Now showing 1 - 10 of 38
  • 2022Journal Article
    [["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Scientific Reports"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Baier, Eva"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-12-01T08:30:57Z"],["dc.date.available","2022-12-01T08:30:57Z"],["dc.date.issued","2022"],["dc.description.abstract","Abstract\n Antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis (AAV) is a small vessel vasculitis often leading to critical illness by multi-organ failure. Data for patients with specifically ANCA-associated renal vasculitis requiring intensive care unit (ICU) supportive care are limited and have mainly focused on long-term renal and overall outcome. Particularly, data on critical illness during the initial course of disease are scarce and remain poorly determined. Therefore, the purpose of this retrospective study was to identify predictors of critical illness in a cohort of patients with ANCA-associated renal vasculitis. We retrospectively included a total number of 53 cases with confirmed ANCA-associated renal vasculitis between 2015 till 2020 in a single-center cohort study. We here identified an association between low hemoglobin levels and requirement of ICU supportive care in patients with ANCA-associated renal vasculitis. Furthermore, levels of hemoglobin below 9.8 g/dL at admission independently predicted prolonged requirement of ICU supportive care in critically ill patients with ANCA-associated renal vasculitis. These findings confirm that low levels of hemoglobin negatively affect short-term outcome and could further improve our current understanding for the role of anemia in ANCA-associated renal vasculitis."],["dc.description.sponsorship","Else-Kröner research program"],["dc.description.sponsorship","Research program, University Medical Center, University of Göttingen"],["dc.description.sponsorship"," Georg-August-Universität Göttingen 501100003385"],["dc.identifier.doi","10.1038/s41598-022-23313-7"],["dc.identifier.pii","23313"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118027"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-621"],["dc.relation.eissn","2045-2322"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Low levels of hemoglobin associate with critical illness and predict disease course in patients with ANCA-associated renal vasculitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2021Journal Article
    [["dc.bibliographiccitation.journal","Journal of Nephrology"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-01-11T14:05:40Z"],["dc.date.available","2022-01-11T14:05:40Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Background Renal involvement is a common and severe complication of ANCA (antineutrophil cytoplasmic antibody) associated vasculitis (AAV) potentially resulting in a pauci-immune necrotizing and crescentic antineutrophil cytoplasmic antibody (ANCA) glomerulonephritis (GN) with acute kidney injury (AKI), end-stage renal disease (ESRD) or death. We recently described that Bowman’s capsule rupture links glomerular damage to tubulointerstitial inflammation in ANCA-associated glomerulonephritis. Herein we provide a comprehensive histological subtyping of immune cell infiltrates in association with Bowman’s capsule rupture in ANCA GN. Methods A total of 44 kidney biopsies with ANCA GN were retrospectively included in a single-center observational study. Within a renal biopsy specimen, each glomerulus was scored separately for the presence of extensive and focal Bowman’s capsule rupture in injured glomeruli. Infiltrates of neutrophils, eosinophils, plasma cells, and mononucleated cells (macrophages, lymphocytes) were quantified as a fraction of the area of total cortical inflammation. Results Extensive Bowman’s capsule rupture was associated with tubulointerstitial inflammation containing infiltrates of neutrophils, eosinophils and plasma cells. A similar association was observed for the presence of focal Bowman’s capsule rupture, correlating with tubulointerstitial inflammation containing neutrophils, eosinophils and plasma cells. Multiple logistic regression confirmed that extensive Bowman’s capsule rupture correlated with tubulointerstitial inflammation containing neutrophils, and focal Bowman’s capsule rupture correlated with neutrophil and plasma cell infiltration. Furthermore, this association was specifically observed in PR3-ANCA GN. Conclusion To our knowledge, this is the first report linking Bowman’s capsule rupture directly to tubulointerstitial inflammation by immune cell subtypes. This underscores a pathomechanistic link between tubulointerstitial and glomerular lesions in ANCA GN and needs further investigation. Graphical abstract"],["dc.description.abstract","Abstract Background Renal involvement is a common and severe complication of ANCA (antineutrophil cytoplasmic antibody) associated vasculitis (AAV) potentially resulting in a pauci-immune necrotizing and crescentic antineutrophil cytoplasmic antibody (ANCA) glomerulonephritis (GN) with acute kidney injury (AKI), end-stage renal disease (ESRD) or death. We recently described that Bowman’s capsule rupture links glomerular damage to tubulointerstitial inflammation in ANCA-associated glomerulonephritis. Herein we provide a comprehensive histological subtyping of immune cell infiltrates in association with Bowman’s capsule rupture in ANCA GN. Methods A total of 44 kidney biopsies with ANCA GN were retrospectively included in a single-center observational study. Within a renal biopsy specimen, each glomerulus was scored separately for the presence of extensive and focal Bowman’s capsule rupture in injured glomeruli. Infiltrates of neutrophils, eosinophils, plasma cells, and mononucleated cells (macrophages, lymphocytes) were quantified as a fraction of the area of total cortical inflammation. Results Extensive Bowman’s capsule rupture was associated with tubulointerstitial inflammation containing infiltrates of neutrophils, eosinophils and plasma cells. A similar association was observed for the presence of focal Bowman’s capsule rupture, correlating with tubulointerstitial inflammation containing neutrophils, eosinophils and plasma cells. Multiple logistic regression confirmed that extensive Bowman’s capsule rupture correlated with tubulointerstitial inflammation containing neutrophils, and focal Bowman’s capsule rupture correlated with neutrophil and plasma cell infiltration. Furthermore, this association was specifically observed in PR3-ANCA GN. Conclusion To our knowledge, this is the first report linking Bowman’s capsule rupture directly to tubulointerstitial inflammation by immune cell subtypes. This underscores a pathomechanistic link between tubulointerstitial and glomerular lesions in ANCA GN and needs further investigation. Graphical abstract"],["dc.identifier.doi","10.1007/s40620-021-01208-6"],["dc.identifier.pii","1208"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/97717"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-507"],["dc.relation.eissn","1724-6059"],["dc.relation.issn","1121-8428"],["dc.title","Neutrophils associate with Bowman’s capsule rupture specifically in PR3-ANCA glomerulonephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2021Journal Article
    [["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"]]
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  • 2020Journal Article
    [["dc.bibliographiccitation.firstpage","annrheumdis-2020-218491"],["dc.bibliographiccitation.journal","Annals of the Rheumatic Diseases"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Franz, Jonas"],["dc.contributor.author","Larsen, Jörg"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Winkler, Martin Sebastian"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-06-01T10:47:36Z"],["dc.date.available","2021-06-01T10:47:36Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1136/annrheumdis-2020-218491"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85655"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1468-2060"],["dc.relation.issn","0003-4967"],["dc.title","Repeated false-negative tests delayed diagnosis of COVID-19 in a case with granulomatosis with polyangiitis under maintenance therapy with rituximab and concomitant influenza pneumonia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2021Journal Article
    [["dc.bibliographiccitation.firstpage","annrheumdis-2021-219970"],["dc.bibliographiccitation.journal","Annals of the Rheumatic Diseases"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-06-01T10:47:36Z"],["dc.date.available","2021-06-01T10:47:36Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1136/annrheumdis-2021-219970"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85659"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1468-2060"],["dc.relation.issn","0003-4967"],["dc.title","Correspondence on ‘Bowman’s capsule rupture on renal biopsy improves the outcome prediction of ANCA-associated glomerulonephritis classifications’"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2022Journal Article
    [["dc.bibliographiccitation.journal","Journal of Nephrology"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Kluge, Ingmar Alexander"],["dc.contributor.author","Baier, Eva"],["dc.contributor.author","Korsten, Peter"],["dc.contributor.author","Tampe, Desiree"],["dc.contributor.author","Ströbel, Philipp"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2022-05-02T08:09:46Z"],["dc.date.available","2022-05-02T08:09:46Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1007/s40620-022-01320-1"],["dc.identifier.pii","1320"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/107458"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-561"],["dc.relation.eissn","1724-6059"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","pANCA autoantibody testing by indirect immunofluorescence indicates interstitial arteritis independent of MPO-ANCA immunoassays in ANCA-associated glomerulonephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2021Journal Article
    [["dc.bibliographiccitation.journal","Journal of Nephrology"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Gersmann, Ann-Kathrin"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-12-01T09:23:33Z"],["dc.date.available","2021-12-01T09:23:33Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1007/s40620-021-01169-w"],["dc.identifier.pii","1169"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94688"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1724-6059"],["dc.relation.issn","1121-8428"],["dc.title","Histopathological and ultrastructural monitoring of remission induction in crescentic C3 glomerulonephritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2021Journal Article
    [["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"]]
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  • 2021Journal Article
    [["dc.bibliographiccitation.firstpage","2974"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of the American Society of Nephrology"],["dc.bibliographiccitation.lastpage","2975"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-12-01T09:23:11Z"],["dc.date.available","2021-12-01T09:23:11Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1681/ASN.2021081057"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/94583"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-478"],["dc.relation.eissn","1533-3450"],["dc.relation.issn","1046-6673"],["dc.title","Incidence of Arteritis and Peritubular Capillaritis in ANCA-associated Vasculitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2021Journal Article
    [["dc.bibliographiccitation.firstpage","annrheumdis-2020-219687"],["dc.bibliographiccitation.journal","Annals of the Rheumatic Diseases"],["dc.contributor.author","Hakroush, Samy"],["dc.contributor.author","Tampe, Björn"],["dc.date.accessioned","2021-06-01T10:47:36Z"],["dc.date.available","2021-06-01T10:47:36Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1136/annrheumdis-2020-219687"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85657"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1468-2060"],["dc.relation.issn","0003-4967"],["dc.title","Correspondence on ‘What comes after the lockdown? Clustering of ANCA-associated vasculitis: single-centre observation of a spatiotemporal pattern’"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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