Summary Diabetic nephropathy is associated with functional changes in the glomerular filtration barrier but the structural counterpart remains unknown. Width of glomerular epithelial cell foot processes and of filtration slits were determined by morphometric methods in 11 non-diabetic kidney donors and in 28 diabetic patients with albumin excretion rates ranging from normal to proteinuria. Foot process width was estimated from the ratio of tuft surface density to length density of slits. At high magnification independently sampled, perpendicularly cut slits were classified. Foot process width on peripheral basement membrane was increased in microalbuminuric compared to normoalbuminuric diabetic patients (p < 0.05) but showed no significant correlation with the level of albumin excretion when patients with increased barrier permeability were considered. Width of filtration slits in normo-and microalbuminuric diabetic patients exceeded that in nondiabetic control subjects (p < 0.05). Filtration slits were narrower in patients with overt proteinuria than in patients with microalbuminuria (p < 0.05) and correlated with glomerular filtration rate in all of the diabetic patients (r = 0.65, p < 0.005). The results show that insulin-dependent diabetic patients with nephropathy present changes of epithelial cells and filtration slits, demonstrable already in the stage of microalbuminuria. The mechanism of albumin leakage is not achieved by these measures. The dimension of filtration slits may play a contributing role in the level of glomerular filtration rate in diabetic patients. [Diabetologia (1995[Diabetologia ( ) 38: 1197[Diabetologia ( -1204
Conventional insulin treatment used during the latter part of this century has been unsuccessful in giving most patients with insulin-dependent diabetes mellitus (IDDM) a long normal life. During the last 10 years, however, our knowledge has improved dramatically. We concluded in 1987: "The accumulating evidence for the relationship between blood glucose control and the development and progression of diabetic microangiopathy, and the demonstration that early microangiopathy responds favourably to nearnormoglycaemia, calls for action to improve the care for diabetics. The question regarding blood glucose control is not in essence 'why', but 'how'?" [1]. This statement was based on the results from several Scandinavian trials which started 10-12 years ago [1][2][3][4][5][6][7]. Since then further evidence has strengthened the basis of the above conclusion, particularly results from the Stockholm study [8] and the Diabetes Control and Complications Trial (DCCT) [9]. In this review we will summarize the evidence of the benefits of near-normal blood glucose control on the development and progression of late diabetic complications, we will also focus on important areas of future research and how they apply in the clinical environment.
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