Acute tubular necrosis

Most common cause of ARF of the renal type.

Second most common cause of acute renal failure in hospitalized patients, after prerenal azotemia.

Usually results from an acute ischemic or toxic event.

Initially characterized by decrease in glomerular filtration rate (GFR), with marked increases in serum creatinine and blood urea nitrogen (BUN).

The maintenance phase continues with sustained reduction in GFR for 1-2 weeks, with continued rising creatinine and BUN.

The recovery phase is manifested by increased urinary volume, with improved tubular function, and decreasing BUN and serum creatinine.

When hypoperfusion occurs it initiates cell injury that can lead to cell death.

The tubular cells of the straight portion of the proximal tubules, and the thick ascending limb of the loop of Henle are the most vulnerable to hypoperfusion injury, especially as it enters the relatively hypoxic medulla.

Reduced filtration occurs with hypoxic injury and GFR and is reduced by the presence of casts and debris that obstructs the tubule lumen, as well.

As the lumen of the tubule is obstructed leakage of filtrate through the damaged epithelium.

Ischemia leads to the production of nitric oxide and prostacylcin by tubule epithelial cells which lead to vasoconstriction and further hypoperfusion.

Ischemia of the kidney causes depletion of ATP, increased cytoplasmic calcium, free radical formation, impaired membrane phospholipid function and creates cell volume abnormalities.

depletion of ATP associated with ischemic causes impaired cellular function and ineffective membrane transport results in the swelling of cells and accumulation of intracellular sodium and calcium.

Results in phosholipid membrane metabolism abnormalities with peroxidation.

Associated with free radical formation with toxic effects.

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