THE CAPACITY OF THE RENAL VASCULAR BED IN HYPERTENSION

By using kerosene and avoiding postmortem rigor one can obtain perfusion rates in kidneys nearly five times faster than those reported by observers who perfused kidneys immediately post mortem with saline solution, only half as viscous as kerosene. The results obtained by kerosene perfusion indicate possible renal blood flow 50 to 100 per cent greater than that measured by Smith and his coworkers (7) in living men by diodrast clearance under normal conditions, and about as high as those observed in febrile subjects. Like the diodrast method, kerosene perfusion shows a striking decrease in renal vascular bed between early matuity (age 18 to 35) and senescence (45 to 60). This decrease is about 25 per cent. Most kidneys from patients with hypertension without uremia have vascular beds in the normal range, but a few show great decreases in capacity for blood flow. This evidence is interpreted as another indication that renal arteriosclerosis is often a result, rarely a cause of hypertension. Significant occlusion of large renal arteries is rare. Uremia due to amyloid may occur with no significant decrease in renal vascular bed, but the uremia of renal sclerosis, glomerulo- or pyelonephritis is associated with reduction of vascular bed to very low levels.