Acute tubular necrosis is a syndrome of physiologic and pathologic dissociation.

Acute tubular necrosis (ATN) is a syndrome of intrinsic renal failure secondary to ischemic or toxic insults. The histopathologic findings of ATN are inconstant. When present, they are limited to the tubulo-interstitium and often subtle despite profound dysfunction. Experimental models of ATN in healthy animals commonly use single insults that result in extensive injury, circumstances that do not parallel the human situation. Recently, there has been a shift to more clinically relevant models using an acute insult superimposed on predisposing factors. This review discusses the complex hemodynamic interrelationships of hypoxia, tubular injury, and altered glomerular filtration, suggesting new ways to understand the pathophysiology of ATN.