Glomerular capillary hemodynamics influence glomerular permselectivity to macromolecules, and alterations in these factors can evoke proteinuria. Changes in hemodynamic patterns can alter protein flux by changing its diffusion- or concentration-driven movement in the presence of a constant membrane barrier. Alternatively, hemodynamic forces may disrupt, transiently or irreversibly, the permeability characteristics of the capillary barrier. Maneuvers that lower glomerular capillary pressure appear capable of reversing, at least in part, these latter permeability defects. Angiotensin II, provoked by higher levels of dietary protein intake, may be a particularly important mediator of proteinuria, both through its effects on diffusion-mediated protein leakage and its tendency to provoke permeability defects due to the heightening of glomerular capillary hydraulic pressures.