Oliver Gross's Publications List

Living donor kidney transplantation from relatives with mild urinary abnormalities in Alport syndrome: long-term risk, benefit and outcome.

2010-01-07T16:14:24Z

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 protei...

Oliver Gross, Manfred Weber, Jochen W U Fries, Gerhard-Anton Müller (2009) Nephrol Dial Transplant 24: 5 1626-1630

Mycophenolic Acid Predose Concentrations and Renal Function in a Mouse Model for Progressive Renal Fibrosis.

2010-01-07T16:14:24Z

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 somnolen...

Gunnar Brandhorst, Franziska Brehmer, Darinka T Petrova, Oliver Gross, Nicolai Miosge, Victor W Armstrong, Michael Oellerich (2009) Ther Drug Monit :

Stem cell therapy for Alport syndrome: the hope beyond the hype.

2010-01-07T16:14:24Z

Oliver Gross, Dorin-Bogdan Borza, Hans-Joachim Anders, Christoph Licht, Manfred Weber, Stephan Segerer, Roser Torra, Marie-Claire Gubler, Laurence Heidet, Scott Harvey, Dominic Cosgrove, George Lees, Clifford Kashtan, Martin Gregory, Judy Savige, Jie Ding, Paul Thorner, Dale R Abrahamson, Corinne Antignac, Karl Tryggvason, Billy Hudson, Jeffrey H Miner (2009) Nephrol Dial Transplant 24: 3 731-734

Ccl2/Mcp-1 blockade reduces glomerular and interstitial macrophages but does not ameliorate renal pathology in collagen4A3-deficient mice with autosomal recessive Alport nephropathy.

2010-01-07T16:14:24Z

Lack of the alpha3 or alpha4 chain of type IV collagen (COL4) causes autosomal recessive Alport nephropathy in humans and mice that is characterized by progressive glomerulosclerosis and tubulointerstitial disease. Renal pathology is associated with chemokine-mediated macrophage infiltrates but their contribution to the progression of Alport nephropathy is unclear. We found Ccl2 to be expressed in...

Sebastian Clauss, Oliver Gross, Onkar Kulkarni, Alejandro Avila-Ferrufino, Ewa Radomska, Stephan Segerer, Dirk Eulberg, Sven Klussmann, Hans-Joachim Anders (2009) J Pathol 218: 1 40-47

Interstitial inflammation in Alport syndrome.

2010-01-07T16:14:24Z

The Alport syndrome is a hereditary glomerular disease linked to structural abnormalities of collagen IV. In a mouse model of Alport syndrome, the interstitial lymphocyte influx was important for disease progression. CXCR3 is a chemokine receptor involved in lymphocyte recruitment to the kidney. We hypothesized that CXCR3-positive T cells might be involved in human Alport syndrome. Immunohistochem...

Jan Jedlicka, Afschin Soleiman, Dan Draganovici, Jana Mandelbaum, Urs Ziegler, Heinz Regele, Rudolf P Wüthrich, Oliver Gross, Hans-Joachim Anders, Stephan Segerer (2009) Hum Pathol :

Treatment of Alport syndrome: beyond animal models.

2010-01-07T16:14:24Z

Alport syndrome (AS) is a hereditary glomerulopathy due to abnormal composition of the glomerular basement membrane, leading to end-stage renal disease (ESRD). Studies of animal models of AS have suggested a variety of potentially effective therapies, but none of these has been definitely shown to prevent or delay ESRD in human AS. Studies in Alport mice suggest that angiotensin inhibition not onl...

Oliver Gross, Clifford E Kashtan (2009) Kidney Int 76: 6 599-603

Inner ear defects and hearing loss in mice lacking the collagen receptor DDR1.

2010-01-07T16:14:24Z

Discoidin domain receptor 1 (DDR1) is a tyrosine kinase receptor that is activated by native collagen. The physiological functions of DDR1 include matrix homeostasis and cell growth, adhesion, branching, and migration, but the specific role of DDR1 in the development and function of the inner ear has not been analyzed. Here, we show that deletion of the DDR1 gene in mouse is associated with a seve...

Angela M Meyer zum Gottesberge, Oliver Gross, Ursula Becker-Lendzian, Thomas Massing, Wolfgang F Vogel (2008) Lab Invest 88: 1 27-37

Understanding renal disorders as systemic diseases: the fascinating world of basement membranes beyond the glomerulus.

2010-01-07T16:14:24Z

Oliver Gross (2008) Nephrol Dial Transplant 23: 6 1823-1825

Nephroprotective effect of the HMG-CoA-reductase inhibitor cerivastatin in a mouse model of progressive renal fibrosis in Alport syndrome.

2010-01-07T16:14:24Z

BACKGROUND: Alport syndrome is caused by mutations in genes encoding for the alpha3, alpha4 or alpha5 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-Co...

Marie-Louise Koepke, Manfred Weber, Eckhard Schulze-Lohoff, Bogdan Beirowski, Stephan Segerer, Oliver Gross (2007) Nephrol Dial Transplant 22: 4 1062-1069

Multipotent mesenchymal stem cells reduce interstitial fibrosis but do not delay progression of chronic kidney disease in collagen4A3-deficient mice.

2010-01-07T16:14:24Z

Multipotent mesenchymal stem or stromal cells (MSC) have shown to improve outcome of acute renal injury models, but whether MSC can delay renal failure in chronic kidney disease is not known. We injected primary MSC or saline into mice that lack the alpha3-chain of type IV collagen (COL4A3), a model of chronic kidney disease with close similarities to human Alport disease. Weekly injections of MSC...

V Ninichuk, O Gross, S Segerer, R Hoffmann, E Radomska, A Buchstaller, R Huss, N Akis, D Schlöndorff, H-J Anders (2006) Kidney Int 70: 1 121-129

Chronic renal failure and shortened lifespan in COL4A3+/- mice: an animal model for thin basement membrane nephropathy.

2010-01-07T16:14:24Z

A heterozygous mutation in autosomal Alport genes COL4A3 and COL4A4 can be found in 20 to 50% of individuals with familial benign hematuria and diffuse glomerular basement membrane thinning (thin basement membrane nephropathy [TBMN]). Approximately 1% of humans are heterozygous carriers of mutations in the autosomal Alport genes and at risk for developing renal failure as a result of TBMN. The inc...

Bogdan Beirowski, Manfred Weber, Oliver Gross (2006) J Am Soc Nephrol 17: 7 1986-1994

Bone marrow transplantation rescues Alport mice.

2010-01-07T16:14:24Z

Jürgen Floege, Uta Kunter, Manfred Weber, Oliver Gross (2006) Nephrol Dial Transplant 21: 10 2721-2723

Nephroprotection by antifibrotic and anti-inflammatory effects of the vasopeptidase inhibitor AVE7688.

2010-01-07T16:14:24Z

BACKGROUND: Chronic renal disease substantially increases the risk of cardiovascular events and death. Vasopeptidase inhibitors are known to show a strong antihypertensive effect. In the present study, we investigated the nephroprotective potential of the vasopeptidase inhibitor AVE7688 beyond its antihypertensive effects in a mouse model of progressive renal fibrosis. METHODS: COL4A3 -/- mice rec...

Oliver Gross, Marie-Louise Koepke, Bogdan Beirowski, Eckhard Schulze-Lohoff, Stephan Segerer, Manfred Weber (2005) Kidney Int 68: 2 456-463

Delayed chemokine receptor 1 blockade prolongs survival in collagen 4A3-deficient mice with Alport disease.

2010-01-07T16:14:24Z

Human Alport disease is caused by a lack of the alpha3-, 4-, or 5-chain of type IV collagen (COL4A). Affected humans and COL4A3-deficient mice develop glomerulosclerosis and progressive renal fibrosis in the presence of interstitial macrophages, but their contribution to disease progression is under debate. This question was addressed by treating COL4A3-deficient mice with BX471, an antagonist of ...

Volha Ninichuk, Oliver Gross, Christoph Reichel, Andrej Khandoga, Rahul D Pawar, Raluca Ciubar, Stephan Segerer, Emilia Belemezova, Ewa Radomska, Bruno Luckow, Guillermo Perez de Lema, Philip M Murphy, Ji-Liang Gao, Anna Henger, Matthias Kretzler, Richard Horuk, Manfred Weber, Fritz Krombach, Detlef Schlöndorff, Hans-Joachim Anders (2005) J Am Soc Nephrol 16: 4 977-985

Novel COL4A5, COL4A4, and COL4A3 mutations in Alport syndrome.

2010-01-07T16:14:24Z

This study summarizes 47 novel mutations identified during routine molecular diagnostics for Alport syndrome. We detected 34 in COL4A5, the gene responsible for X-linked Alport syndrome, and 13 in COL4A3 and COL4A4, the genes responsible for autosomal recessive Alport syndrome. A high detection rate of 90% was achieved among patients with typical clinical symptoms and a characteristic family histo...

Mato Nagel, Sylvia Nagorka, Oliver Gross (2005) Hum Mutat 26: 1

From the molecular genetics of Alport's syndrome to principles of organo-protection in chronic renal diseases

2010-01-07T16:14:24Z

BACKGROUND: Scarring is known to be the endpoint of most chronic kidney diseases. Therefore, prevention of renal fibrosis is a very important topic. The hereditary type IV collagen disease Alport's syndrome is a rare, but challenging cause of chronic renal fibrosis. PATHOGENESIS OF GLOMERULAR AND INTERSTITIAL RENAL FIBROSIS IN HUMANS: Increasing knowledge about the pathogenesis of Alport's syndrom...

Oliver Gross, Manfred Weber (2005) Med Klin (Munich) 100: 12 826-831

DDR1-deficient mice show localized subepithelial GBM thickening with focal loss of slit diaphragms and proteinuria.

2010-01-07T16:14:24Z

BACKGROUND: Type IV collagen in basement membranes is a ligand for the receptor tyrosine kinase discoidin domain receptor 1 (DDR1). DDR1 is expressed in renal cells and regulates cell adhesion and proliferation ex vivo. The interaction between type IV collagen and cell surface receptors is believed important for normal renal function as well as significant in chronic renal diseases and we therefor...

Oliver Gross, Bogdan Beirowski, Scott J Harvey, Catherine McFadden, Dilys Chen, Stephanie Tam, Paul S Thorner, Neil Smyth, Klaus Addicks, Wilhelm Bloch, Yoshifumi Ninomiya, Yoshikazu Sado, Manfred Weber, Wolfgang F Vogel (2004) Kidney Int 66: 1 102-111

Antifibrotic, nephroprotective potential of ACE inhibitor vs AT1 antagonist in a murine model of renal fibrosis.

2010-01-07T16:14:24Z

BACKGROUND: Several studies have shown antifibrotic effects of angiotensin converting enzyme (ACE) inhibitors as well as of angiotensin receptor 1 (AT1) antagonists, however, prospective trials with clinical end points comparing these effects do not exist. COL4A3-/- mice develop a non-hypertensive progressive renal fibrosis. We used this animal model to compare the potential of ACE inhibitor vs AT...

Oliver Gross, Eckhard Schulze-Lohoff, Marie-Louise Koepke, Bogdan Beirowski, Klaus Addicks, Wilhelm Bloch, Neil Smyth, Manfred Weber (2004) Nephrol Dial Transplant 19: 7 1716-1723

Preemptive ramipril therapy delays renal failure and reduces renal fibrosis in COL4A3-knockout mice with Alport syndrome.

2010-01-07T16:14:24Z

BACKGROUND: Alport syndrome (AS) is a common hereditary cause of end-stage renal failure in adolescence due to defects in type IV collagen genes. Molecular genetics allows early diagnosis, however, no preventive strategy can be offered. Using the COL4A3 -/- mouse, an animal model for human AS, we evaluated therapy with ramipril in mice. METHODS: One hundred and twenty-two Alport-mice were treated ...

Oliver Gross, Bogdan Beirowski, Marie-Louise Koepke, Jeannine Kuck, Michael Reiner, Klaus Addicks, Neil Smyth, Eckhard Schulze-Lohoff, Manfred Weber (2003) Kidney Int 63: 2 438-446

Novel COL4A4 splice defect and in-frame deletion in a large consanguine family as a genetic link between benign familial haematuria and autosomal Alport syndrome.

2010-01-07T16:14:24Z

BACKGROUND: Alport syndrome (AS) is a common hereditary cause for end-stage renal failure due to a defect in type IV collagen genes. The molecular pathogenesis of benign familial haematuria (BFH) is not fully understood. Evidence from linkage analyses and mutation studies point to a role of the COL4A3/COL4A4 genes. The present study describes molecular changes of the COL4A4 gene that cause both di...

Oliver Gross, Kai-Olaf Netzer, Romy Lambrecht, Stefan Seibold, Manfred Weber (2003) Nephrol Dial Transplant 18: 6 1122-1127

X-linked Alport syndrome: natural history and genotype-phenotype correlations in girls and women belonging to 195 families: a "European Community Alport Syndrome Concerted Action" study.

2010-01-07T16:14:24Z

Alport syndrome (AS) is a type IV collagen hereditary disease characterized by progressive hematuric nephritis, hearing loss, and ocular changes. Mutations in the COL4A5 collagen gene are responsible for the more common X-linked dominant form of the disease characterized by much less severe disease in girls and women. A "European Community Alport Syndrome Concerted Action" (ECASCA) group was estab...

Jean Philippe Jais, Bertrand Knebelmann, Iannis Giatras, Mario De Marchi, Gianfranco Rizzoni, Alessandra Renieri, Manfred Weber, Oliver Gross, Kai-Olaf Netzer, Frances Flinter, Yves Pirson, Karin Dahan, Jörgen Wieslander, Ulf Persson, Karl Tryggvason, Paula Martin, Jens Michael Hertz, Cornelis Schröder, Marek Sanak, Maria Fernanda Carvalho, Juan Saus, Corinne Antignac, Hubert Smeets, Marie Claire Gubler (2003) J Am Soc Nephrol 14: 10 2603-2610

Meta-analysis of genotype-phenotype correlation in X-linked Alport syndrome: impact on clinical counselling.

2010-01-07T16:14:24Z

BACKGROUND: Alport syndrome (AS) is a hereditary nephropathy characterized by progressive renal failure, hearing loss and ocular lesions. Numerous mutations of the COL4A5 gene encoding the alpha 5-chain of type IV collagen have been described, establishing the molecular cause of AS. The goal of the present study was to identify the genotype-phenotype correlations that are helpful in clinical couns...

Oliver Gross, Kai-Olaf Netzer, Romy Lambrecht, Stefan Seibold, Manfred Weber (2002) Nephrol Dial Transplant 17: 7 1218-1227

Regulation of mesangial cell function by vasodilatory signaling molecules.

2010-01-07T16:14:24Z

Proliferation of mesangial cells and expansion of mesangial matrix is a hallmark of glomerular disease leading to end-stage renal failure and requiring renal replacement therapy. Independently from the type of injury, e.g. in glomerulonephritis or diabetic nephropathy, the response to injury is remarkably uniform. Chronic glomerular disease is frequently associated with increases in systemic blood...

L Buschhausen, S Seibold, O Gross, T Matthaeus, M Weber, E Schulze-Lohoff (2001) Cardiovasc Res 51: 3 463-469

Membranous nephropathy from exposure to mercury in the fluorescent-tube-recycling industry.

2010-01-07T16:14:24Z

S Aymaz, O Gross, B Krakamp, M Ortmann, H P Dienes, M Weber (2001) Nephrol Dial Transplant 16: 11 2253-2255

X-linked Alport syndrome: natural history in 195 families and genotype- phenotype correlations in males.

2010-01-07T16:14:24Z

Alport syndrome (AS) is a type IV collagen hereditary disease characterized by the association of progressive hematuric nephritis, hearing loss, and, frequently, ocular changes. Mutations in the COL4A5 collagen gene are responsible for the more common X-linked dominant form of the disease. Considerable allelic heterogeneity has been observed. A "European Community Alport Syndrome Concerted Action"...

J P Jais, B Knebelmann, I Giatras, M De Marchi, G Rizzoni, A Renieri, M Weber, O Gross, K O Netzer, F Flinter, Y Pirson, C Verellen, J Wieslander, U Persson, K Tryggvason, P Martin, J M Hertz, C Schröder, M Sanak, S Krejcova, M F Carvalho, J Saus, C Antignac, H Smeets, M C Gubler (2000) J Am Soc Nephrol 11: 4 649-657

Sporadic case of X-chromosomal Alport syndrome in a consanguineous family.

2010-01-07T16:14:24Z

Alport syndrome (AS) is a genetic disorder of basement membranes caused by mutations in type IV collagen genes that is characterized by chronic hematuria and progressive nephropathy leading to renal failure. The main extrarenal features include sensorineural hearing loss and ocular lesions. The mode of inheritance is X-linked dominant in about 80%-85% of the affected families, whereas autosomal tr...

B Ermisch, O Gross, K O Netzer, M Weber, M Brandis, L B Zimmerhackl (2000) Pediatr Nephrol 14: 8-9 758-761

Management of lupus nephritis.

2010-01-07T16:14:24Z

Summary : Renal disease is common in systemic lupus erythematosus (SLE) and significantly influences patient prognosis. Immunosuppressive therapy has markedly improved outcome, however, it increases the risk of infection and cancer induction. Although several therapeutic regimens have proved to be effective in controlling lupus nephritis (LN), optimal therapy is still a matter of discussion. The f...

F Merkel, O Gross, M Weber (2000) Saudi J Kidney Dis Transpl 11: 3 381-395

Therapeutic options for critically ill patients suffering from progressive lupus nephritis or Goodpasture's syndrome.

2010-01-07T16:14:24Z

Systemic lupus erythematosus is a chronic disease with many clinical features, while Goodpasture's syndrome usually becomes manifest with progressive glomerulonephritis and pulmonary hemorrhage. Rapidly declining renal function and even pulmonary hemorrhage may be the common feature. Early and precise diagnosis is most important as it may provide general prognostic information and serve as a guide...

F Merkel, K O Netzer, O Gross, M Marx, M Weber (1998) Kidney Int Suppl 64: S31-S38

Alport syndrome: clinical and genetic correlation in a type-IV collagen disease.

2010-01-07T16:14:24Z

K O Netzer, O Gross, C Jung, R Kirsten, S Seibold, A Leinonen, M Weber (1997) Contrib Nephrol 122: 116-123

Exploring the role of oxygen in Fanconi's anemia.

2010-01-07T16:14:24Z

W Liebetrau, T M Rünge, A Baumer, C Henning, O Gross, D Schindler, M Poot, H Hoehn (1997) Recent Results Cancer Res 143: 353-367

Use of psoralen-coupled nucleotide primers for screening of COL4A5 mutations in Alport syndrome.

2010-01-07T16:12:28Z

K O Netzer, S Seibold, O Gross, R Lambrecht, M Weber (1996) Kidney Int 50: 4 1363-1367

Cell cycle defect in connection with oxygen and iron sensitivity in Fanconi anemia lymphoblastoid cells.

2010-01-07T16:12:28Z

Fanconi anemia (FA) is an autosomal recessive disorder involving progressive pancytopenia, skeletal malformations, and a predisposition to leukemia. The in vitro growth of FA fibroblasts is impaired, due to a defective G2 phase traverse of the cell cycle. Analyzing the cell cycle of lymphoid cell lines (LCLs) obtained from peripheral blood of FA patients by transformation with Epstein-Barr virus, ...

M Poot, O Gross, B Epe, M Pflaum, H Hoehn (1996) Exp Cell Res 222: 2 262-268