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","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.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"]]

[["dc.bibliographiccitation.firstpage","916"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Nephrology Dialysis Transplantation"],["dc.bibliographiccitation.lastpage","924"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Kashtan, Clifford E."],["dc.contributor.author","Rheault, Michelle N."],["dc.contributor.author","Flinter, Frances"],["dc.contributor.author","Savige, Judith"],["dc.contributor.author","Miner, Jeffrey H."],["dc.contributor.author","Torra, Roser"],["dc.contributor.author","Ars, Elisabet"],["dc.contributor.author","Deltas, Constantinos"],["dc.contributor.author","Savva, Isavella"],["dc.contributor.author","Perin, Laura"],["dc.contributor.author","Renieri, Alessandra"],["dc.contributor.author","Ariani, Francesca"],["dc.contributor.author","Mari, Francesca"],["dc.contributor.author","Baigent, Colin"],["dc.contributor.author","Judge, Parminder"],["dc.contributor.author","Knebelman, Bertrand"],["dc.contributor.author","Heidet, Laurence"],["dc.contributor.author","Lagas, Sharon"],["dc.contributor.author","Blatt, Dave"],["dc.contributor.author","Ding, Jie"],["dc.contributor.author","Zhang, Y."],["dc.contributor.author","Gale, Daniel P."],["dc.contributor.author","Prunotto, Marco"],["dc.contributor.author","Xue, Yong"],["dc.contributor.author","Schachter, Asher D."],["dc.contributor.author","Morton, Lori C. G."],["dc.contributor.author","Blem, Jacqui"],["dc.contributor.author","Huang, Michael"],["dc.contributor.author","Liu, Shiguang"],["dc.contributor.author","Vallee, Sebastien"],["dc.contributor.author","Renault, Daniel"],["dc.contributor.author","Schifter, Julia"],["dc.contributor.author","Skelding, Jules"],["dc.contributor.author","Gear, Susie"],["dc.contributor.author","Friede, Tim"],["dc.contributor.author","Turner, A. Neil"],["dc.contributor.author","Lennon, Rachel"],["dc.date.accessioned","2018-11-07T10:22:52Z"],["dc.date.available","2018-11-07T10:22:52Z"],["dc.date.issued","2017"],["dc.description.abstract","Alport syndrome (AS) is a genetic disease characterized by haematuric glomerulopathy variably associated with hearing loss and anterior lenticonus. It is caused by mutations in the COL4A3, COL4A4 or COL4A5 genes encoding the alpha 3 alpha 4 alpha 5(IV) collagen heterotrimer. AS is rare, but it accounts for > 1% of patients receiving renal replacement therapy. Angiotensin-converting enzyme inhibition slows, but does not stop, the progression to renal failure; therefore, there is an urgent requirement to expand and intensify research towards discovering new therapeutic targets and new therapies. The 2015 International Workshop on Alport Syndrome targeted unmet needs in basic science, genetics and diagnosis, clinical research and current clinical care. In three intensive days, more than 100 international experts including physicians, geneticists, researchers from academia and industry, and patient representatives from all over the world participated in panel discussions and breakout groups. This report summarizes the most important priority areas including (i) understanding the crucial role of podocyte protection and regeneration, (ii) targeting mutations by new molecular techniques for new animal models and potential gene therapy, (iii) creating optimal interaction between nephrologists and geneticists for early diagnosis, (iv) establishing standards for mutation screening and databases, (v) improving widespread accessibility to current standards of clinical care, (vi) improving collaboration with the pharmaceutical/biotech industry to investigate new therapies, (vii) research in hearing loss as a huge unmet need in Alport patients and (viii) the need to evaluate the risk and benefit of novel (including 'repurposing') therapies on an international basis."],["dc.description.sponsorship","Wellcome Trust [WT090006, 088785/Z/09/Z]"],["dc.identifier.doi","10.1093/ndt/gfw095"],["dc.identifier.isi","000404539500003"],["dc.identifier.pmid","27190345"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42352"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1460-2385"],["dc.relation.issn","0931-0509"],["dc.title","Advances and unmet needs in genetic, basic and clinical science in Alport syndrome: report from the 2015 International Workshop on Alport Syndrome"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","73"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Therapeutic Drug Monitoring"],["dc.bibliographiccitation.lastpage","78"],["dc.bibliographiccitation.volume","32"],["dc.contributor.author","Brandhorst, Gunnar"],["dc.contributor.author","Brehmer, Franziska"],["dc.contributor.author","Petrova, Darinka T"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","Miosge, Nicolai"],["dc.contributor.author","Armstrong, Victor W"],["dc.contributor.author","Oellerich, Michael"],["dc.date.accessioned","2021-06-01T10:46:58Z"],["dc.date.available","2021-06-01T10:46:58Z"],["dc.date.issued","2010"],["dc.description.abstract","Within the scope of this study, the potential antifibrotic effect of mycophenolate mofetil (MMF) on COL4A3-deficient mice as an animal model for progressive renal fibrosis was investigated regarding kidney function and survival. Thirty-five animals were randomly assigned to one of five groups and treated with doses of 0, 10, 50, 100, or 150 mg/kg MMF per day, respectively. When increasing somnolence was observed, indicating end-stage renal disease, the mice were euthanized and blood was obtained. Serum concentrations of creatinine, urea nitrogen, total protein, mycophenolic acid (MPA), and mycophenolic acid glucuromide (MPAG) were quantified. The kidney histology was examined using hematoxylin and eosin as well as trichrome staining. The mean overall survival was 65.9 (+/- 6.1) days with no significant difference between the treatment groups (P > 0.05, Mantel-Cox test). Serum predose concentrations of MPA and MPAG showed considerable interindividual variability. There was no correlation between Survival time and MPA or MPAG concentrations (P > 0.05, Spearman rank correlation). However, an apparent decrease in serum creatinine and urea nitrogen concentrations was observed at higher doses of MMF, eg, -54% for creatinine in the 150-mg/kg/day group compared with placebo. A highly significant reciprocal correlation between MPA concentrations and serum creatinine was demonstrated (P < 0.01, r = -0.655, Spearman rank correlation). In conclusion, MMF may be a candidate drug for preserving kidney function in progressive renal fibrosis."],["dc.identifier.doi","10.1097/FTD.0b013e3181c91fc4"],["dc.identifier.isi","000274072000011"],["dc.identifier.pmid","20042922"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85439"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Lippincott Williams & Wilkins"],["dc.relation.issn","0163-4356"],["dc.title","Mycophenolic Acid Predose Concentrations and Renal Function in a Mouse Model for Progressive Renal Fibrosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2117"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Pediatric Nephrology"],["dc.bibliographiccitation.lastpage","2123"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Pohl, Michael"],["dc.contributor.author","Danz, Karin"],["dc.contributor.author","Gross, Oliver"],["dc.contributor.author","John, Ulrike"],["dc.contributor.author","Urban, Johannes"],["dc.contributor.author","Patzer, Ludwig"],["dc.contributor.author","Habbig, Sandra"],["dc.contributor.author","Feldkoetter, Markus"],["dc.contributor.author","Witzke, Oliver"],["dc.contributor.author","Walther, Mario"],["dc.contributor.author","Rhode, Heidrun"],["dc.date.accessioned","2018-11-07T09:18:22Z"],["dc.date.available","2018-11-07T09:18:22Z"],["dc.date.issued","2013"],["dc.description.abstract","The hereditary kidney disease Alport syndrome (AS) has become a treatable disease: intervention with angiotensin-converting enzyme (ACE)-inhibitors delays end stage renal failure by years. The efficiency of ACE inhibition depends on the onset of therapy-the earlier the better. Therefore, early diagnosis has become increasingly important. To date, robust diagnosis requires renal biopsy and/or expensive genetic analysis, which is mostly performed late after onset of the profound clinical symptoms of this progressive renal disease. Thus, disease biomarkers enabling low-invasive screening are urgently required. Fourteen potential proteomic candidate markers (proteins) identified in a previous study in sera from patients exhibiting manifest AS were evaluated in the plasma, serum, and urine collected from a cohort of 132 subjects, including patients with AS and other nephropathies and healthy controls. Quantitation was performed by immunoassays. The serum and plasma levels of none of the 14 proteins evaluated were significantly different among the three groups and therefore could not be used to discriminate between the groups. In contrast, the levels of various biomarker combinations in the urine were significantly different between AS patients and healthy controls. Importantly, some combinations had the potential to discriminate between AS and other nephropathies. These findings open a window of opportunity for the sensitive and specific early diagnosis of AS. Our results increase the potential for larger scale evaluation of an increased number of patients."],["dc.identifier.doi","10.1007/s00467-013-2533-5"],["dc.identifier.isi","000325433100007"],["dc.identifier.pmid","23793922"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28394"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0931-041X"],["dc.title","Diagnosis of Alport syndrome-search for proteomic biomarkers in body fluids"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]