C lassically, albuminuria has been attributed to hypertension: in a chicken or egg scenario, albuminuria appears to be the product that 'hatches' from hypertension (Figure 1).Hypertension promotes shearing stress and oxidative stress in endothelial cells.These injured endothelial cells lose the glycocalyx that covers their fenestrae (Figure 2); therefore, they cannot prevent albumin from moving through the basal membrane. 1Accordingly, albuminuria is attributed to endothelial cell injury, whereas macroproteinuria is attributed to either injured podocytes or their foot processes.The juxtamedullary nephrons often face conditions characterized by intense hypertension due to vessel strain.Albuminuria has served as an indicator of pressure-associated injury to nephrons. 2everal disease conditions, as well as hypertension, also cause proteinuria in a similar manner. 3,4Diabetes mellitus is a well-known inducer of albuminuria. 5The endothelial surface layer is diminished by the increased expression of heparanase, which is induced by oxidative stress 6 in the setting of diabetes mellitus; this phenomenon may explain the albuminuria observed in diabetic nephropathy.The negatively charged sugar chains attached to proteoglycans mediate the permselective properties of glomerular endothelial cells. 1 High concentrations of glucose increase the expression of both dysfunctional endothelial nitric oxide synthase and reactive oxygen species, whereas high doses of free fatty acids do not increase oxidative stress.