CELLULAR MECHANISMS OF ACUTE ISCHEMIC-INJURY IN THE KIDNEY

Hypoxic injury to tubular cells represents an early event in acute renal failure. Although important advances have been made in the understanding of hypoxic injury at the cellular level (e.g. loss of cell polarity, production of free radicals, calcium entry, and the activation of genes for protection or regeneration), the basic mechanisms responsible for organ failure remain elusive. The renal medulla, working on the brink of anoxia and being the site of concentration for many toxins, may be an important target for the synergistic events of hypoperfusion and nephrotoxic exposure that often precede human acute renal failure.