Gross, Oliver

[["dc.bibliographiccitation.firstpage","131"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Pediatric Nephrology"],["dc.bibliographiccitation.lastpage","137"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Stock, Johanna"],["dc.contributor.author","Kuenanz, Johannes"],["dc.contributor.author","Glonke, Niklas"],["dc.contributor.author","Sonntag, Joseph"],["dc.contributor.author","Frese, Jenny"],["dc.contributor.author","Toenshoff, Burkhard"],["dc.contributor.author","Hoecker, Britta"],["dc.contributor.author","Hoppe, Bernd"],["dc.contributor.author","Feldkoetter, Markus"],["dc.contributor.author","Pape, Lars"],["dc.contributor.author","Lerch, Christian"],["dc.contributor.author","Wygoda, Simone"],["dc.contributor.author","Weber, Manfred"],["dc.contributor.author","Mueller, Gerhard-Anton"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2018-11-07T10:29:37Z"],["dc.date.available","2018-11-07T10:29:37Z"],["dc.date.issued","2017"],["dc.description.abstract","Patients with autosomal or X-linked Alport syndrome (AS) with heterozygous mutations in type IV collagen genes have a 1-20 % risk of progressing to end-stage renal disease during their lifetime. We evaluated the long-term renal outcome of patients at risk of progressive disease (chronic kidney disease stages 1-4) with/without nephroprotective therapy. This was a prospective, non-interventional, observational study which included data from a 4-year follow-up of AS patients with heterozygous mutations whose datasets had been included in an analysis of the 2010 database of the European Alport Registry. Using Kaplan-Meier estimates and logrank tests, we prospectively analyzed the updated datasets of 52 of these patients and 13 new datasets (patients added to the Registry after 2011). The effects of therapy, extrarenal symptoms and inheritance pattern on renal outcome were analyzed. The mean prospective follow-up was 46 +/- 10 months, and the mean time on therapy was 8.4 +/- 4.4 (median 7; range 2-18) years. The time from the appearance of the first symptom to diagnosis was 8.1 +/- 14.2 (range 0-52) years. At the time of starting therapy, 5.4 % of patients had an estimated glomerular filtration rate of < 60 ml/min, 67.6 % had proteinuria and 27.0 % had microalbuminuria. Therapeutic strategies included angiotensin-converting enzymer inhibitors (97.1 %), angiotensin receptor antagonists (1 patient), dual therapy (11.8 %) and statins (8.8 %). Among patients included in the prospective dataset, prevented the need for dialysis. Among new patients, no patient at risk for renal failure progressed to the next disease stage after 4 years follow-up; three patients even regressed to a lower stage during therapy. Treatment with blockers of the renin-angiotensin-aldosterone system prevents progressive renal failure in AS patients with heterozygous mutations in the genes causing AS. Considerable numbers of aging AS patients on dialysis may have heterozygous mutations in these genes (present in 1 % of total population) as underlying disease. Hence, greater alertness towards timely diagnosis and therapy has the potential to prevent progressive renal failure in most-if not all-AS patients with heterozygous mutations in the causal genes."],["dc.identifier.doi","10.1007/s00467-016-3452-z"],["dc.identifier.isi","000388976400015"],["dc.identifier.pmid","27402170"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/43676"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Springer"],["dc.relation.issn","1432-198X"],["dc.relation.issn","0931-041X"],["dc.title","Prospective study on the potential of RAAS blockade to halt renal disease in Alport syndrome patients with heterozygous mutations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Therapeutic Drug Monitoring"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Brandhorst, Gunnar"],["dc.contributor.author","Brehmer, Franziska"],["dc.contributor.author","Petrova, Darinka Todorova"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Armstrong, Victor William"],["dc.contributor.author","Oellerich, M."],["dc.date.accessioned","2018-11-07T11:24:07Z"],["dc.date.available","2018-11-07T11:24:07Z"],["dc.date.issued","2009"],["dc.format.extent","664"],["dc.identifier.isi","000270484600225"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56334"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.publisher.place","Philadelphia"],["dc.relation.conference","11th International Congress of Therapeutic Drug Monitoring and Clinical Toxicology"],["dc.relation.eventlocation","Montreal, CANADA"],["dc.relation.issn","0163-4356"],["dc.title","Mycophenolate Mofetil improves Kidney Function but not Survival in a COL4A3-deficient Mouse Model for Progressive Renal Fibrosis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","76"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of the American Society of Nephrology"],["dc.bibliographiccitation.lastpage","83"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Andersen, Kirstin"],["dc.contributor.author","Kesper, Marie Sophie"],["dc.contributor.author","Marschner, Julian A."],["dc.contributor.author","Konrad, Lukas"],["dc.contributor.author","Ryu, Mi"],["dc.contributor.author","Kumar VR, Santhosh"],["dc.contributor.author","Kulkarni, Onkar P."],["dc.contributor.author","Mulay, Shrikant R."],["dc.contributor.author","Romoli, Simone"],["dc.contributor.author","Demleitner, Jana"],["dc.contributor.author","Schiller, Patrick"],["dc.contributor.author","Dietrich, Alexander"],["dc.contributor.author","Müller, Susanna"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Ruscheweyh, Hans-Joachim"],["dc.contributor.author","Huson, Daniel H."],["dc.contributor.author","Stecher, Bärbel"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.date.accessioned","2020-12-10T18:42:47Z"],["dc.date.available","2020-12-10T18:42:47Z"],["dc.date.issued","2017"],["dc.description.abstract","CKD associates with systemic inflammation, but the underlying cause is unknown. Here, we investigated the involvement of intestinal microbiota. We report that collagen type 4 alpha 3-deficient mice with Alport syndrome related progressive CKD displayed systemic inflammation, including increased plasma levels of pentraxin-2 and activated antigen presenting cells, CD4 and CD8 T cells, and Th17 or IFN gamma-producing T cells in the spleen as well as regulatory T cell suppression. CKD related systemic inflammation in these mice associated with intestinal dysbiosis of proteobacterial blooms, translocation of living bacteria across the intestinal barrier into the liver, and increased serum levels of bacterial endotoxin. Uremia did not affect secretory IgA release into the ileum lumen or mucosal leukocyte subsets. To test for causation between dysbiosis and systemic inflammation in CKD, we eradicated facultative anaerobic microbiota with antibiotics. This eradication prevented bacterial translocation, significantly reduced serum endotoxin levels, and fully reversed all markers of systemic inflammation to the level of nonuremic controls. Therefore, we conclude that uremia associates with intestinal dysbiosis, intestinal barrier dysfunction, and bacterial trans location, which trigger the state of persistent systemic inflammation in CKD. Uremic dysbiosis and intestinal barrier dysfunction may be novel therapeutic targets for intervention to suppress CKD related systemic inflammation and its consequences."],["dc.identifier.doi","10.1681/ASN.2015111285"],["dc.identifier.eissn","1533-3450"],["dc.identifier.isi","000391647700012"],["dc.identifier.issn","1046-6673"],["dc.identifier.pmid","27151924"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/78080"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Amer Soc Nephrology"],["dc.relation.issn","1533-3450"],["dc.relation.issn","1046-6673"],["dc.title","Intestinal Dysbiosis, Barrier Dysfunction, and Bacterial Translocation Account for CKD–Related Systemic Inflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","482"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The Journal of Pathology"],["dc.bibliographiccitation.lastpage","494"],["dc.bibliographiccitation.volume","228"],["dc.contributor.author","Ryu, M. I."],["dc.contributor.author","Migliorini, Adriana"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Shankland, Stuart"],["dc.contributor.author","Brinkkoetter, Paul T."],["dc.contributor.author","Hagmann, Henning"],["dc.contributor.author","Romagnani, Paola"],["dc.contributor.author","Liapis, Helen"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.date.accessioned","2018-11-07T09:02:32Z"],["dc.date.available","2018-11-07T09:02:32Z"],["dc.date.issued","2012"],["dc.description.abstract","Glomerular crescents are most common in rapidly progressive glomerulonephritis but also occur in noninflammatory chronic glomerulopathies; thus, factors other than inflammation should trigger crescent formation, eg vascular damage and plasma leakage. Here we report that Alport nephropathy in Col4A3-deficient Sv129 mice is complicated by diffuse and global crescent formation in which proliferating parietal epithelial cells are the predominant cell type. Laminin staining and transmission and acellular scanning electron microscopy of acellular glomeruli documented disruptions and progressive disintegration of the glomerular basement membrane in Col4A3-deficient mice. FITC-dextran perfusion further revealed vascular leakage from glomerular capillaries into Bowman's space, further documented by fibrin deposits in the segmental crescents. Its pathogenic role was validated by showing that the fibrinolytic activity of recombinant urokinase partially prevented crescent formation. In addition, in vitro studies confirmed an additional mitogenic potential of serum on murine and human parietal epithelial cells. Furthermore, loss of parietal cell polarity and unpolarized secretion of extracellular matrix components were evident within fibrocellular crescents. Among 665 human Alport nephropathy biopsies, crescent formation was noted in 0.4%. We conclude that glomerular vascular injury and GBM breaks cause plasma leakage which triggers a wound healing programme involving the proliferation of parietal cells and their loss of polarity. This process can trigger cellular and fibrocellular crescent formation even in the absence of cellular inflammation and rupture of the Bowman's capsule. Copyright (C) 2012 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd."],["dc.identifier.doi","10.1002/path.4046"],["dc.identifier.isi","000313949800007"],["dc.identifier.pmid","22553158"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/24705"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.relation.issn","0022-3417"],["dc.title","Plasma leakage through glomerular basement membrane ruptures triggers the proliferation of parietal epithelial cells and crescent formation in non-inflammatory glomerular injury"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","731"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Pediatric Nephrology"],["dc.bibliographiccitation.lastpage","731"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Kashtan, Clifford E."],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2021-04-14T08:30:39Z"],["dc.date.available","2021-04-14T08:30:39Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1007/s00467-020-04892-x"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83324"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1432-198X"],["dc.relation.iserratumof","/handle/2/83836"],["dc.relation.issn","0931-041X"],["dc.title","Correction to: Clinical practice recommendations for the diagnosis and management of Alport syndrome in children, adolescents, and young adults–an update for 2020"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","erratum_ja"],["dspace.entity.type","Publication"]]

[["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.firstpage","1626"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","1630"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Weber, Manfred"],["dc.contributor.author","Fries, Jochen W. U."],["dc.contributor.author","Mueller, Gerhard-Anton"],["dc.date.accessioned","2018-11-07T08:30:29Z"],["dc.date.available","2018-11-07T08:30:29Z"],["dc.date.issued","2009"],["dc.description.abstract","Background. Alport syndrome is a hereditary nephropathy leading to renal failure during adolescence. This study evaluates the outcome of living donor transplantation (Tx) from heterozygous mothers to their affected children. Methods. Seven mothers were evaluated, and donation was refused in one because of proteinuria. Results. All of the remaining six donors had microhaematuria, and one had proteinuria. Renal function was monitored after Tx (average 6.7 years in donors and 5.3 years in acceptors). Three of six donors developed new onset hypertension, and two new onset of proteinuria. Renal function declined significantly in four donors: (1) -35% after 2 years; (2) -25% after 3 years; (3) -30% after 4 years and (4) -60% after 14 years versus before Tx. However, creatinine clearance remained > 40 ml/min in all donors. All transplanted kidneys worked well 1 and 5 years after Tx, and one failed after 10 years. One patient died from meningitis, and the remaining four remained stable. Conclusion. Living donor Tx from relatives in Alport families is an ambivalent option. Proteinuria should be an exclusion criterion. Yet, even in donors with isolated microhaematuria, families and their physicians should be aware of an increased risk of renal failure in donor and recipient. This risk might be minimized by careful donor evaluation including biopsy and nephroprotective strategies after Tx in both donor and recipient."],["dc.identifier.doi","10.1093/ndt/gfn635"],["dc.identifier.isi","000265275000045"],["dc.identifier.pmid","19028755"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16900"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.conference","Annual Meeting of the American-and-German-Society-of-Nephrology"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0931-0509"],["dc.title","Living donor kidney transplantation from relatives with mild urinary abnormalities in Alport syndrome: long-term risk, benefit and outcome"],["dc.type","conference_paper"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","855"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Der Urologe"],["dc.bibliographiccitation.lastpage","864"],["dc.bibliographiccitation.volume","57"],["dc.contributor.author","Gross, O."],["dc.contributor.author","Bramlage, C."],["dc.date.accessioned","2020-12-10T14:08:40Z"],["dc.date.available","2020-12-10T14:08:40Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00120-018-0691-6"],["dc.identifier.eissn","1433-0563"],["dc.identifier.issn","0340-2592"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70517"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Nephrologie für Urologen"],["dc.title.alternative","Nephrology for urologists"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]