107 research outputs found
The podocyte and parietal epithelial cell in proteinuria and glomerulosclerosis.
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51043.pdf (Publisher’s version ) (Open Access)FSGS has become one of the most common glomerular diseases and is characterized by focal and segmental occurrence of lesions. Proteinuria is an important hallmark of glomerular diseases. Based on findings in a mouse model of FSGS we questioned if PECs play a role in human FSGS. Until now epithelial hyperplasia, which can be prominent in FSGS has been attributed to dedifferentiation and proliferation of podocytes. We performed a detailed study of lesions by serial sectioning, marker analysis and three-dimensional reconstruction of glomeruli. Our study demonstrated that the proliferating epithelial cells in FSGS lesions were negative for podocyte and macrophage markers, but stained for PEC markers. Also the staining characteristics of the matrix deposited by these cells was identical to Bowman's capsule. Taken together, these data argue that proliferating epithelial cells in active FSGS lesions are PECs and question the contribution of the socalled 'de-differentiated' podocyte. The concept of the dedifferentiated-proliferating podocyte needs revision. Progressive FSGS will eventually lead to global glomerulosclerosis. Global glomerulosclerosis is often observed in patients with renal disease or patients with nephrosclerosis. Two types of global glomerulosclerosis are described: the obsolescent type and the solidified type. We noticed the presence of abnormal glomeruli in biopsies of children with a recurrent nephrotic syndrome and we have suggested the term involution to describe this process. We have developed a mouse model of glomerular involution. In this model the small glomeruli had the same characteristics as the involuted glomeruli described in children with minimal change disease. Our mouse model will enable us to investigate in more detail the pathogenesis of glomerular involution. We propose a new scheme for the development of FSGS and glomerular involution. We attribute a central role to parietal epithelial cell injury in determining if podocyte injury and proteinuria progress to FSGS or glomerular involution. If confirmed by further studies the PEC might become a new target for therapy.RU Radboud Universiteit Nijmegen, 28 november 2006Promotor : Wetzels, J.F.M. Co-promotores : Assmann, K.J.M., Steenbergen, E.211 p
Glomerulonephritis in the mouse
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mmubn000001_000495700.pdf (Publisher’s version ) (Open Access)Promotor : R. Koene123 p
Albuminuria induced by monoclonal antibodies against aminopeptidase A: a mouse model of membranous glomerulonephritis?
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145567.pdf (Publisher’s version ) (Open Access)173 p
Fabricage van freon-22
No full textDocument(en) uit de collectie Chemische ProcestechnologieDelftChemTechApplied Science
Aminopeptidase A: a key enzyme in the intrarenal degradation of angiotensin II
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Acute renal failure in patients with glomerular diseases: a consequence of tubular cell damage caused by haematuria?
No full textItem does not contain fulltextWe describe three patients with acute renal failure after the onset of gross haematuria. In all patients a presumptive diagnosis of rapidly progressive glomerulonephritis was made and immunosuppressive therapy initiated. A renal biopsy was performed in two patients, which showed evidence of IgA nephropathy. Extracapillary proliferation was seen in a few glomeruli. The most notable abnormality was acute tubular necrosis with intraluminal erythrocytes and cell debris. In the third patient, who was known to have longstanding glomerular haematuria, acute tubular necrosis was considered likely after review of the urinary sediment. Despite the fact that immunosuppressive therapy was stopped, renal function rapidly returned to normal in all these patients. We feel that our patients and additional literature data demonstrate that in patients with glomerular disease a reversible acute renal failure can occur that is caused by acute tubular necrosis mediated by haematuria. Recognition of this entity will prevent unnecessary long-term immunosuppressive therapy
Glomerulonefritis door acute serumziekte
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25918___.PDF (Publisher’s version ) (Open Access
Atheroembolic disease in a female patient
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25333___.PDF (Publisher’s version ) (Open Access
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