Acute tubular necrosis
Also known as acute tubulointerstitial nephritis, acute tubular necrosis (ATN) is the most common cause of acute renal failure in critically ill patients, and it accounts for about 75% of all cases of acute renal failure. ATN injures the tubular segment of the nephron, causing renal failure and uremic syndrome. Mortality ranges from 40% to 70%, depending on complications from underlying diseases. Patients with non-oliguric forms of ATN have a better prognosis.
ATN results from ischemic or nephrotoxic injury, most commonly in debilitated patients, such as the critically ill and those who have undergone extensive surgery.
With ischemic injury, disruption of blood flow to the kidneys may result from circulatory collapse, severe hypotension, trauma, hemorrhage, dehydration, cardiogenic or septic shock, surgery, anesthetics, or reactions to transfusions. Ischemic ATN can damage the epithelial and basement membranes and can cause lesions in the renal interstitium.
With nephrotoxic injury, damage may follow ingestion of certain chemical agents or result from a hypersensitive reaction of the kidneys. Because nephrotoxic ATN doesn’t damage the basement membrane of the nephron, it’s potentially reversible.
ATN may result from:
diseased tubular epithelium that allows leakage of glomerular filtrate across the membranes and reabsorption of filtrate into the blood
obstruction of urine flow by the collection of damaged cells, casts, red blood cells (RBCs), and other cellular debris within the tubular walls
ischemic injury to glomerular epithelial cells, resulting in cellular collapse and decreased glomerular capillary permeability
ischemic injury to vascular endothelium, eventually resulting in cellular swelling and obstruction.