Management of Nutrition in Acute Kidney Injury and Renal Replacement Therapy

Protein and Energy Metabolism and Requirements

Macronutrient metabolism and requirements are detailed in Chapter 72, Chapter 73, Chapter 74, Chapter 75 . In short, ICU-acquired AKI results in increased protein catabolism and sustained negative nitrogen balance. The mechanisms associated to this response may be specific to the acute uremic state or RRT but also are associated with the underlying disease and its complications ( Fig. 78.1 ). As a result, loss of lean body mass with marked muscle wasting is already evident in the early days of ICU stay, resulting in protein energy wasting (PEW).

The optimal protein intake of patients with AKI still has not been defined. Protein intake should be quantitatively adequate to blunt skeletal muscle wasting, while providing the amino acids needed for the acute-phase response. Patients with AKI undergoing RRT, especially when the most efficient modalities such as CRRT or SLED are applied, are at greater risk of PEW, because of the amino acid losses in the dialysate/ultrafiltrate, and they may require higher protein intakes. A protein catabolic rate of 1.4 to 1.8 g/kg/day has been documented in patients undergoing continuous RRT (CRRT) or SLED.

Energy intake in the ICU setting should never exceed actual energy requirements, because overfeeding is much more deleterious to the patient than slightly underfeeding. In patients with AKI, an energy provision of 40 kcal/kg/day was associated with more severe metabolic complications, such as hypertriglyceridemia and hyperglycemia than lower intakes (30 kcal/kg/day) without any positive effects on nitrogen balance. Indirect calorimetry (IC) is the gold standard for assessing resting energy expenditure (REE) in critically ill patients and should be used to guide energy support also in this clinical setting.

Nonprotein energy should be provided as glucose and lipids, aiming to prevent or reduce protein breakdown for gluconeogenesis and preserve muscle mass.

Glucose always has represented the most important source of calories for patients with AKI; however, because these patients are at increased risk for hyperglycemia and hypoglycemia, a tight, but not overly aggressive glucose control is necessary. Data on critically ill patients show that both complications are associated with poor outcomes and that insulin resistance in AKI patients is associated with increased mortality ( Table 78.1 ).

Despite the fact that exogenous lipid particles have a reduced clearance rate in AKI patients, fatty acid oxidation is increased and lipids are a key energy substrate. A complete diet including all of the macronutrients is important to avoid essential fatty acid deficiency and to provide the right amount of energy, with lipids up to 30% to 35% of total calories. In the case of parenteral nutrition, when the commercially available all-in-one admixtures are not used, patients should receive 0.8 to 1.2 g/kg/day of lipid from lipid emulsions. Serum triglycerides should be monitored, and lipid administration should be interrupted when it exceeds 400 mg/dL (4 mmol/L).

Few data are currently available on measured energy and protein needs in critically ill patients with AKI. A mean energy requirement of 27 kcal/kg/day has been documented in critically ill patients with AKI on RRT, with no major differences with patients with preserved renal function. Protein catabolic rates of 1.5 to 1.8 g/kg/day measured by urea kinetic methods were obtained in small groups of patients with AKI on different modalities of RRT. Finally, no data are currently available in the literature on protein/energy intakes in patients with AKI not on RRT. In this specific clinical setting, a protein intake of 0.8 to 1 g/kg/day has been suggested also in recent guidelines as an expert opinion. Table 78.1 reports the recommendations of the latest guidelines regarding nutritional practices for AKI patients.

Fluid, Vitamins, and Micronutrient Requirements

Fluid overload is not uncommon among patients with AKI and is a well-known poor outcome determinant. Thus it is important to provide the right amount of nutrients in the minimum volume of fluids. This can be achieved using the most concentrated all-in-one parenteral admixtures and the disease-specific enteral formulae ( Table 78.2 ). Micronutrient requirements have been poorly investigated in AKI patients. However, it has been demonstrated that trace elements and water soluble vitamins can be lower than normal. These alterations are likely to be the consequence of many interfering factors, including acute phase reaction/critical illness, redistribution of elements between plasma and tissues, acute losses of biologic fluids, dilution, varying concentrations of trace elements in dialysis/hemofiltration fluids, and effects of enteral or parenteral nutrition fluid. Moreover, RRT fluids may have variable content of trace elements, at concentrations often neglected. Finally, the effects of RRT on the removal of mainly protein-bound trace elements are far from clearly defined. Data from in vitro studies indicate that selenium, chromium, copper, and zinc can be removed from plasma by convective/diffusive RRTs. The levels of water-soluble vitamins, such as vitamin C, folic acid, and thiamin are reduced mainly because of the losses occurring through the extracorporeal circuit. In continuous venovenous hemofiltration (CVVH), vitamin C losses can reach up to 600 µmol/day (100 mg/day) and folate losses up to 600 nmol/day. In continuous venovenous hemodiafiltration (CVVHDF), thiamin losses may exceed 1.5 times the daily provision of the vitamin from standard total parenteral nutrition solutions. Vitamin C administration should not usually exceed 50 to 100 mg/day, because inappropriate supplementation may lead to secondary oxalosis. Higher intakes (up to 150 to 200 mg) may be needed when CRRT is used (see Table 78.1 ). No supplementation of fat-soluble vitamins usually is needed in AKI.