Hypertension and nephrosclerosis: a reappraisal and a new theory of renal ischemia.

An observation in human autopsy material showing a statistically close relationship between complicated atherosclerosis of the aorta, at or above the renal artery take-off, and nephrosclerosis of usual type (i.e. the "granular kidney" of essential hypertension) led to a study of platelet aggregates as a cause of renal lesions. The renal cortical surface is peculiarly sensitive to ischemic damage. When an embolic source, which sheds repeatedly, was placed in the thoracic aorta of rabbits, they became hypertensive. The hypertension persisted for six months, at which time the kidneys showed nephrosclerosis characterized by surface cortical lesions consisting of shrunken glomeruli and atrophical tubules, subtended by arterioles whose intimas showed fibrous thickening. It is suggested that the renal component of the hypertension so induced is transitory, serving as a trigger mechanism for sustained hypertension.