Renal changes in shock treated with levarterenol (levophed).

Abstract

I t is generally recognized that a variety of conditions or situations such as crushing injuries, transfusions of incompatible blood, black water fever, burns, administration of sulfa drugs, uteroplacental damage, and certain others may result in clinically similar episodes of anuria. There is also fairly uniform agreement among many observers that shock, with its associated renal ischemia, constitutes the etiologic bond that is common to such conditions or situations. On the other hand, the exact relation of the ischemia to the anuria is not quite so evident. Bywaters and Dible and Luck6 postulated that the chief damage occurred in the distal convoluted tubules and that tubular casts were an important part of the pathologic picture. Oliver et al. believed that all segments of the tubular system were damaged, but that the most significant was that in the proximal convoluted tubules. Sheehan and Moore, however, thought that vasospasm resulted in a whole spectrum of lesions, ranging from albuminuria (with formation of casts in the collecting tubules) to gross cortical necrosis of the kidneys. Why do vasospasm and ischemia lead to so many different lesions? May the differences be the result of variable durations or severity of spasm? We recently observed some interesting changes in the kidneys of people who died of various clinical conditions with terminal shock. In each instance, liberal amounts of levarterenol (Levophed), a pressor amine, were administered in attempts to counteract the condition.