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Abstract
The main functional change in patients with acute renal failure (ARF) is a decrease
in glomerular filtration rate (GFR). The virtual complete recovery of renal function
in those patients who survive ARF, as well as the minimal renal histological abnormalities
during ARF when the GFR is less than 10 ml/min, suggest that a major component of
the renal tubular cell injury is sublethal or reversible. Experimental models of acute
tubular necrosis frequently have placed the emphasis on irreversible proximal tubular
cell death. The nature of the renal tubular cell injury in ischemic acute renal failure,
however, includes not only cell death (necrosis or apoptosis) but also sublethal injury
causing cell dysfunction. The role of intracellular calcium, the calcium-dependent
enzymes calpain, phospholipase A2 and nitric oxide synthase (NOS), in the pathophophysiology
of this renal tubular cell injury during hypoxia/ischemia is described. The effects
of calpain and nitric oxide (NO) on the cytoskeleton and cell adhesion are discussed.
Potential mechanisms whereby tubular injury leads to a profound fall in GFR, including
increased tubuloglomerular feedback and increased distal tubular obstruction, in ischemic
acute renal failure are proposed.