Bench-to-bedside review: Metabolism and nutrition
Critical Care
Bench-to-bedside review: Metabolism and nutrition Michal P Casaer, Dieter Mesotten and Miet RC Schetz
Corresponding author: Michal P Casaer 0
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0 Department of Intensive Care Medicine, University Hospital Leuven, Catholic University of Leuven , Herestraat 49, B-3000 Leuven , Belgium
Acute kidney injury (AKI) develops mostly in the context of critical illness and multiple organ failure, characterized by alterations in substrate use, insulin resistance, and hypercatabolism. Optimal nutritional support of intensive care unit patients remains a matter of debate, mainly because of a lack of adequately designed clinical trials. Most guidelines are based on expert opinion rather than on solid evidence and are not fundamentally different for critically ill patients with or without AKI. In patients with a functional gastrointestinal tract, enteral nutrition is preferred over parenteral nutrition. The optimal timing of parenteral nutrition in those patients who cannot be fed enterally remains controversial. All nutritional regimens should include tight glycemic control. The recommended energy intake is 20 to 30 kcal/kg per day with a protein intake of 1.2 to 1.5 g/kg per day. Higher protein intakes have been suggested in patients with AKI on continuous renal replacement therapy (CRRT). However, the inadequate design of the trials does not allow firm conclusions. Nutritional support during CRRT should take into account the extracorporeal losses of glucose, amino acids, and micronutrients. Immunonutrients are the subject of intensive investigation but have not been evaluated specifically in patients with AKI. We suggest a protocolized nutritional strategy delivering enteral nutrition whenever possible and providing at least the daily requirements of trace elements and vitamins.
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Introduction
Patients with acute kidney injury (AKI) have a high prevalence
of malnutrition, a condition that is associated with morbidity
and mortality [1]. AKI develops mostly in the context of critical
illness and multiple organ failure, which are associated with
major changes in substrate metabolism and body
composition, overwhelming the alterations induced by AKI itself. Key
effectors of these changes are inflammatory mediators and
neuroendocrine alterations. The development of AKI further
adds fluid overload, azotemia, acidosis, and electrolyte
disturbances. In addition, AKI is associated with increased
inflammation and oxidative stress [2]. The most severe cases
of AKI require renal replacement therapy (RRT), with
continuous treatments (continuous renal replacement therapy,
CRRT) being the modality of choice in most intensive care
units (ICUs) [3]. These extracorporeal treatments facilitate
nutritional support but may, on the other hand, induce
derangements of nutrient balances. The rationale for nutrition
during critical illness is mainly to attenuate the catabolism and
the loss of lean body mass in the hypermetabolic critically ill
patient. However, the concept of improving clinical outcome
by improving energy and nitrogen balance is still being
challenged [4]. The purposes of this paper were to review the
metabolic alterations underlying critical illness and AKI, to
discuss nutritional and metabolic support in these patients,
and to address the nutritional implications of CRRT. The
reader is also referred to several other reviews on this subject
[5-10].
Metabolic alterations in critical illness and
acute kidney injury
Critical illness is generally recognized as a hypermetabolic
state, with energy expenditure (EE) being proportional to the
amount of stress [11,12]. Although active solute transport in
a functioning kidney is an energy-consuming process, the
presence of AKI by itself (in the absence of critical illness)
does not seem to affect resting EE (REE) [13]. EE in AKI
patients is therefore determined mainly by the underlying
condition. Studies in chronic kidney disease yield conflicting
results varying between increased [14,15], normal [16], or
even decreased REE [17].
A characteristic of critical illness is the so-called diabetes of
stress with hyperglycemia and insulin resistance. Hepatic
gluconeogenesis (from amino acids and lactate) increases
mainly due to the action of catabolic hormones such as
glucagon, epinephrine, and cortisol. In addition, the normal
suppressive action of exogenous glucose and insulin on
hepatic gluconeogenesis is decreased. Peripheral glucose
utilization in insulin-dependent tissues (muscle and fat) is also
decreased [18,19]. Since most patients with AKI also have
an underlying critical illness, it is not surprising that the same
AKI = acute kidney injury; CO2 = carbon dioxide; CRRT = continuous renal replacement therapy; EE = energy expenditure; EN = enteral nutrition;
ESPEN = European Society for Enteral and Parenteral Nutrition; ICU = intensive care unit; MOD = multiple organ dysfunction; PN = parenteral
nutrition; RCT = randomized controlled trial; REE = resting energy expendi (...truncated)