Abstract
Acute ischemic or toxic injury to the kidney induces alterations in the expression of many genes. Some of these molecular responses have been termed 'maladaptive' because they exacerbate the tubular damage induced by the initiating insult. Some maladaptive responses include alterations in the activity of nitric oxide synthases and expression of cytokines and adhesion molecules that mediate an inflammatory response. This review focuses on the role of nitric oxide and inflammation in influencing the course of acute renal failure due to ischemic and toxic tubular injury.