I have a nine year old daughter with type 1 diabetes. My friend is involved in researching kidney disease. Although diabetes is not his major interest, one of his preliminary findings is that in the in vitro situation, exposing kidney cells to high glucose nutrient does cause increased laying down of connective tissue, but (and this is what I find both disturbing, and interesting) the speed at which the connective tissue forms is more related to the speed of rate of change in glucose concentration in the nutrient, rather than the length of time the cells are exposed to high concentrations of glucose rich nutrient. Admittedly, this is a preliminary finding, and an in vitro situation, but are you aware if this relates also to the “live kidney?” In other words, Are the fluctuations in blood sugar causing more damage the kidneys of people with diabetes rather than sustained high blood glucose levels?

It is difficult to assess whether your friend’s studies on kidney cell cultures have any relevance to diabetes without having a lot more in the way of experimental detail. Suffice it to say that the development of long term vascular complications seems to be primarily related not so much to connective tissue proliferation as to a sequence of complex biochemical reactions that involve the inappropriate attachment of glucose molecules to a variety of proteins, the formation of complexes called advanced glycation end products which attach to receptors on the endothelial cell surface and in turn to blood lipids and the formation of reactive oxygen species e.g. nitric oxide. The progression of all of these factors is related both to the level of blood sugar and to the duration of that level above normal. It is really not possible in the ordinary clinical situation to disentangle the short from the long term effect. However, the measurement of A1c or fructosamine seems to be a valid assessment of the combined risk.

DOB