Estimation Of Energy Requirements

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Calculation of resting energy expenditure (REE) (Harris Benedict equation): Males: 66.47 ^ (13.75 X BW) ^ (5 X height) - (6.76 X age) Females: 655.1 ^ (9.56 X BW) ^ (1.85 X height) - (4.67 X age) The average REE is approximately 25 kcal/kg BW/day Stress factors to correct calculated energy requirement for hypermetabolism: Postoperative (no complications) 1.0 Long bone fracture 1.15-1.30 Cancer 1.10-1.30 Peritonitis/sepsis 1.20-1.30 Severe infection/polytrauma 1.20-1.40

Burns (= approxim. REE + % burned body surface area) 1.20-2.00 Corrected energy requirements (kcal/d) = REE X stress factor

FIGURE 18-4

Estimation of energy requirements. Energy requirements of patients with acute renal failure (ARF) have been grossly overestimated in the past and energy intakes of more than 50 kcal/kg of body weight (BW) per day (ie, about 100% above resting energy expenditure (REE) haven been advocated [6]. Adverse effects of overfeeding have been extensively documented during the last decades, and it should be noted that energy intake must not exceed the actual energy consumption. Energy requirements can be calculated with sufficient accuracy by standard formulas such as the Harris Benedict equation. Calculated REE should be multiplied with a stress factor to correct for hypermetabolic disease; however, even in hypercatabolic conditions such as sepsis or multiple organ dysfunction syndrome, energy requirements rarely exceed 1.3 times calculated REE [1].

Protein metabolism

FIGURE 18-5

Protein metabolism in acute renal failure (ARF): activation of protein catabolism. Protein synthesis and degradation rates in acutely uremic and sham-operated rats. The hallmark of metabolic alterations in ARF is activation of protein catabolism with excessive release of amino acids from skeletal muscle and sustained negative nitrogen balance [7, 8]. Not only is protein breakdown accelerated, but there also is defective muscle utilization of amino acids for protein synthesis. In muscle, the maximal rate of insulin-stimulated protein synthesis is depressed by ARF and protein degradation is increased, even in the presence of insulin [9]. (From [8]; with permission.)

FIGURE 18-6

Protein metabolism in acute renal failure (ARF): impairment of cellular amino acid transport. A, Amino acid transport into skeletal muscle is impaired in ARF [10]. Transmembranous uptake of the amino acid analogue methyl-amino-isobutyrate (MAIB) is reduced in uremic tissue in response to insulin (muscle tissue from uremic animals, black circles, and from sham-operated animals, open circles, respectively). Thus, insulin responsiveness is reduced in ARF tissue, but, as can be seen from the parallel shift of the curves, insulin sensitivity is maintained (see also Fig. 18-14). This abnormality can be linked both to insulin resistance and to a generalized defect in ion transport in uremia; both the activity and receptor density of the sodium pump are abnormal in adipose cells and muscle tissue [11]. B, The impairment of rubidium uptake (Rb) as a measure of Na-K-ATPase activity is tightly correlated to the reduction in amino acid transport. (From [10,11]; with permission.)

FIGURE 18-7

Protein catabolism in acute renal failure (ARF). Amino acids are redistributed from muscle tissue to the liver. Hepatic extraction of amino acids from the circulation—hepatic gluconeogenesis, A, and ureagenesis, B, from amino acids all are increased in ARF [12]. The dominant mediator of protein catabolism in ARF is this accel erated hepatic gluconeogenesis, which cannot be suppressed by exogenous substrate infusions (see Fig. 18-15). In the liver, protein synthesis and secretion of acute phase proteins are also stimulated. Circles—livers from acutely uremic rats; squares—livers from sham operated rats. (From Fröhlich [12]; with permission.).

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