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Carbohydrate metabolism in AKI is characterized by hyperglycemia due to peripheral insulin resistance158,159 and accelerated hepatic gluconeogenesis, mainly from conversion of amino acids released during protein catabolism that cannot be suppressed by exogenous glucose infusions.160 In addition, hypertriglyceridemia commonly occurs due to inhibition of lipolysis. The clearance of exogenously administered lipids can be reduced.161 The modifications of energy metabolism are usually not caused by AKI per se but related to acute comorbidities and complications.162 Energy consumption is not increased by AKI. Even in multiple-organ failure, the energy expenditure of critically ill patients amounts to not more than 130% of resting energy expenditure. The optimal energy-to-nitrogen ratio during AKI has not been clearly determined. In a retrospective study of AKI patients undergoing continuous venovenous hemofiltration (CVVH), less negative or weakly positive nitrogen balance was associated with an energy intake of approximately 25 kcal/kg/d.163 In a randomized trial in AKI patients comparing 30 and 40 kcal/kg/d energy provision, the higher energy prescription did not induce a more positive nitrogen balance but was associated with a higher incidence of hyperglycemia and hypertriglyceridemia and a more positive fluid balance.164 These observations provide a rationale to maintain a total energy intake of at least 20, but not more than 25–30 kcal/kg/d, equivalent to 100–130% of resting energy expenditure. Energy provision should be composed of 3–5 (maximum 7) g per kilogram body weight carbohydrates and 0.8–1.0 g per kilogram body weight fat.
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