointestinal Oncology and Endocrinology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Tampe, Björn; \r\n1\r\nDepartment of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.author","Plüß, Marlene"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Schwörer, Harald"],["dc.contributor.author","Bremer, Sebastian Christopher Benjamin"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-08-31T07:08:38Z"],["dc.date.available","2022-08-31T07:08:38Z"],["dc.date.issued","2022-08-17"],["dc.date.updated","2022-08-31T07:05:37Z"],["dc.description.abstract","Potassium para-aminobenzoate (POTABA) is used to treat Peyronie’s disease by decreasing fibrosis and plaque size progression. Among potential side effects, drug-induced liver injury (DILI) attributed to POTABA administration has been reported in a few cases and inferred to immune hypersensitivity. In the present case, we investigated clinical, biochemical, and serological features as well as searched for non-drug-related causes, and applied the updated Roussel Uclaf Causality Assessment Method (RUCAM) confirming a highly probable causality of POTABA-induced liver injury. Moreover, we here observed specific activated CD3+ T lymphocytes during the acute phase of liver injury by monitoring of human leukocyte antigen receptor (HLA-DR) expression. Furthermore, improvement of biochemical markers of liver injury after POTABA withdrawal was associated with a rapid decline of CD3+ HLA-DR+ immune cells. In contrast, CD14+ monocytes expressing HLA-DR remained stable during recovery from liver injury. These observations implicate a specific involvement of activated T lymphocytes in liver injury mediated by POTABA. Clinicians should be aware of POTABA-induced liver injury, and measurement of activated immune cells by assessment of HLA-DR could provide pathomechanistic insights enabling biomonitoring of recovery from DILI."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3389/fphar.2022.966910"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113317"],["dc.language.iso","en"],["dc.relation.eissn","1663-9812"],["dc.rights","CC BY 4.0"],["dc.rights.uri","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Case report: Kinetics of human leukocyte antigen receptor HLA-DR during liver injury induced by potassium para-aminobenzoate as assessed for causality using the updated RUCAM"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2014"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Schridde, Laura"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-10-01T09:58:23Z"],["dc.date.available","2021-10-01T09:58:23Z"],["dc.date.issued","2021"],["dc.description.abstract","Kidney fibrosis is a common manifestation and hallmark of a wide variety of chronic kidney disease (CKD) that appears in different morphological patterns, suggesting distinct pathogenic causes. Broad macroscopically visible scars are the sequelae of severe focal injury and complete parenchymal destruction, reflecting a wound healing response as a consequence of infarction. In the kidney, chronic glomerular injury leads to atrophy of the corresponding tubule, degeneration of this specific nephron, and finally interstitial fibrosis/tubular atrophy (IF/TA). Compared to this glomerulus-induced focal replacement scar, diffuse fibrosis independent of tubular atrophy appears to be a different pathogenic process. Kidney fibrosis appears to develop in a compartment-specific manner, but whether focal and diffuse fibrosis has distinct characteristics associated with other glomerular or tubulointerstitial lesions remains elusive. In the present study, we aimed to analyze renal fibrotic patterns related to renal lesions, which directly contribute to renal fibrogenesis, to unravel fibrotic patterns and manifestations upon damage to distinct renal compartments. Patterns of kidney fibrosis were analyzed in experimental models of CKD and various renal pathologies in correlation with histopathological and ultrastructural findings. After the induction of isolated crescentic glomerulonephritis (GN) in nephrotoxic serum-nephritis (NTN), chronic glomerular damage resulted in predominantly focal fibrosis adjacent to atrophic tubules. By contrast, using unilateral ureteral obstruction (UUO) as a model of primary injury to the tubulointerstitial compartment revealed diffuse fibrosis as the predominant pattern of chronic lesions. Finally, folic acid-induced nephropathy (FAN) as a model of primary tubular injury with consecutive tubular atrophy independent of chronic glomerular damage equally induced predominant focal IF/TA. By analyzing several renal pathologies, our data also suggest that focal and diffuse fibrosis appear to contribute as chronic lesions in the majority of human renal disease, mainly being present in antineutrophil cytoplasmic antibody (ANCA)-associated GN, lupus nephritis, and IgA nephropathy (IgAN). Focal IF/TA correlated with glomerular damage and irreversible injury to nephrons, whereas diffuse fibrosis in ANCA GN was associated explicitly with interstitial inflammation independent of glomerular damage and nephron loss. Ultrastructural analysis of focal IF/TA versus diffuse fibrosis revealed distinct matrix compositions, further supported by different collagen signatures in transcriptome datasets. With regard to long-term renal outcome, only the extent of focal IF/TA correlated with the development of end-stage kidney disease (ESKD) in ANCA GN. In contrast, diffuse kidney fibrosis did not associate with the long-term renal outcome. In conclusion, we here provide evidence that a focal pattern of kidney fibrosis seems to be associated with nephron loss and replacement scarring. In contrast, a diffuse pattern of kidney fibrosis appears to result from primary interstitial inflammation and injury."],["dc.description.abstract","Kidney fibrosis is a common manifestation and hallmark of a wide variety of chronic kidney disease (CKD) that appears in different morphological patterns, suggesting distinct pathogenic causes. Broad macroscopically visible scars are the sequelae of severe focal injury and complete parenchymal destruction, reflecting a wound healing response as a consequence of infarction. In the kidney, chronic glomerular injury leads to atrophy of the corresponding tubule, degeneration of this specific nephron, and finally interstitial fibrosis/tubular atrophy (IF/TA). Compared to this glomerulus-induced focal replacement scar, diffuse fibrosis independent of tubular atrophy appears to be a different pathogenic process. Kidney fibrosis appears to develop in a compartment-specific manner, but whether focal and diffuse fibrosis has distinct characteristics associated with other glomerular or tubulointerstitial lesions remains elusive. In the present study, we aimed to analyze renal fibrotic patterns related to renal lesions, which directly contribute to renal fibrogenesis, to unravel fibrotic patterns and manifestations upon damage to distinct renal compartments. Patterns of kidney fibrosis were analyzed in experimental models of CKD and various renal pathologies in correlation with histopathological and ultrastructural findings. After the induction of isolated crescentic glomerulonephritis (GN) in nephrotoxic serum-nephritis (NTN), chronic glomerular damage resulted in predominantly focal fibrosis adjacent to atrophic tubules. By contrast, using unilateral ureteral obstruction (UUO) as a model of primary injury to the tubulointerstitial compartment revealed diffuse fibrosis as the predominant pattern of chronic lesions. Finally, folic acid-induced nephropathy (FAN) as a model of primary tubular injury with consecutive tubular atrophy independent of chronic glomerular damage equally induced predominant focal IF/TA. By analyzing several renal pathologies, our data also suggest that focal and diffuse fibrosis appear to contribute as chronic lesions in the majority of human renal disease, mainly being present in antineutrophil cytoplasmic antibody (ANCA)-associated GN, lupus nephritis, and IgA nephropathy (IgAN). Focal IF/TA correlated with glomerular damage and irreversible injury to nephrons, whereas diffuse fibrosis in ANCA GN was associated explicitly with interstitial inflammation independent of glomerular damage and nephron loss. Ultrastructural analysis of focal IF/TA versus diffuse fibrosis revealed distinct matrix compositions, further supported by different collagen signatures in transcriptome datasets. With regard to long-term renal outcome, only the extent of focal IF/TA correlated with the development of end-stage kidney disease (ESKD) in ANCA GN. In contrast, diffuse kidney fibrosis did not associate with the long-term renal outcome. In conclusion, we here provide evidence that a focal pattern of kidney fibrosis seems to be associated with nephron loss and replacement scarring. In contrast, a diffuse pattern of kidney fibrosis appears to result from primary interstitial inflammation and injury."],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.identifier.doi","10.3390/cells10082014"],["dc.identifier.pii","cells10082014"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/90053"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-469"],["dc.publisher","MDPI"],["dc.relation.eissn","2073-4409"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Different Patterns of Kidney Fibrosis Are Indicative of Injury to Distinct Renal Compartments"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1231"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Kluge, Ingmar Alexander"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-06-01T09:42:37Z"],["dc.date.available","2021-06-01T09:42:37Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a systemic vasculitis, most frequently presenting as microscopic polyangiitis (MPA) or granulomatosis with polyangiitis (GPA). Kidney involvement is a common and severe complication of ANCA AAV which is observed in a considerable subset of patients, mainly affecting glomeruli. However, tubulointerstitial lesions have also been described in ANCA glomerulonephritis (GN). Therefore, we aim to describe active and chronic tubulointerstitial lesions in ANCA GN subtypes by systematic scoring analogous to the Banff scoring system while also utilizing clinical and laboratory findings. Methods: A total of 49 kidney biopsies with ANCA GN were retrospectively included in a single-center cohort study between 2015–2020. Results: We report that MPO-ANCA GN is associated with more severe deterioration of kidney function independent of systemic markers of AAV disease activity, and is also associated with increased proteinuria in MPO-ANCA GN and a decreased fraction of normal glomeruli. Finally, MPO-ANCA GN showed distinct, active, and chronic tubulointerstitial lesions. Conclusion: New insights into the pathophysiology of both entities, as well as differences in the clinical presentation of MPO- versus PR3-ANCA GN, could potentially pave the way for more precise treatment regimens. Therefore, it is important to understand the differences in histopathological presentation, especially in yet underestimated active tubulointerstitial lesions of ANCA GN subtypes. This research could further improve our understanding of distinct pathophysiological mechanisms."],["dc.description.sponsorship","Georg-August-Universität Göttingen"],["dc.identifier.doi","10.3390/jcm10061231"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85302"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Systematic Histological Scoring Reveals More Prominent Interstitial Inflammation in Myeloperoxidase-ANCA Compared to Proteinase 3-ANCA Glomerulonephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3526"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-07-01T07:35:33Z"],["dc.date.available","2022-07-01T07:35:33Z"],["dc.date.issued","2022"],["dc.date.updated","2022-07-08T11:30:46Z"],["dc.description.abstract","Background: We have previously reported that the ultrasound (US)-guided tip positioning is an accurate and safe procedure for placement of retrograde- and antegrade-tunneled hemodialysis catheters (HDCs). However, determinants of tunneled hemodialysis catheter implantation time by using US guidance have not been described yet. Therefore, we here report a comparative analysis to identify determinants of implantation time for retrograde- and antegrade-tunneled HDCs placement by US guidance. Methods: We performed a cross-sectional study to compare implantation time for US-guided tip positioning of retrograde- and antegrade-tunneled HDCs. We included a total number of 47 tunneled HDC insertions, including 23 retrograde tunneled and 24 antegrade-tunneled HDCs in patients requiring placement of an HDC for the temporary or permanent treatment of end-stage kidney disease (ESKD) in a single-center, cross-sectional pilot study. Results: We show that clinical and laboratory parameters did not differ between retrograde- and antegrade-tunneled HDC implantations. There was a tendency for shorter implantation time in antegrade-tunneled HDCs, although not statistically significant. Finally, we identified an independent inverse association between body weight (BW) and platelet counts with HDC implantation time specifically in antegrade-tunneled HDCs. Conclusion: In this study, we identified determinants for tunneled HDC implantation time that might be relevant for patients and interventionists."],["dc.description.sponsorship","Georg August University Göttingen"],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3390/jcm11123526"],["dc.identifier.pii","jcm11123526"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112200"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/112419"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-581"],["dc.relation.eissn","2077-0383"],["dc.rights","CC BY 4.0"],["dc.title","Determinants of Tunneled Hemodialysis Catheter Implantation Time by Ultrasound Guidance: A Single-Center Cross-Sectional Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","19"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","EBioMedicine"],["dc.bibliographiccitation.lastpage","36"],["dc.bibliographiccitation.volume","2"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Müller, Gerhard A."],["dc.contributor.author","Bechtel-Walz, Wibke"],["dc.contributor.author","Koziolek, Michael"],["dc.contributor.author","Kalluri, Raghu"],["dc.contributor.author","Zeisberg, Michael"],["dc.date.accessioned","2019-02-27T10:29:15Z"],["dc.date.available","2019-02-27T10:29:15Z"],["dc.date.issued","2015"],["dc.description.abstract","Progression of chronic kidney disease remains a principal problem in clinical nephrology and there is a pressing need for novel therapeutics and biomarkers. Aberrant promoter CpG island methylation and subsequent transcriptional silencing of specific genes have emerged as contributors to progression of chronic kidney disease. Here, we report that transcriptional silencing of the Ras-GTP suppressor RASAL1 contributes causally to progression of kidney fibrosis and we identified that circulating methylated RASAL1 promoter DNA fragments in peripheral blood correspond with levels of intrarenal levels of RASAL1 promoter methylation and degree of fibrosis in kidney biopsies, enabling non-invasive longitudinal analysis of intrarenal CpG island methylation. Retrospective analysis of patients with hypertensive nephrosclerosis revealed that circulating methylated RASAL1 promoter DNA fragments in peripheral blood decrease with Dihydralazine treatment in patients with hypertensive nephrosclerosis, and provided evidence that low-dose Dihydralazine delays decline of excretory kidney function, whereas Dihydralazine at standard doses had no protective effect. We demonstrate that the protective effect of Dihydralazine is due to induction of endogenous Tet3/Tdg-mediated DNA-de-methylation activity reversing aberrant promoter CpG island methylation, while HIF1α induction at standard doses counterbalances its protective activity. We conclude that RASAL1 promoter methylation is a therapeutic target and a biomarker of renal fibrosis. Our study suggests therapeutic use of low-dose Dihydralazine in patients with chronic kidney disease and fibrosis deserves further consideration."],["dc.identifier.doi","10.1016/j.ebiom.2014.11.005"],["dc.identifier.pmid","25717475"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11368"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/57639"],["dc.identifier.url","https://sfb1002.med.uni-goettingen.de/production/literature/publications/62"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation","SFB 1002: Modulatorische Einheiten bei Herzinsuffizienz"],["dc.relation","SFB 1002 | C01: Epigenetische Kontrolle der Herzfibrose"],["dc.relation.issn","2352-3964"],["dc.relation.workinggroup","RG E. Zeisberg (Kardiales Stroma)"],["dc.relation.workinggroup","RG M. Zeisberg (Renale Fibrogenese)"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Induction of Tet3-dependent Epigenetic Remodeling by Low-dose Hydralazine Attenuates Progression of Chronic Kidney Disease"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","original_ja"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1054457"],["dc.bibliographiccitation.journal","Frontiers in Immunology"],["dc.bibliographiccitation.volume","13"],["dc.contributor.affiliation","Baier, Eva; \r\n1\r\nDepartment of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Tampe, Désirée; \r\n1\r\nDepartment of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Kluge, Ingmar Alexander; \r\n2\r\nInstitute of Pathology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Hakroush, Samy; \r\n2\r\nInstitute of Pathology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.affiliation","Tampe, Björn; \r\n1\r\nDepartment of Nephrology and Rheumatology, University Medical Center Göttingen, Göttingen, Germany"],["dc.contributor.author","Baier, Eva"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Kluge, Ingmar Alexander"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-12-01T08:31:31Z"],["dc.date.available","2022-12-01T08:31:31Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-28T18:41:30Z"],["dc.description.abstract","Introduction\r\n Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a potentially life-threatening systemic small-vessel vasculitis that is characterized by pauci-immune glomerulonephritis, depicting in turn a major denominator of AAV mortality. It is well established that AAV patients feature an increased risk of developing thrombotic events, and platelets are activated in AAV patients being triggered by the alternative complement pathway. Platelets guard vessels integrity and initiate thrombus formation in response to endothelial damage, further constituting a triangular interconnection with the activation of neutrophils and the complement system. We here aimed to systematically assess the relevance of platelet counts and systemic complement system activation regarding distinct histopathological lesions in ANCA-associated renal vasculitis.\r\n \r\n \r\n Methods\r\n A cohort of 53 biopsy-proven cases of ANCA-associated renal vasculitis were retrospectively enrolled in a single-center observational study. Univariate and multivariate regression analysis was performed to identify parameters associated with platelet counts in ANCA-associated renal vasculitis compared to disease controls. Finally, the relevance of platelets for disease course and recovery was assessed by survival analysis.\r\n \r\n \r\n Results\r\n \r\n Lower platelet counts correlated with markers of kidney injury including eGFR loss (\r\n p=0.0004\r\n ) and lower complement C3 levels (\r\n p=0.0037\r\n ). Multivariate and subgroup analysis revealed that this association was only present in the subgroup with MPO-ANCA seropositivity (eGFR loss:\r\n p=0.0009\r\n , lower C3:\r\n p=0.0032\r\n ). While lower platelet counts correlated with kidney injury in the PR3-ANCA subgroup (eGFR loss:\r\n p=0.0272\r\n ), we did not observe an independent association with complement C3 levels (\r\n p=0.4497\r\n ). Independent of any glomerular lesion, lower platelet counts correlated with interstitial fibrosis (\r\n p=0.0313\r\n ), tubular atrophy (\r\n p=0.0073\r\n ), and tubulitis in areas of interstitial fibrosis and tubular atrophy (\r\n p=0.0033\r\n ). Finally, we observed significant differences with increased requirement of kidney replacement therapy (KRT) or death in the subgroup below median platelet counts (HR: 4.1, 95% CI: 1.6-10,\r\n p=0.0047\r\n ), associated with a lower probability of discharge and prolonged hospitalization in this subgroup (HR: 0.5, 95% CI: 0.3-0.9,\r\n p=0.0113\r\n ).\r\n \r\n \r\n \r\n Conclusion\r\n Based on our observation that an association between platelets and complement system activation is only observed in the MPO-ANCA subgroup, this could implicate that platelets and complement C3 link innate immunity to tubulointerstitial injury in the presence of MPO-ANCA autoantibodies."],["dc.identifier.doi","10.3389/fimmu.2022.1054457"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118191"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","1664-3224"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Implication of platelets and complement C3 as link between innate immunity and tubulointerstitial injury in renal vasculitis with MPO-ANCA seropositivity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Frontiers in Medicine"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Bösherz, Mark-Sebastian"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Hofmann-Winkler, Heike"],["dc.contributor.author","Pöhlmann, Stefan"],["dc.contributor.author","Kluge, Stefan"],["dc.contributor.author","Moerer, Onnen"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Tampe, Björn"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.date.accessioned","2021-07-05T14:57:53Z"],["dc.date.available","2021-07-05T14:57:53Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Acute kidney injury (AKI) is very common in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) disease 2019 (COVID-19) and considered as a risk factor for COVID-19 severity. SARS-CoV-2 renal tropism has been observed in COVID-19 patients, suggesting that direct viral injury of the kidneys may contribute to AKI. We examined 20 adult cases with confirmed SARS-CoV-2 infection requiring ICU supportive care in a single-center prospective observational study and investigated whether urinary markers for viral infection (SARS-CoV-2 N) and shedded cellular membrane proteins (ACE2, TMPRSS2) allow identification of patients at risk for AKI and outcome of COVID-19. Objectives: The objective of the study was to evaluate whether urinary markers for viral infection (SARS-CoV-2 N) and shedded cellular membrane proteins (ACE2, TMPRSS2) allow identification of patients at risk for AKI and outcome of COVID-19. Results: Urinary SARS-CoV-2 N measured at ICU admission identified patients at risk for AKI in COVID-19 (HR 5.9, 95% CI 1.4–26, p = 0.0095 ). In addition, the combination of urinary SARS-CoV-2 N and plasma albumin measurements further improved the association with AKI (HR 11.4, 95% CI 2.7–48, p = 0.0016 ). Finally, combining urinary SARS-CoV-2 N and plasma albumin measurements associated with the length of ICU supportive care (HR 3.3, 95% CI 1.1–9.9, p = 0.0273 ) and premature death (HR 7.6, 95% CI 1.3–44, p = 0.0240 ). In contrast, urinary ACE2 and TMPRSS2 did not correlate with AKI in COVID-19. Conclusions: In conclusion, urinary SARS-CoV-2 N levels associate with risk for AKI and correlate with COVID-19 severity."],["dc.description.abstract","Background: Acute kidney injury (AKI) is very common in severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) disease 2019 (COVID-19) and considered as a risk factor for COVID-19 severity. SARS-CoV-2 renal tropism has been observed in COVID-19 patients, suggesting that direct viral injury of the kidneys may contribute to AKI. We examined 20 adult cases with confirmed SARS-CoV-2 infection requiring ICU supportive care in a single-center prospective observational study and investigated whether urinary markers for viral infection (SARS-CoV-2 N) and shedded cellular membrane proteins (ACE2, TMPRSS2) allow identification of patients at risk for AKI and outcome of COVID-19. Objectives: The objective of the study was to evaluate whether urinary markers for viral infection (SARS-CoV-2 N) and shedded cellular membrane proteins (ACE2, TMPRSS2) allow identification of patients at risk for AKI and outcome of COVID-19. Results: Urinary SARS-CoV-2 N measured at ICU admission identified patients at risk for AKI in COVID-19 (HR 5.9, 95% CI 1.4–26, p = 0.0095 ). In addition, the combination of urinary SARS-CoV-2 N and plasma albumin measurements further improved the association with AKI (HR 11.4, 95% CI 2.7–48, p = 0.0016 ). Finally, combining urinary SARS-CoV-2 N and plasma albumin measurements associated with the length of ICU supportive care (HR 3.3, 95% CI 1.1–9.9, p = 0.0273 ) and premature death (HR 7.6, 95% CI 1.3–44, p = 0.0240 ). In contrast, urinary ACE2 and TMPRSS2 did not correlate with AKI in COVID-19. Conclusions: In conclusion, urinary SARS-CoV-2 N levels associate with risk for AKI and correlate with COVID-19 severity."],["dc.identifier.doi","10.3389/fmed.2021.644715"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/87765"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-441"],["dc.publisher","Frontiers Media S.A."],["dc.relation.eissn","2296-858X"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Urinary Levels of SARS-CoV-2 Nucleocapsid Protein Associate With Risk of AKI and COVID-19 Severity: A Single-Center Observational Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1538"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Tampe, Désirée"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-06-01T09:42:37Z"],["dc.date.available","2021-06-01T09:42:37Z"],["dc.date.issued","2021"],["dc.description.abstract","Background: Renal involvement is a common and severe complication of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV), potentially resulting in a pauci-immune necrotizing and crescentic ANCA glomerulonephritis (GN) with acute kidney injury (AKI), end-stage renal disease (ESRD) or death. There is recent evidence that the degree of proteinuria at diagnosis is associated with long-term renal outcome in ANCA GN. Therefore, we here aimed to systematically describe the association between proteinuria and clinicopathological characteristics in 53 renal biopsies with ANCA GN and corresponding urinary samples at admission. Methods: A total number of 53 urinary samples at admission and corresponding renal biopsies with confirmed renal involvement of AAV were retrospectively included from 2015 to 2021 in a single-center study. Results: Proteinuria correlated with myeloperoxidase (MPO) subtype, diagnosis of microscopic polyangiitis (MPA) and severe deterioration of kidney function. Proteinuria was most prominent in sclerotic class ANCA GN and ANCA renal risk score (ARRS) high risk attributed to nonselective proteinuria, including both glomerular and tubular proteinuria. Finally, there was no association between proteinuria and systemic disease activity, suggesting that proteinuria reflected specific renal involvement in AAV rather that systemic disease activity. Conclusions: In conclusion, proteinuria correlated with distinct clinicopathological characteristics in ANCA GN, mostly attributed to a reduced fraction of normal glomeruli. Furthermore, proteinuria in ANCA GN reflected specific renal involvement in AAV rather than systemic disease activity. Therefore, urinary findings could further improve our understanding of mechanisms promoting kidney injury and progression of ANCA GN."],["dc.description.sponsorship","Research program, University Medical Center, University of Göttingen"],["dc.identifier.doi","10.3390/jcm10071538"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85303"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Proteinuria Indicates Decreased Normal Glomeruli in ANCA-Associated Glomerulonephritis Independent of Systemic Disease Activity"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","339"],["dc.bibliographiccitation.journal","BMC Musculoskeletal Disorders"],["dc.bibliographiccitation.volume","17"],["dc.contributor.author","Patschan, Susann A."],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Mueller, C."],["dc.contributor.author","Seitz, C."],["dc.contributor.author","Herink, Claudia"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Zeisberg, Elisabeth M."],["dc.contributor.author","Zeisberg, Michael"],["dc.contributor.author","Henze, Elvira"],["dc.contributor.author","Patschan, Daniel"],["dc.date.accessioned","2018-11-07T10:10:11Z"],["dc.date.available","2018-11-07T10:10:11Z"],["dc.date.issued","2016"],["dc.description.abstract","Background: Patients with systemic sclerosis (SSc) are endagered by tissue fibrosis and by microvasculopathy, with the latter caused by endothelial cell expansion/proliferation. SSc-associated fibrosis potentially results from mesenchymal transdifferentiation of endothelial cells. Early Endothelial Progenitor Cells (eEPCs) act proangiogenic under diverse conditions. Aim of the study was to analyze eEPC regeneration and mesenchymal transdifferentiation in patients with limited and diffuse SSs (lSSc and dSSc). Methods: Patients with both, lSSc and dSSc were included into the study. The following parameters were evaluated: eEPC numbers and regeneration, concentrations of vasomodulatory mediators, mesenchymal properties of blood-derived eEPC. Serum samples of healthy subjects and SS patients were used for stimulation of cultured human eEPC, subsequently followed by analysis of mesenchymal cell characteristics and mobility. Results: Twenty-nine patients were included into the study. Regenerative activity of blood-derived eEPCs did not differ between Controls and patients. Circulating eEPC were significantly lower in all patients with SSc, and in limited and diffuse SSc (lSSc/dSSc). Serum concentrations of promesenchymal TGF-b was elevated in all patients with SSc. Cultured mononuclear cells from SS patients displayed higher abundances of CD31 and of CD31 and aSMA combined. Finally, serum from SSc patients inhibited migration of cultured eEPCs and the cells showed lower sensitivity towards the endothelin antagonist Bosentan. Conclusions: The eEPC system, which represents an essential element of the endogenous vascular repair machinery is affected in SSc. The increased appearance of mesenchymal properties in eEPC may indicate that alterations of the cells potentially contribute to the accumulation of connective tissue and to vascular malfunction."],["dc.description.sponsorship","Heidenreich von-Siebold Programm"],["dc.identifier.doi","10.1186/s12891-016-1197-2"],["dc.identifier.isi","000395017600003"],["dc.identifier.pmid","27519706"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13866"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39808"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Biomed Central Ltd"],["dc.relation.issn","1471-2474"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Early Endothelial Progenitor Cells (eEPCs) in systemic sclerosis (SSc) - dynamics of cellular regeneration and mesenchymal transdifferentiation"],["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"]]