Putative pathophysiologic mechanisms in the development of atherosclerotic vascular and albuminuric diabetic kidney disease. The investigated markers have been associated with development, progression or complications of atherosclerotic vascular disease. The changes in their levels presented in the left box are based on published study data summarized in the reference list of Supplementary Table S8. The results of our study are shown in the right box. ▲ denotes increases and ▼ decreases. For many of the markers, the changes in patients with future microalbuminuria (right box), were concordant with the changes observed in patients with future major cardiovascular events or adverse outcomes after a cardiovascular event (left box). The concordant changes in the markers included in the analysis are in bold. ANGP-1, angiopoietin-1; ANGP-2, angiopoietin-2; CXCL16, C-X-C motif chemokine ligand 16; MCP-1, monocyte chemotactic protein 1; RAGE, receptor for advanced glycation endproducts; S100A8, S100 calcium binding protein A8/myeloid related protein 8; sTNF-RI, soluble tumor necrosis factor receptor I; sTNF-RII, soluble tumor necrosis factor receptor II; sST2, soluble ST2; sThrombo, sThrombomodulin; TGFβ-1, transforming growth factor beta 1; VAP-1, vascular adhesion protein 1; VEGF, vascular endothelial growth factor.