ABSTRACT
Cora Weigert and Erwin D. Schleicher Department of Medicine, Division of Endocrinology, Metabolism and Pathobiochemistry, University of Tübingen, Germany
The dominant histological feature of diabetic nephropathy is the thickening of the glomerular basement membrane (GBM) and expansion of the mesangial matrix [1-3]. The changes correlate strongly with the clinical onset of proteinuria, hypertension and kidney failure. Although more than 60 years have elapsed since Kimmelstiel and Wilson [4] described in diabetic glomeruli the distinctive periodic acid-schiff (PAS)-reactive nodular deposits, progress in elucidating the pathobiochemistry has been slow. Recent investigations with electron microscopic, immunochemical and biochemical methods have led to an improved understanding of the structure-function relationship of the glomerular filtration unit in normal and pathological conditions [5].
