In normoalbuminuric patients with DM1, poor glycemic control is an independent predictor of progression to development of proteinuria (albuminuria) and/or ESRD (14).Two landmark trials conducted with patients with early-stage DM1 or DM2 showed that intensive blood glucose control early in the course of disease exhibits a long-lasting favorable effect on the risk of DKD development (15,16).Segmental mesangiolysis is observed with progression of diabetes and thought to be associated with development of Kimmelstiel–Wilson nodules and microaneurysms, which often present together (29,30) (Figure 3).The exudative lesions result from subendothelial deposits of plasma proteins, which form periodic acid–Schiff-positive and electron-dense deposits and accumulate in small arterial branches, arterioles, and glomerular capillaries as well as microaneurysms.
Similarly, in patients with newly diagnosed DM2, 10 years of an intensive glycemic control intervention targeting an Hb A1C of 7% produced a 24% reduction in development of microvascular complications, including DKD, compared with conventional therapy (20,21).
Introduction It took more than three millennia from the first description of diabetes in 1552 BC to the recognition of an association between diabetes and kidney disease, but it took only several decades for diabetic kidney disease (DKD) to become the leading cause of ESRD in the United States (1,2).
This microvascular complication develops in approximately 30% of patients with type 1 diabetes mellitus (DM1) and approximately 40% of patients with type 2 diabetes mellitus (DM2) (2,3).
After 12 years, intensive glycemic control resulted in a 33% reduction in the risk of development of microproteinuria or “clinical grade” proteinuria and a significant reduction in the proportion of patients with a doubling of the blood creatinine level (0.9% versus 3.5%) relative to the conventional therapy group (20,21).
Development of DKD is associated with many alterations in the structure of multiple kidney compartments.