Between 25 and 40 per cent of cases of ARF are ascribed to intrinsic renal damage, predominantly induced by prolonged renal hypoperfusion (as for prerenal failure)
or nephrotoxins (contrast, antibiotics, rhabdomyolysis), and most often by their combination ( Dinour and Brezis 1998). Acute intrinsic renal failure is synonymous with vasomotor nephropathy and acute tubular necrosis. Although acute intrinsic renal failure and the prerenal state represent two extremes of renal hypoperfusion, intrinsic failure implies renal parenchymal damage (tubular epithelium) that is not immediately reversible upon elimination of the precipitating factor and restoration of blood flow.
Putative mechanisms by which renal ischemia impairs glomerular filtration include reduction in glomerular perfusion, renal tubule cast or cellular debris obstruction, and backleak of glomerular filtrate through injured tubule epithelium. ARF is often multifactorial, involving more than one mechanism of injury.
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