The mortality rate in patients with acute renal failure (ARF) has not declined during the past two to three decades, despite advances in medical technology and improvements in renal replacement therapy (1-3). Although associated illnesses contribute to the high mortality rate in ARF, metabolic alterations induced by acute uremia also stimulate protein catabolism and loss of lean body mass (4). It is well known that malnutrition is a risk factor for morbidity and mortality in hospitalized patients, as well as patients with end-stage renal failure receiving maintenance hemodialysis (5). These findings provide circumstantial evidence that malnutrition may also be an important and potentially treatable risk factor for morbidity and mortality in patients with ARF. Factors which have been implicated as contributing to wasting in ARF include: 1) the presence of preexisting malnutrition and the adequacy of nutritional support; 2) concomitant catabolic condition(s) (e.g., trauma, sepsis, surgery, chemotherapy, etc.); 3) alterations in intermediary metabolism due to the loss of renal function; and 4) intradialytic losses of amino acids and protein, as well as catabolism induced by the hemodialysis procedure per se (6).In this review we have summarized the current knowledge regarding the mechanism(s) responsible for catabolism in ARF as well as potential therapeutic approaches to this difficult problem.
