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Abstract

Acute renal failure (ARF) is defined clinically as the sudden loss of renal function that may result from inadequate renal perfusion associated with a decrease in effective circulation, arterial or venous obstruction, renal cell injury, or obstruction to urine flow as occurs in obstructive uropathy. Renal cell injury, commonly termed intrinsic ARF, results from an ischemic or toxicant insult that causes acute tubular damage with accompanying loss of ability to reabsorb filtered solute. The resulting decrease in glomerular filtration rate (GFR), an invariable component of ARF, is then a successful adaptive response, since continued filtration of plasma across the glomerular basement membrane without reabsorption of the filtrate by injured renal tubules would result in massive losses of salt and water (1). Thus, the decreased GFR associated with ARF prevents severe depletion of extracellular fluid.

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