Patients with hypertension and diabetes are frequently salt-sensitive. Consequently, increasing dietary salt intake results in a rise in systemic arterial pressure and an increase in proteinuria, as well as a progressive risk for developing renal injury. A difference in the renal hemodynamic response to salt appears, at least in part, to determine how the salt intake affects blood pressure. Greater dietary salt intake in salt-sensitive patients results in a blunted rise in renal plasma flow and an increase in body weight. Greater dietary salt consumption also results in a rise in glomerular filtration fraction and increasing proteinuria. Pharmacologic antagonism of the renin-angiotensin system helps restore the blunted renal plasma flow response to high salt intake and correlates with the fall in mean arterial pressure. Consequently, the pressor response to increasing dietary salt consumption in patients with diabetes and hypertension may be related to insufficient renal vasodilation, perhaps due to inadequate suppression of the renin-angiotensin system. Moreover, inadequate suppression of the renin-angiotensin system within the kidney results in an increase in efferent glomerular arteriolar tone and a rise in glomerular capillary pressure, increased proteinuria and a greater risk for renal injury. Many of the coexisting cardiovascular risk factors associated with salt sensitivity may be explainable in part by the overactivity of the renin-angiotensin system.