Research team

Scientific Chair Nephrology. 20/12/2011 - 19/12/2012

Abstract

This project represents a formal research agreement between UA and on the other hand a private institution. UA provides the private institution research results mentioned in the title of the project under the conditions as stipulated in this contract.

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  • Research Project

Chronic kidney disease and cardiovascular risk: endothelial dysfunction at the interface? 01/10/2010 - 30/09/2011

Abstract

In the present project, we focus on endothelial dysfunction in CKD patients. Endothelial dysfunction precedes overt atherosclerotic changes of the vascular wall by many years. Interestingly, in the absence of structural changes, endothelial dysfunction is still reversible, which offers therapeutic perspectives to tackle the progression towards atherosclerosis in an early stage. Several mechanisms for the development of endothelial dysfunction will be investigated, with special emphasize on mechanisms that repair the vascular wall. Moreover, we will study the possible beneficial effect of physical exercise on endothelial function in CKD patients.

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  • Research Project

Pharmaco-epidemiological research on the relationship between drug interactions and polypharmacy based on data from the database Farmanet. 20/07/2009 - 31/07/2010

Abstract

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  • Research Project

BOF - University Research Fund: 1 year doctoral fellowship in view of a second IWT application (Kristien Ledeganck). 01/01/2008 - 31/12/2008

Abstract

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  • Research Project

Expression of genes involved in inflammation and fibrosis in protocolbiopsies of renal allografts. A study of the pathophysiologic mechanisms of chronic allograft nephropathy. 01/01/2004 - 31/12/2007

Abstract

In a prospective, randomized study in de novo kidney transplant recipients, we will compare the influence of a combination therapy with prednisolone, mycophenolate mofetil, and cyclosporine with a combination therapy with prednisolone, mycophenolate mofetil, and rapamycine, on the expression of genes, associated with inflammation and fibrosis in protocol biopsies of the graft, six months after transplantation. Glomeruli, tubulo-epithelial cells and interstitial cells will be isolated by means of the laser capture microscope. After RNA-extraction, we will perform semiquantitative RT amplification with Taqman PCR for the genes of interest: i.e. IL 10, IL 12, TNF alpha, B7-1, B7-RP1, CD40, CXCR3, CCR5, perforine, granzyme, angiotensine II, TGF-ß1, PAI-1, TIMP-1, and endotheline.

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  • Research Project

The plasminogen activator/plasmin system in the kidney and cyclosporine nephrotoxicity. 01/01/1997 - 31/12/1998

Abstract

The different elements of the plasminogen activator/plasmin system are determined in rat kidney using biochemical and immunohistochemical techniques. Furthermore, the influence of cyclosporine in the system is studied.

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    • Research Project

    A prospective clinical and experimental study of the effects of blood lipid disturbances and cytomegalovirus infection on the development of chronic cyclosporine toxicity. 01/01/1996 - 31/12/1997

    Abstract

    Blood lipid disturbances and cytomegalovirus infections will be prospectively monitored in renal transplant recipients. The renal lesions induced by cyclosporine will be evaluated in a renal biopsy and related to the metabolic and clinical events.

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      • Research Project

      The plasminogen activator/plasmin system in the kidney and cyclosporine nephrotoxicity. 01/01/1995 - 31/12/1996

      Abstract

      The plasmin system is a proteolytic system involved in the development of fibrosis, which is an important feature of cyclosporine nephrotoxicity. In a rat model of cyclosporine nephrotoxicity, the activity of the plasmin system is downregulated by the increased expression of the plasminogen activatior inhibitor.

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        • Research Project

        The role of growth factors in the initiation of chronic cyclosporine nephrotoxicity 01/01/1992 - 31/12/1992

        Abstract

        Chronic cyclosporine nephrotoxicity is characterized by renal interstitial cellular infiltration and fibrosis... In a rat model the pathogenesis of this disorder is investigated by means of immunochemical characterisation of the infiltrating cells and by Northern analysis of the mRNA expression of growth factors and cytokines.

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          • Research Project

          The role of growth factors in the development of the renal fibrosis of chronic cyclosporine nephrotoxicity. 01/10/1991 - 30/09/1993

          Abstract

          Cyclosporine is one of the basic therapies after kidney-, heart- and liver transplantation and is also used for the treatment of systemic diseases, but is toxic for the kidney. We will try to find an answer to the following question : which growth factors play a role in the initiation and development of interstitial fibrosis in the kidney during chronic cyclosporine administration. An experimental animal model will be used.

          Researcher(s)

          Research team(s)

            Project type(s)

            • Research Project