acute kidney injury

Apoptotic cell death is consistently found in both distal and proximal tubules in human ischemic and nephrotoxic acute kidney injury.

The prognosis for patients with intrinsic acute renal failure remains poor, with mortality of 40 to 80 percent in the intensive care setting.

Acute kidney injury was proposed as a standardized term to reflect the spectrum of intrinsic acute renal failure while excluding prerenal azotemia and other fully reversible causes.

Intrinsic acute renal failure is associated with intense and persistent renal vasoconstriction that reduces overall kidney blood flow to approximately 50 percent of normal.

Endothelial cell injury is presented as a primary mechanism underlying hemodynamic alterations in ischemic acute kidney injury, including imbalance between endothelin and nitric oxide.

Human ischemic acute kidney injury is characterized by proximal tubule brush border loss, patchy tubule cell loss, proximal tubular dilation, distal tubular casts, and areas of cellular regeneration.

Endothelin receptor antagonists ameliorate ischemic acute kidney injury in animals, but human data are lacking.

Postischemic kidneys show persistent outer medullary congestion and hypoperfusion even when cortical blood flow improves during reperfusion.