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Molecular biology of diabetic glomerulosclerosis Del Prete D; Anglani F; Ceol M; D'Angelo A; Forino M; Vianello D; Baggio B; Gambaro GNephrol Dial Transplant 1998[]; 13 Suppl 8 (ä): 20-5Diabetic nephropathy is one of the leading causes of renal failure in Western countries, where diabetic patients account for nearly half of all patients on haemodialysis. Progressive expansion of the mesangial matrix, and thickening of the glomerular and tubular basement membranes without signs of major cell proliferation are hallmarks of human and experimental diabetic nephropathy. These lesions eventually lead to glomerular fibrosis, a central pathological feature in many human acute and chronic kidney diseases, which progressively destroys the renal filtration unit, and may finally cause renal failure. Indeed, structure function relationship studies have shown that mesangial matrix expansion is strongly related to the clinical manifestation of diabetic nephropathy.|*Molecular Biology[MESH]|Diabetic Nephropathies/*genetics/physiopathology[MESH]|Endothelial Growth Factors/physiology[MESH]|Extracellular Matrix/metabolism[MESH]|Glomerular Mesangium/metabolism[MESH]|Glomerulosclerosis, Focal Segmental/*genetics/physiopathology[MESH]|Growth Substances/physiology[MESH]|Humans[MESH]|Lymphokines/physiology[MESH]|Renin-Angiotensin System/physiology[MESH]|Vascular Endothelial Growth Factor A[MESH]|Vascular Endothelial Growth Factors[MESH] |
