The vast majority of patients with essential hypertension have structural changes in their kidneys consisting of preglomerular vascular disease ('arteriolosclerosis') and tubulointerstitial injury. Most authorities have assumed that these structural changes occur secondary to hypertensive renal injury. However, Goldblatt proposed that primary renal microvascular disease might be the cause of some forms of hypertension. In this paper we present recent studies from our group that support a role for both preglomerular vascular disease as well as the tubulointerstitial inflammatory response in mediating salt-sensitivity. We propose that subtle acquired renal injury may underlie the etiology of some forms of salt-sensitive hypertension.