Gross, Oliver

[["dc.bibliographiccitation.firstpage","1815"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Cells"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Boeckhaus, Jan"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2021-08-12T07:45:53Z"],["dc.date.available","2021-08-12T07:45:53Z"],["dc.date.issued","2021"],["dc.description.abstract","Hereditary diseases of the glomerular filtration barrier are characterized by a more vulnerable glomerular basement membrane and dysfunctional podocytes. Recent clinical trials have demonstrated the nephroprotective effect of sodium-glucose cotransporter-2 inhibitors (SGLT2i) in chronic kidney disease (CKD). SGLT2-mediated afferent arteriole vasoconstriction is hypothesized to correct the hemodynamic overload of the glomerular filtration barrier in hereditary podocytopathies. To test this hypothesis, we report data in a case series of patients with Alport syndrome and focal segmental glomerulosclerosis (FSGS) with respect of the early effect of SGLT2i on the kidney function. Mean duration of treatment was 4.5 (±2.9) months. Mean serum creatinine before and after SGLT-2i initiation was 1.46 (±0.42) and 1.58 (±0.55) mg/dL, respectively, with a median estimated glomerular filtration rate of 64 (±27) before and 64 (±32) mL/min/1.73 m2 after initiation of SGLT2i. Mean urinary albumin-creatinine ratio in mg/g creatinine before SGLT-2i initiation was 1827 (±1560) and decreased by almost 40% to 1127 (±854) after SGLT2i initiation. To our knowledge, this is the first case series on the effect and safety of SGLT2i in patients with hereditary podocytopathies. Specific large-scale trials in podocytopathies are needed to confirm our findings in this population with a tremendous unmet medical need for more effective, early on, and safe nephroprotective therapies."],["dc.description.abstract","Hereditary diseases of the glomerular filtration barrier are characterized by a more vulnerable glomerular basement membrane and dysfunctional podocytes. Recent clinical trials have demonstrated the nephroprotective effect of sodium-glucose cotransporter-2 inhibitors (SGLT2i) in chronic kidney disease (CKD). SGLT2-mediated afferent arteriole vasoconstriction is hypothesized to correct the hemodynamic overload of the glomerular filtration barrier in hereditary podocytopathies. To test this hypothesis, we report data in a case series of patients with Alport syndrome and focal segmental glomerulosclerosis (FSGS) with respect of the early effect of SGLT2i on the kidney function. Mean duration of treatment was 4.5 (±2.9) months. Mean serum creatinine before and after SGLT-2i initiation was 1.46 (±0.42) and 1.58 (±0.55) mg/dL, respectively, with a median estimated glomerular filtration rate of 64 (±27) before and 64 (±32) mL/min/1.73 m2 after initiation of SGLT2i. Mean urinary albumin-creatinine ratio in mg/g creatinine before SGLT-2i initiation was 1827 (±1560) and decreased by almost 40% to 1127 (±854) after SGLT2i initiation. To our knowledge, this is the first case series on the effect and safety of SGLT2i in patients with hereditary podocytopathies. Specific large-scale trials in podocytopathies are needed to confirm our findings in this population with a tremendous unmet medical need for more effective, early on, and safe nephroprotective therapies."],["dc.identifier.doi","10.3390/cells10071815"],["dc.identifier.pii","cells10071815"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88568"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-448"],["dc.publisher","MDPI"],["dc.relation.eissn","2073-4409"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Sodium-Glucose Cotransporter-2 Inhibitors in Patients with Hereditary Podocytopathies, Alport Syndrome, and FSGS: A Case Series to Better Plan a Large-Scale Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2225"],["dc.bibliographiccitation.issue","23"],["dc.bibliographiccitation.journal","New England Journal of Medicine"],["dc.bibliographiccitation.lastpage","2236"],["dc.bibliographiccitation.volume","373"],["dc.contributor.author","Rauen, Thomas"],["dc.contributor.author","Eitner, Frank"],["dc.contributor.author","Fitzner, Christina"],["dc.contributor.author","Sommerer, Claudia"],["dc.contributor.author","Zeier, Martin"],["dc.contributor.author","Otte, Britta"],["dc.contributor.author","Panzer, Ulf"],["dc.contributor.author","Peters, Harm"],["dc.contributor.author","Benck, Urs"],["dc.contributor.author","Mertens, Peter R."],["dc.contributor.author","Kuhlmann, Uwe"],["dc.contributor.author","Witzke, Oliver"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Vielhauer, Volker"],["dc.contributor.author","Mann, Johannes F. E."],["dc.contributor.author","Hilgers, Ralf-Dieter"],["dc.contributor.author","Floege, Juergen"],["dc.date.accessioned","2018-11-07T09:47:50Z"],["dc.date.available","2018-11-07T09:47:50Z"],["dc.date.issued","2015"],["dc.description.abstract","BACKGROUND The outcomes of immunosuppressive therapy, when added to supportive care, in patients with IgA nephropathy are uncertain. METHODS We conducted a multicenter, open-label, randomized, controlled trial with a two-group, parallel, group-sequential design. During a 6-month run-in phase, supportive care (in particular, blockade of the renin-angiotensin system) was adjusted on the basis of proteinuria. Patients who had persistent proteinuria with urinary protein excretion of at least 0.75 g per day were randomly assigned to receive supportive care alone (supportive-care group) or supportive care plus immunosuppressive therapy (immunosuppression group) for 3 years. The primary end points in hierarchical order were full clinical remission at the end of the trial (protein-to-creatinine ratio < 0.2 [with both protein and creatinine measured in grams] and a decrease in the estimated glomerular filtration rate [eGFR] of < 5 ml per minute per 1.73 m(2) of body-surface area from baseline) and a decrease in the eGFR of at least 15 ml per minute per 1.73 m(2) at the end of the trial. The primary end points were analyzed with the use of logistic-regression models. RESULTS The run-in phase was completed by 309 of 337 patients. The proteinuria level decreased to less than 0.75 g of urinary protein excretion per day in 94 patients. Of the remaining 162 patients who consented to undergo randomization, 80 were assigned to the supportive-care group, and 82 to the immunosuppression group. After 3 years, 4 patients (5%) in the supportive-care group, as compared with 14 (17%) in the immunosuppression group, had a full clinical remission (P = 0.01). A total of 22 patients (28%) in the supportive-care group and 21 (26%) in the immunosuppression group had a decrease in the eGFR of at least 15 ml per minute per 1.73 m(2) (P = 0.75). There was no significant difference in the annual decline in eGFR between the two groups. More patients in the immunosuppression group than in the supportive-care group had severe infections, impaired glucose tolerance, and weight gain of more than 5 kg in the first year of treatment. One patient in the immunosuppression group died of sepsis. CONCLUSIONS The addition of immunosuppressive therapy to intensive supportive care in patients with high-risk IgA nephropathy did not significantly improve the outcome, and during the 3-year study phase, more adverse effects were observed among the patients who received immunosuppressive therapy, with no change in the rate of decrease in the eGFR. (Funded by the German Federal Ministry of Education and Research; STOP-IgAN ClinicalTrials.gov number, NCT00554502.)"],["dc.description.sponsorship","German Federal Ministry of Education and Research"],["dc.identifier.doi","10.1056/NEJMoa1415463"],["dc.identifier.isi","000365743100006"],["dc.identifier.pmid","26630142"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13836"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35183"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Massachusetts Medical Soc"],["dc.relation.issn","1533-4406"],["dc.relation.issn","0028-4793"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Intensive Supportive Care plus Immunosuppression in IgA Nephropathy"],["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.journal","Frontiers in Pediatrics"],["dc.bibliographiccitation.volume","7"],["dc.contributor.author","Macheroux, Eva Pauline"],["dc.contributor.author","Braunisch, Matthias C."],["dc.contributor.author","Pucci Pegler, Stephanie"],["dc.contributor.author","Satanovskij, Robin"],["dc.contributor.author","Riedhammer, Korbinian M."],["dc.contributor.author","Günthner, Roman"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Nagel, Mato"],["dc.contributor.author","Renders, Lutz"],["dc.contributor.author","Hoefele, Julia"],["dc.date.accessioned","2020-12-10T18:44:36Z"],["dc.date.available","2020-12-10T18:44:36Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.3389/fped.2019.00485"],["dc.identifier.eissn","2296-2360"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/17105"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78523"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The Hypomorphic Variant p.(Gly624Asp) in COL4A5 as a Possible Cause for an Unexpected Severe Phenotype in a Family With X-Linked Alport Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Pediatric Nephrology"],["dc.bibliographiccitation.lastpage","10"],["dc.contributor.author","Rheault, Michelle N."],["dc.contributor.author","Savige, Judith"],["dc.contributor.author","Randles, Michael J."],["dc.contributor.author","Weinstock, André"],["dc.contributor.author","Stepney, Melissa"],["dc.contributor.author","Turner, A Neil"],["dc.contributor.author","Parziale, Gina"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Flinter, Frances A"],["dc.contributor.author","Miner, Jeffrey H"],["dc.contributor.author","Lagas, Sharon"],["dc.contributor.author","Gear, Susie"],["dc.contributor.author","Lennon, Rachel"],["dc.date.accessioned","2019-07-09T11:51:36Z"],["dc.date.available","2019-07-09T11:51:36Z"],["dc.date.issued","2019"],["dc.description.abstract","Alport syndrome is caused by mutations in the genes COL4A3, COL4A4 or COL4A5 and is characterised by progressive glomerular disease, sensorineural hearing loss and ocular defects. Occurring in less than 1:5000, Alport syndrome is a rare genetic disorder but still accounts for > 1% of the prevalent population receiving renal replacement therapy. There is also increasing awareness about the risk of chronic kidney disease in individuals with heterozygous mutations in Alport syndrome genes. The mainstay of current therapy is the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers, yet potential new therapies are now entering clinical trials. The 2017 International Workshop on Alport Syndrome in Glasgow was a pre-conference workshop ahead of the 50th anniversary meeting of the European Society for Pediatric Nephrology. It focussed on updates in clinical practice, genetics and basic science and also incorporated patient perspectives. More than 80 international experts including clinicians, geneticists, researchers from academia and industry, and patient representatives took part in panel discussions and breakout groups. This report summarises the workshop proceedings and the relevant contemporary literature. It highlights the unique clinician, patient and researcher collaborations achieved by regular engagement between the groups."],["dc.identifier.doi","10.1007/s00467-019-04241-7"],["dc.identifier.pmid","31044288"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59970"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1432-198X"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","The importance of clinician, patient and researcher collaborations in Alport syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","3049"],["dc.bibliographiccitation.issue","14"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Moerer, Onnen"],["dc.contributor.author","Rauen, Thomas"],["dc.contributor.author","Böckhaus, Jan"],["dc.contributor.author","Hoxha, Elion"],["dc.contributor.author","Jörres, Achim"],["dc.contributor.author","Kamm, Matthias"],["dc.contributor.author","Elfanish, Amin"],["dc.contributor.author","Windisch, Wolfram"],["dc.contributor.author","Blaschke, Sabine"],["dc.contributor.author","Dreher, Michael"],["dc.contributor.author","Floege, Juergen"],["dc.contributor.author","Kluge, Stefan"],["dc.contributor.author","Schmidt-Lauber, Christian"],["dc.contributor.author","Turner, Jan-Eric"],["dc.contributor.author","Huber, Samuel"],["dc.contributor.author","Addo, Marylyn M."],["dc.contributor.author","Scheithauer, Simone"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Braun, Gerald S."],["dc.contributor.author","Huber, Tobias B."],["dc.date.accessioned","2021-08-12T07:46:00Z"],["dc.date.available","2021-08-12T07:46:00Z"],["dc.date.issued","2021"],["dc.description.abstract","In COVID-19, guidelines recommend a urinalysis on hospital admission as SARS-CoV-2 renal tropism, post-mortem, was associated with disease severity and mortality. Following the hypothesis from our pilot study, we now validate an algorithm harnessing urinalysis to predict the outcome and the need for ICU resources on admission to hospital. Patients were screened for urinalysis, serum albumin (SA) and antithrombin III activity (AT-III) obtained prospectively on admission. The risk for an unfavorable course was categorized as (1) “low”, (2) “intermediate” or (3) “high”, depending on (1) normal urinalysis, (2) abnormal urinalysis with SA ≥ 2 g/dL and AT-III ≥ 70%, or (3) abnormal urinalysis with SA or AT-III abnormality. Time to ICU admission or death served as the primary endpoint. Among 223 screened patients, 145 were eligible for enrollment, 43 falling into the low, 84 intermediate, and 18 into high-risk categories. An abnormal urinalysis significantly elevated the risk for ICU admission or death (63.7% vs. 27.9%; HR 2.6; 95%-CI 1.4 to 4.9; p = 0.0020) and was 100% in the high-risk group. Having an abnormal urinalysis was associated with mortality, a need for mechanical ventilation, extra-corporeal membrane oxygenation or renal replacement therapy. In conclusion, our data confirm that COVID-19-associated urine abnormalities on admission predict disease aggravation and the need for ICU (ClinicalTrials.gov number NCT04347824)."],["dc.description.abstract","In COVID-19, guidelines recommend a urinalysis on hospital admission as SARS-CoV-2 renal tropism, post-mortem, was associated with disease severity and mortality. Following the hypothesis from our pilot study, we now validate an algorithm harnessing urinalysis to predict the outcome and the need for ICU resources on admission to hospital. Patients were screened for urinalysis, serum albumin (SA) and antithrombin III activity (AT-III) obtained prospectively on admission. The risk for an unfavorable course was categorized as (1) “low”, (2) “intermediate” or (3) “high”, depending on (1) normal urinalysis, (2) abnormal urinalysis with SA ≥ 2 g/dL and AT-III ≥ 70%, or (3) abnormal urinalysis with SA or AT-III abnormality. Time to ICU admission or death served as the primary endpoint. Among 223 screened patients, 145 were eligible for enrollment, 43 falling into the low, 84 intermediate, and 18 into high-risk categories. An abnormal urinalysis significantly elevated the risk for ICU admission or death (63.7% vs. 27.9%; HR 2.6; 95%-CI 1.4 to 4.9; p = 0.0020) and was 100% in the high-risk group. Having an abnormal urinalysis was associated with mortality, a need for mechanical ventilation, extra-corporeal membrane oxygenation or renal replacement therapy. In conclusion, our data confirm that COVID-19-associated urine abnormalities on admission predict disease aggravation and the need for ICU (ClinicalTrials.gov number NCT04347824)."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft"],["dc.description.sponsorship","Bundesministerium für Bildung und Forschung"],["dc.identifier.doi","10.3390/jcm10143049"],["dc.identifier.pii","jcm10143049"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88595"],["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","Validation of a Prospective Urinalysis-Based Prediction Model for ICU Resources and Outcome of COVID-19 Disease: A Multicenter Cohort Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","19"],["dc.bibliographiccitation.journal","Fibrogenesis & Tissue Repair"],["dc.bibliographiccitation.lastpage","10"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Martin, Maria"],["dc.contributor.author","Kruegel, Jenny"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Temme, Johanna"],["dc.contributor.author","Eckes, Beate"],["dc.contributor.author","Müller, Gerhard-Anton"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2019-07-09T11:52:48Z"],["dc.date.available","2019-07-09T11:52:48Z"],["dc.date.issued","2010"],["dc.description.abstract","Background: Integrins are important cellular receptors for collagens. Within the glomerulus, podocytes regulate the integrity of the glomerular basement membrane (GBM) by sensing the presence of collagen and regulating collagen IV synthesis. The present study evaluates the role of integrin a2 (ITGA2) in cell-matrix interaction. Methods and Results: ITGA2-deficient mice had normal renal function but moderate proteinuria and enhanced glomerular and tubulointerstitial matrix deposition. Electron microscopy demonstrated irregular podocyte-matrix interaction, causing pathological protrusions towards the urinary (podocyte) side of the GBM. These characteristic subepithelial bulges mimic the renal phenotype of mice, which are deficient in another collagen receptor, discoidin domain receptor (DDR)1. Using immunogold staining, ITGA2 expression was found to localize to the basolateral site of the podocyte foot processes. ITGA2-deficient mice overexpressed transforming growth factor (TGF)b and connective tissue growth factor (CTGF) compared with wild-type mice. Using in situ hybridization, tubular cells were found to be the primary site of TGFb synthesis and podocytes the source of CTGF in ITGA2- deficient mice. Conclusion: These findings support our hypothesis that both these collagen receptors (ITGA2 and DDR1) play a similar role within the kidney. Further, cell-matrix interaction via collagen receptors seems to be crucial for maintenance of normal GBM architecture and function. Targeting collagen receptors such as ITGA2 might be a new form of treatment for progressive fibrotic diseases."],["dc.identifier.doi","10.1186/1755-1536-3-19"],["dc.identifier.fs","575629"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6018"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60281"],["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-1/6905 but duplicate"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Integrin a2-deficient mice provide insights into specific functions of collagen receptors in the kidney"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","360"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Life"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Boeckhaus, Jan"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Storz, Celine"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2021-04-14T08:24:02Z"],["dc.date.available","2021-04-14T08:24:02Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.3390/life10120360"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81139"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2075-1729"],["dc.rights","https://creativecommons.org/licenses/by/4.0/"],["dc.title","Characterization of Sensorineural Hearing Loss in Children with Alport Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","5101"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Journal of Clinical Medicine"],["dc.bibliographiccitation.volume","11"],["dc.contributor.affiliation","Feltgen, Nicolas; 1Clinic of Ophthalmology, University Medical Centre Goettingen, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Ach, Thomas; 2Department of Ophthalmology, University Hospital Bonn, 53127 Bonn, Germany"],["dc.contributor.affiliation","Ziemssen, Focke; 3Department of Ophthalmology, University Leipzig, 04103 Leipzig, Germany"],["dc.contributor.affiliation","Quante, Carolin Sophie; 5Medical School, University Medical Centre Goettingen, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Gross, Oliver; 6Clinic of Nephrology and Rheumatology, University Medical Centre Goettingen, 37075 Goettingen, Germany"],["dc.contributor.affiliation","Abdin, Alaa Din; 7Department of Ophthalmology, Saarland University Medical Centre UKS, 66421 Homburg/Saar, Germany"],["dc.contributor.affiliation","Aisenbrey, Sabine; 8Department of Ophthalmology, Vivantes Health Network Ltd., Neukoelln Hospital, 12351 Berlin, Germany"],["dc.contributor.affiliation","Bartram, Martin C.; 9Department of Ophthalmology, Hannover Medical School, 30625 Hannover, Germany"],["dc.contributor.affiliation","Blum, Marcus; 10Department of Ophthalmology, Helios Hospital Erfurt, 99089 Erfurt, Germany"],["dc.contributor.affiliation","Brockmann, Claudia; 11Department of Ophthalmology, Universitätsmedizin Rostock, 18057 Rostock, Germany"],["dc.contributor.affiliation","Dithmar, Stefan; 12Department of Ophthalmology, Helios HSK Wiesbaden, 65191 Wiesbaden, Germany"],["dc.contributor.affiliation","Friedrichs, Wilko; 13Charlottenklinik Ophthalmology, 70176 Stuttgart, Germany"],["dc.contributor.affiliation","Guthoff, Rainer; 14Department of Ophthalmology, Faculty of Medicine, University Hospital Duesseldorf, 40225 Dusseldorf, Germany"],["dc.contributor.affiliation","Hattenbach, Lars-Olof; 15Department of Ophthalmology, Ludwigshafen Hospital, 67063 Ludwigshafen am Rhein, Germany"],["dc.contributor.affiliation","Herrlinger, Klaus R.; 16Department of Internal Medicine I, Asklepios Klinik Nord, 22417 Hamburg, Germany"],["dc.contributor.affiliation","Kaskel-Paul, Susanne; 17Department of Ophthalmology, Maerkische Kliniken GmbH, 58515 Luedenscheid, Germany"],["dc.contributor.affiliation","Khoramnia, Ramin; 18The David J Apple Centre for Vision Research, Department of Ophthalmology, University Hospital Heidelberg, 69120 Heidelberg, Germany"],["dc.contributor.affiliation","Klaas, Julian E.; 19Department of Ophthalmology, University Hospital, LMU Munich, 80336 Munich, Germany"],["dc.contributor.affiliation","Krohne, Tim U.; 20Department of Ophthalmology, Faculty of Medicine and University Hospital of Cologne, University of Cologne, 50937 Cologne, Germany"],["dc.contributor.affiliation","Lommatzsch, Albrecht; 21Department of Ophthalmology, St. Franziskus-Hospital, 48145 Muenster, Germany"],["dc.contributor.affiliation","Lueken, Sabine; 22Department of Ophthalmology, University of Luebeck, 23538 Luebeck, Germany"],["dc.contributor.affiliation","Maier, Mathias; 23Ophthalmology Department, Hospital Rechts der Isar, Technical University of Munich (TUM), 81675 Munich, Germany"],["dc.contributor.affiliation","Nassri, Lina; 24Department of Ophthalmology, University Hospital RWTH Aachen, 52074 Aachen, Germany"],["dc.contributor.affiliation","Nguyen-Dang, Thien A.; 25Praxis Prof. Laube, 40212 Duesseldorf, Germany"],["dc.contributor.affiliation","Radeck, Viola; 26Department of Ophthalmology, University Hospital of Regensburg, 93049 Regensburg, Germany"],["dc.contributor.affiliation","Rau, Saskia; 27Department of Ophthalmology, Charité-University Medicine Berlin, Corporate Member of Freie Universitaet Berlin, Humboldt-Universitaet zu Berlin and Berlin Institute of Health, 13353 Berlin, Germany"],["dc.contributor.affiliation","Roider, Johann; 28Clinic of Ophthalmology, University Hospital Schleswig-Holstein, Kiel Campus, 24105 Kiel, Germany"],["dc.contributor.affiliation","Sandner, Dirk; 29Department of Ophthalmology, University Hospital Carl Gustav Carus, Technical University of Dresden, 01307 Dresden, Germany"],["dc.contributor.affiliation","Schmalenberger, Laura; 30Municipal Clinic Braunschweig, 38126 Braunschweig, Germany"],["dc.contributor.affiliation","Schmidtmann, Irene; 31Institute of Medical Biostatistics, Epidemiology and Informatics, University Medical Centre of the Johannes Gutenberg-University Mainz, 55131 Mainz, Germany"],["dc.contributor.affiliation","Schubert, Florian; 32Department of Ophthalmology, Phillips University of Marburg, 35043 Marburg, Germany"],["dc.contributor.affiliation","Siegel, Helena; 33Eye Centre, Faculty of Medicine, University of Freiburg, 79106 Freiburg, Germany"],["dc.contributor.affiliation","Spitzer, Martin S.; 34Department of Ophthalmology, University Medical Centre Hamburg-Eppendorf, 20251 Hamburg, Germany"],["dc.contributor.affiliation","Stahl, Andreas; 35Department of Ophthalmology, University Medical Centre Greifswald, 17475 Greifswald, Germany"],["dc.contributor.affiliation","Stingl, Julia V.; 36Department of Ophthalmology, Medical Centre of the Johannes Gutenberg-University Mainz, 55131 Mainz, Germany"],["dc.contributor.affiliation","Treumer, Felix; 37Department of Ophthalmology, Klinikum Kassel, 34125 Kassel, Germany"],["dc.contributor.affiliation","Viestenz, Arne; 38Department of Ophthalmology, Martin-Luther University Halle-Wittenberg, 06120 Halle (Saale), Germany"],["dc.contributor.affiliation","Wachtlin, Joachim; 39Department of Ophthalmology, Sankt-Gertrauden Krankenhaus, 10713 Berlin, Germany"],["dc.contributor.affiliation","Wolf, Armin; 41Department of Ophthalmology, Ulm University Medical Centre, 89075 Ulm, Germany"],["dc.contributor.affiliation","Zimmermann, Julian; 42Department of Ophthalmology, University of Muenster Medical Centre, 48149 Muenster, Germany"],["dc.contributor.affiliation","Schargus, Marc; 43Asklepios Augenklinik Nord, 22417 Hamburg, Germany"],["dc.contributor.affiliation","Schuster, Alexander K.; 36Department of Ophthalmology, Medical Centre of the Johannes Gutenberg-University Mainz, 55131 Mainz, Germany"],["dc.contributor.author","Feltgen, Nicolas"],["dc.contributor.author","Ach, Thomas"],["dc.contributor.author","Ziemssen, Focke"],["dc.contributor.author","Quante, Carolin Sophie"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Abdin, Alaa Din"],["dc.contributor.author","Aisenbrey, Sabine"],["dc.contributor.author","Bartram, Martin C."],["dc.contributor.author","Blum, Marcus"],["dc.contributor.author","Brockmann, Claudia"],["dc.contributor.author","Schuster, Alexander K."],["dc.contributor.editor","Ascaso, Francisco Javier"],["dc.date.accessioned","2022-10-04T10:21:14Z"],["dc.date.available","2022-10-04T10:21:14Z"],["dc.date.issued","2022"],["dc.date.updated","2022-11-11T13:14:59Z"],["dc.description.abstract","Background: To investigate whether vaccination against SARS-CoV-2 is associated with the onset of retinal vascular occlusive disease (RVOD). Methods: In this multicentre study, data from patients with central and branch retinal vein occlusion (CRVO and BRVO), central and branch retinal artery occlusion (CRAO and BRAO), and anterior ischaemic optic neuropathy (AION) were retrospectively collected during a 2-month index period (1 June–31 July 2021) according to a defined protocol. The relation to any previous vaccination was documented for the consecutive case series. Numbers of RVOD and COVID-19 vaccination were investigated in a case-by-case analysis. A case–control study using age- and sex-matched controls from the general population (study participants from the Gutenberg Health Study) and an adjusted conditional logistic regression analysis was conducted. Results: Four hundred and twenty-one subjects presenting during the index period (61 days) were enrolled: one hundred and twenty-one patients with CRVO, seventy-five with BRVO, fifty-six with CRAO, sixty-five with BRAO, and one hundred and four with AION. Three hundred and thirty-two (78.9%) patients had been vaccinated before the onset of RVOD. The vaccines given were BNT162b2/BioNTech/Pfizer (n = 221), followed by ChadOx1/AstraZeneca (n = 57), mRNA-1273/Moderna (n = 21), and Ad26.COV2.S/Johnson & Johnson (n = 11; unknown n = 22). Our case–control analysis integrating population-based data from the GHS yielded no evidence of an increased risk after COVID-19 vaccination (OR = 0.93; 95% CI: 0.60–1.45, p = 0.75) in connection with a vaccination within a 4-week window. Conclusions: To date, there has been no evidence of any association between SARS-CoV-2 vaccination and a higher RVOD risk."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2022"],["dc.identifier.doi","10.3390/jcm11175101"],["dc.identifier.pii","jcm11175101"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/114357"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-600"],["dc.publisher","MDPI"],["dc.relation.eissn","2077-0383"],["dc.rights","CC BY 4.0"],["dc.title","Retinal Vascular Occlusion after COVID-19 Vaccination: More Coincidence than Causal Relationship? Data from a Retrospective Multicentre Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","429"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Medizinische Genetik"],["dc.bibliographiccitation.lastpage","437"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Hoefele, Julia"],["dc.date.accessioned","2019-07-09T11:50:42Z"],["dc.date.available","2019-07-09T11:50:42Z"],["dc.date.issued","2019"],["dc.description.abstract","Patients with the hereditary disease Alport syndrome (AS) develop progressive renal fibrosis due to variants in type IV collagen genes. In the first years of life, AS starts with hematuria and proteinuria, finally leading to end-stage renal disease and extrarenal symptoms such as hearing impairment and ocular changes. Variants in three different genes can cause AS, COL4A5 (X-chromosomal) in 85%, COL4A3 or COL4A4 (autosomal) in 10%, and digenic variants in less than 5% of the cases. In the past, the symptomatic form in patients with a heterozygous variant was classified as thin basement membrane disease or benign familial hematuria. However, patients with a heterozygous variant often have a non-benign disease course. Therefore, these patients are now also given the diagnosis “Alport syndrome.” If diagnosed early, AS is treatable. Renal failure can be delayed by years and life expectancy can be improved. Because of the available treatment options, the molecular genetic diagnosis should be made as soon as possible in every affected child and in all patients with a heterozygous variant. Unfortunately, the diagnosis is often made too late during early adolescence. This article serves as a guideline for the genetic background of AS, possible additional (genetic) modifiers, possible additional complications, and the current therapeutic approach for the optimal lifelong care of patients living with AS. For genetic experts, it is important to know that this nephroprotective approach begins with an early genetic diagnosis guiding the timeline of possible therapeutic interventions."],["dc.description.abstract","Bei der Typ IV Kollagen-Erkrankung Alport-Syndrom (AS) handelt es sich um eine progressive hereditäre Nephropathie. Klinische Zeichen sind zunächst Hämaturie und Proteinurie, im weiteren Verlauf kommt es zu einem terminalen Nierenversagen. Zusätzlich werden extrarenale Manifestationen wie Innenohr-Schwerhörigkeit und Augenveränderungen beobachtet. Man unterscheidet drei Erbgänge: 85 % der Fälle sind X-chromosomal, ca. 10 % autosomal und weniger als 5 % digenisch. Ursächlich sind Varianten in den Kollagen Typ IV-Genen COL4A3, COL4A4 (beide autosomal) und COL4A5 (X-chromosomal). Die Symptomatik heterozygoter Anlageträger wurde früher als benigne familiäre Hämaturie bezeichnet. Da Anlageträger jedoch häufig keinen benignen Verlauf zeigen, werden sie inzwischen auch unter der Diagnose „Alport-Syndrom“ geführt. Der Humangenetiker hat daher beim AS eine wichtige Lotsenfunktion: Bei früher Diagnose ist das AS inzwischen gut behandelbar, wodurch das terminale Nierenversagen um mehrere Jahre hinausgezögert und damit die Lebenserwartung verbessert werden kann. Aufgrund der Therapiemöglichkeiten sollte die (molekulargenetische) Diagnose bei Betroffenen, auch bei heterozygoten Anlageträgern, frühzeitig gestellt werden. Mit diesem Artikel sollen die genetischen Ursachen des AS, mögliche genetische Einflussfaktoren auf den variablen Phänotyp, die unterschiedlichen Krankheitsstadien, Komplikationen sowie die derzeit zugelassene Behandlung aufgezeigt werden, um eine bestmögliche lebenslange Betreuung des Patienten zu gewährleisten."],["dc.identifier.doi","10.1007/s11825-018-0214-2"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15981"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59812"],["dc.language.iso","de"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1863-5490"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Genetische Ursachen und Therapie beim Alport-Syndrom"],["dc.title.translated","Genetic causes and therapy in Alport Syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","ISRN Pediatrics"],["dc.bibliographiccitation.lastpage","6"],["dc.bibliographiccitation.volume","2012"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Hilgers, Reinhard"],["dc.contributor.author","Görlitz, Anke"],["dc.contributor.author","Gavénis, Karsten"],["dc.contributor.author","Ahmed, Raees"],["dc.contributor.author","Dürr, Ulrike"],["dc.date.accessioned","2019-07-09T11:54:04Z"],["dc.date.available","2019-07-09T11:54:04Z"],["dc.date.issued","2012"],["dc.description.abstract","Introduction. Retrospective observational data show that ACE-inhibitor therapy delays renal failure and improves life expectancy in Alport patients with proteinuria. The EARLY PRO-TECT Alport trial assesses the safety and efficacy of early therapy onset with ramipril in pediatric Alport patients.Methods and analysis. This double-blind, randomized, placebo-controlled, multicenter phase III trial (NCT01485978; EudraCT-number 2010-024300-10) includes 120 pediatric patients aged 24 months to 18 years with early stages of Alport syndrome (isolated hematuria or microalbuminuria). From March 2012, up to 80 patients will be randomized 1:1 to ramipril or placebo. In the event of disease progression during 3-year treatment, patients are unblinded and ramipril is initiated, if applicable. Approximately 40 patients receive open-label ramipril contributing to the safety database. Primary endpoints are “time to progression to next disease level” and “incidence of adverse drug events before disease progression.” Treatment effect estimates from the randomized comparison and Alport registry data will be combined in supportive analyses to maximize evidence. Conclusion. Without this trial, ACE inhibitors may become standard off-label treatment in Alport syndrome without satisfactory evidence base. The results are expected to be of relevance for therapy of all pediatric patients with kidney disease, and the trial protocol might serve as a model for other rare pediatric glomerulopathies."],["dc.identifier.doi","10.5402/2012/436046"],["dc.identifier.fs","587146"],["dc.identifier.pmid","22811928"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8396"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60563"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","2090-4703"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Safety and Efficacy of the ACE-Inhibitor Ramipril in Alport Syndrome: The Double-Blind, Randomized, Placebo-Controlled, Multicenter Phase III EARLY PRO-TECT Alport Trial in Pediatric Patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]