Abstract
Increased extracellular matrix (ECM) is the ultrastructural hallmark of diabetic microangiopathy. Its accumulation within the kidney is directly linked to the clinical manifestations of diabetic nephropathy, namely proteinuria and declining renal function. The pathogenesis of ECM changes in diabetes is not well understood, but is likely to involve interaction between cells, growth factors, structural proteins, and cell receptors for these molecules. Molecular biological techniques may offer the necessary tools for gaining insight into the pathogenetic processes that eventually lead to renal failure in diabetes.
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