The mechanism of development of microangiopathy is incompletely understood, but relates to a number of ultrastructural, biochemical and haemostatic processes. These include capillary basement membrane thickening, non-enzymatic glycosylation, possibly increased free radical activity, increased flux through the polyol pathway and haemostatic abnormalities. The central feature appears to be hyperglycaemia, which is causally related to the above processes and culminates in tissue ischaemia. This article will briefly describe these processes and will discuss possible pathogenic interactions which may lead to the development of the pathological lesion.
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