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CBMT remains a key marker of diabetic microangiopathy; leaves open the relative roles of metabolic and environmental drivers.
Microangiopathy has been recognized as a critical complication which afflicts the human diabetic population and magnifies the risk for permanent injury and/or mortality. One of the major manifestations of diabetic microvascular disease in man appears to be capillary basement membrane thickening (CBMT) which has been termed the “hallmark of diabetic microangiopathy”. CBMT of diabetic patients seems to be a product of vascular injury imposed by the interaction of metabolic derangement, environmental factors and genetics (1). Although the degree of thickening varies with age, duration of diabetes, severity of metabolic impairment and location in the body, capillary basement membranes from the kidney, skeletal muscle and heart are usually expanded in diabetic man. However, due to the sparsity of systematic studies and inherent problems with human experimentation, the pathogenesis of CBMT remains controversial. In an attempt to achieve a better understanding of the etiology and progression of CBMT, diabetic animal models have recently been the focal point of intensive research (2).
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Diani et al. (1984) studied this question.
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