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.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","Transplant International"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Reinhardt, Joanna"],["dc.contributor.author","Weber, Manfred"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2018-11-07T10:59:28Z"],["dc.date.available","2018-11-07T10:59:28Z"],["dc.date.issued","2007"],["dc.format.extent","315"],["dc.identifier.isi","000249954001257"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50707"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.issn","0934-0874"],["dc.title","Living donor kidney transplanation from relatives with mild urinary abnormalities in Alport syndrome: Risk, benefit and outcome in five families"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2721"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","2723"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Floege, Juergen"],["dc.contributor.author","Kunter, Uta"],["dc.contributor.author","Weber, Manfred"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2018-11-07T09:12:19Z"],["dc.date.available","2018-11-07T09:12:19Z"],["dc.date.issued","2006"],["dc.identifier.doi","10.1093/ndt/gfl367"],["dc.identifier.isi","000240694900010"],["dc.identifier.pmid","16861735"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26923"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0931-0509"],["dc.title","Bone marrow transplantation rescues Alport mice"],["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","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","734"],["dc.bibliographiccitation.volume","24"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Borza, Dorin-Bogdan"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.contributor.author","Licht, Christoph"],["dc.contributor.author","Weber, Manfred"],["dc.contributor.author","Segerer, Stephan"],["dc.contributor.author","Torra, Roser"],["dc.contributor.author","Gubler, Marie-Claire"],["dc.contributor.author","Heidet, Laurence"],["dc.contributor.author","Harvey, Scott"],["dc.contributor.author","Cosgrove, Dominic"],["dc.contributor.author","Lees, George"],["dc.contributor.author","Kashtan, Clifford E."],["dc.contributor.author","Gregory, Martin"],["dc.contributor.author","Savige, Judy"],["dc.contributor.author","Ding, Jie"],["dc.contributor.author","Thorner, Paul"],["dc.contributor.author","Abrahamson, Dale R."],["dc.contributor.author","Antignac, Corinne"],["dc.contributor.author","Tryggvason, Karl"],["dc.contributor.author","Hudson, Billy"],["dc.contributor.author","Miner, Jeffrey H."],["dc.date.accessioned","2018-11-07T08:32:22Z"],["dc.date.available","2018-11-07T08:32:22Z"],["dc.date.issued","2009"],["dc.identifier.doi","10.1093/ndt/gfn722"],["dc.identifier.isi","000263605000011"],["dc.identifier.pmid","19110486"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17328"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0931-0509"],["dc.title","Stem cell therapy for Alport syndrome: the hope beyond the hype"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","494"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","501"],["dc.bibliographiccitation.volume","81"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Licht, Christoph"],["dc.contributor.author","Anders, Hans-Joachim"],["dc.contributor.author","Hoppe, Bernd"],["dc.contributor.author","Beck, Bodo"],["dc.contributor.author","Toenshoff, Burkhard"],["dc.contributor.author","Hoecker, Britta"],["dc.contributor.author","Wygoda, Simone"],["dc.contributor.author","Ehrich, Jochen H. H."],["dc.contributor.author","Pape, Lars"],["dc.contributor.author","Konrad, Martin"],["dc.contributor.author","Rascher, Wolfgang"],["dc.contributor.author","Doetsch, Joerg"],["dc.contributor.author","Mueller-Wiefel, Dirk E."],["dc.contributor.author","Hoyer, Peter F."],["dc.contributor.author","Knebelmann, Bertrand"],["dc.contributor.author","Pirson, Yves"],["dc.contributor.author","Grunfeld, Jean-Pierre"],["dc.contributor.author","Niaudet, Patrick"],["dc.contributor.author","Cochat, Pierre"],["dc.contributor.author","Heidet, Laurence"],["dc.contributor.author","Lebbah, Said"],["dc.contributor.author","Torra, Roser"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Lange, Katharina"],["dc.contributor.author","Mueller, Georg Anton"],["dc.contributor.author","Weber, Manfred"],["dc.date.accessioned","2018-11-07T09:13:13Z"],["dc.date.available","2018-11-07T09:13:13Z"],["dc.date.issued","2012"],["dc.description.abstract","Alport syndrome inevitably leads to end-stage renal disease and there are no therapies known to improve outcome. Here we determined whether angiotensin-converting enzyme inhibitors can delay time to dialysis and improve life expectancy in three generations of Alport families. Patients were categorized by renal function at the initiation of therapy and included 33 with hematuria or microalbuminuria, 115 with proteinuria, 26 with impaired renal function, and 109 untreated relatives. Patients were followed for a period whose mean duration exceeded two decades. Untreated relatives started dialysis at a median age of 22 years. Treatment of those with impaired renal function significantly delayed dialysis to a median age of 25, while treatment of those with proteinuria delayed dialysis to a median age of 40. Significantly, no patient with hematuria or microalbuminuria advanced to renal failure so far. Sibling pairs confirmed these results, showing that earlier therapy in younger patients significantly delayed dialysis by 13 years compared to later or no therapy in older siblings. Therapy significantly improved life expectancy beyond the median age of 55 years of the no-treatment cohort. Thus, Alport syndrome is treatable with angiotensin-converting enzyme inhibition to delay renal failure and therapy improves life expectancy in a time-dependent manner. This supports the need for early diagnosis and early nephroprotective therapy in oligosymptomatic patients. Kidney International (2012) 81, 494-501; doi:10.1038/ki.2011.407; published online 14 December 2011"],["dc.identifier.doi","10.1038/ki.2011.407"],["dc.identifier.isi","000300377000011"],["dc.identifier.pmid","22166847"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27122"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0085-2538"],["dc.title","Early angiotensin-converting enzyme inhibition in Alport syndrome delays renal failure and improves life expectancy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","779"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Kidney International"],["dc.bibliographiccitation.lastpage","783"],["dc.bibliographiccitation.volume","81"],["dc.contributor.author","Temme, Johanna"],["dc.contributor.author","Peters, Frederick"],["dc.contributor.author","Lange, Katharina"],["dc.contributor.author","Pirson, Yves"],["dc.contributor.author","Heidet, Laurence"],["dc.contributor.author","Torra, Roser"],["dc.contributor.author","Grunfeld, Jean-Pierre"],["dc.contributor.author","Weber, Manfred"],["dc.contributor.author","Licht, Christoph"],["dc.contributor.author","Mueller, Gerhard-Anton"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2018-11-07T09:11:47Z"],["dc.date.available","2018-11-07T09:11:47Z"],["dc.date.issued","2012"],["dc.description.abstract","We studied here the clinical course of heterozygous carriers of X-linked Alport syndrome and a subgroup of patients with thin basement membrane disease due to heterozygous autosomal recessive Alport mutations whose prognosis may be worse than formerly thought. We analyzed 234 Alport carriers, including 29 with autosomal recessive mutations. Using Kaplan-Meier estimates and log-rank tests, autosomal and X-linked carriers were found to have similar incidences of renal replacement therapy, proteinuria, and impaired creatinine clearance. Further, age at onset of renal replacement therapy did not differ between X-chromosomal and autosomal carriers. Both groups showed an impaired life expectancy when reaching renal replacement therapy. RAAS inhibition significantly delayed the onset of end-stage renal failure. Not only carriers of X-linked Alport mutations but also heterozygous carriers of autosomal recessive mutations were found to have an increased risk for worse renal function. The risk of end-stage renal disease in both groups affected life expectancy, and this should cause a greater alertness toward patients presenting with what has been wrongly termed 'familial benign hematuria.' Timely therapy can help to delay onset of end-stage renal failure. Thus, yearly follow-up by a nephrologist is advised for X-linked Alport carriers and patients with thin basement membrane nephropathy, microalbuminuria, proteinuria, or hypertension. Kidney International (2012) 81, 779-783; doi:10.1038/ki.2011.452; published online 11 January 2012"],["dc.identifier.doi","10.1038/ki.2011.452"],["dc.identifier.isi","000302269300010"],["dc.identifier.pmid","22237748"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26799"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","0085-2538"],["dc.title","Incidence of renal failure and nephroprotection by RAAS inhibition in heterozygous carriers of X-chromosomal and autosomal recessive Alport mutations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","346"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Matrix Biology"],["dc.bibliographiccitation.lastpage","356"],["dc.bibliographiccitation.volume","29"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Girgert, Rainer"],["dc.contributor.author","Beirowski, Bogdan"],["dc.contributor.author","Kretzler, Matthias"],["dc.contributor.author","Kang, Hee Gyung"],["dc.contributor.author","Kruegel, Jenny"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Busse, Ann-Christin"],["dc.contributor.author","Segerer, Stephan"],["dc.contributor.author","Vogel, Wolfgang F."],["dc.contributor.author","Mueller, Gerhard-Anton"],["dc.contributor.author","Weber, Manfred"],["dc.date.accessioned","2018-11-07T08:42:54Z"],["dc.date.available","2018-11-07T08:42:54Z"],["dc.date.issued","2010"],["dc.description.abstract","Alport syndrome is a hereditary type IV collagen disease leading to progressive renal fibrosis, hearing loss and ocular changes. End stage renal failure usually develops during adolescence. COL4A3-/- mice serve as an animal model for progressive renal scarring in Alport syndrome. The present study evaluates the role of Discoidin Domain Receptor 1 (DDR1) in cell-matrix interaction involved in pathogenesis of Alport syndrome including renal inflammation and fibrosis. DDR1/COL4A3 Double-knockouts were compared to COL4A3-/- mice with 50% or 100% expression of DDR1, wildtype controls and to DDR1-/- COL4A3+/+ controls for over 6 years. Double-knockouts lived 47% longer, mice with 50% DDR1 lived 29% longer and showed improved renal function (reduction in proteinuria and blood urea nitrogen) compared to animals with 100% DDR1 expression. Loss of DDR1 reduced proinflammtory, profibrotic cells via signaling of TGF beta, CTGF, NF kappa B and IL-6 and decreased deposition of extracellular matrix. Immunogold-staining and in-situ hybridisation identified podocytes as major players in DDR1-mediated fibrosis and inflammation within the kidney. In summary, glomerular epithelial cells (podocytes) express DDR1. Loss of DDR1-expression in the kidney delayed renal fibrosis and inflammation in hereditary type IV collagen disease. This supports our hypothesis that podocyte-matrix interaction via collagen receptors plays an important part in progression of renal fibrosis in Alport disease. The blockade of collagen-receptor DDR1 might serve as an important new therapeutic concept in progressive fibrotic and inflammatory diseases in the future. (C) 2010 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.matbio.2010.03.002"],["dc.identifier.isi","000280726400002"],["dc.identifier.pmid","20307660"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19817"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0945-053X"],["dc.title","Loss of collagen-receptor DDR1 delays renal fibrosis in hereditary type IV collagen disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1062"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","1069"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Koepke, Marie-Louise"],["dc.contributor.author","Weber, Manfred"],["dc.contributor.author","Schulze-Lohoff, Eckhard"],["dc.contributor.author","Beirowski, Bogdan"],["dc.contributor.author","Segerer, Stephan"],["dc.contributor.author","Gross, Oliver"],["dc.date.accessioned","2018-11-07T11:03:46Z"],["dc.date.available","2018-11-07T11:03:46Z"],["dc.date.issued","2007"],["dc.description.abstract","Background. Alport syndrome is caused by mutations in genes encoding for the alpha 3, alpha 4 or alpha 5 chain of type IV collagen leading to excessive production of fibrotic tissue and end-stage renal failure. HMG-CoA-reductase-inhibitors exhibit pleiotropic effects by which they modulate the production of connective tissue. The aim of this study was to examine the anti-fibrotic effect of the HMG-CoA-reductase-inhibitor, cerivastatin, in COL4A3 knockout mice, an animal model of Alport syndrome with progressive renal fibrosis. Methods. Forty homozygous COL4A3 knockout mice received cerivastatin, starting 28 or 49 days after birth. Mice were sacrificed at day 52 or 66 after birth. Immunohistochemistry against laminin and fibronectin was performed. Inflammatory cell infiltration was determined by F4/80- and CD3-staining. Myofibroblasts were identified by an alpha-smooth muscle actin staining. Expression of the profibrotic cytokines, TGF-beta 1 and CTGF, were determined by immunoblot. Results. The lifespan of treated COL4A3 knockout mice was increased by 28% compared with untreated animals (71 +/- 6 vs 91 +/- 9 days, P < 0.01). Early cerivastatin treatment reduced cholesterol levels (113 +/- 13 vs 141 +/- 19 mmol/l in untreated animals, P < 0.05) and serum urea (164 vs 235 mmol/l, day 66, P < 0.05). Treatment also decreased proteinuria (5.5 vs 12 g/l at day 66, P < 0.05). Deposition of laminin and fibronectin, expression of TGF-beta and CTGF was reduced. Infiltration of T-cells and macrophages as well as myofibroblasts appeared to be reduced in kidneys from cerivastatin-treated mice. Conclusion. Cerivastatin prolongs the lifespan of COL4A3 knockout mice, reduces proteinuria and delays uraemia. These effects are associated with decreased renal fibrosis and a reduction of inflammatory cell infiltration."],["dc.identifier.doi","10.1093/ndt/gfl810"],["dc.identifier.isi","000245353600016"],["dc.identifier.pmid","17287218"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51687"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0931-0509"],["dc.title","Nephroprotective effect of the HMG-CoA-reductase inhibitor cerivastatin in a mouse model of progressive renal fibrosis in Alport syndrome"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e87"],["dc.bibliographiccitation.issue","10236"],["dc.bibliographiccitation.journal","The Lancet"],["dc.bibliographiccitation.lastpage","e88"],["dc.bibliographiccitation.volume","395"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Moerer, Onnen"],["dc.contributor.author","Weber, Manfred"],["dc.contributor.author","Huber, Tobias B"],["dc.contributor.author","Scheithauer, Simone"],["dc.date.accessioned","2021-04-14T08:26:48Z"],["dc.date.available","2021-04-14T08:26:48Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1016/S0140-6736(20)31041-2"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/82083"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.issn","0140-6736"],["dc.title","COVID-19-associated nephritis: early warning for disease severity and complications?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]