Diabetic kidney disease (DKD) is a severe microvascular complication traditionally attributed to general metabolic derangement and genetic susceptibility. However, this classic pathophysiological approach overlooks the role of red blood cells in the development and the progression of the disease. Prolonged exposure to high blood glucose and oxidative stress compromises the cell’s membrane architecture and ionic homeostasis, resulting in altered rheological properties. By synthesizing these molecular-to-rheological pathways, this review establishes a novel pathophysiological framework for understanding DKD, repositioning erythrocytes to a primary catalyst of renal injury and a highly sensitive target for early diagnostic intervention.
Garoufis et al. (Fri,) studied this question.