Macronutrients and Critical Illness with AKI

By Lisa Moloney MS, RD, LDN

 When assessing critically ill patients, dietitian’s critical thinking skills are in full swing.  Numerous underlying etiologies are contributors of a multitude of problems.  It can sometimes be difficult to assess the cause of presented symptoms with so much going on.  I personally have found this especially difficult when assessing and determining needs of patients with Acute Kidney Injury (AKI). 

Per Gervasio etal, AKI is associated with sudden decline of glomerular filtration rate with a buildup of metabolic waste products, toxins, and drugs along with alteration in kidney function.  The kidneys regulate acid base equilibrium, fluid and electrolyte balance, gluconeogenesis, secrete erythropoietin and convert vitamin D3 to its active form.  All of these functions can become impaired with AKI. 

 The main goal of nutrition support in patients with AKI is to prevent    protein energy wasting (PEW).  Per Gervasio etal, PEW is diagnosed if 3 characteristics are present: (1) low serum albumin, prealbumin, or cholesterol (2) reduced body mass and (3) reduced muscle mass.  Diagnosis of PEW in patients with AKI can be difficult.  Inflammation, edema and renal excretion of prealbumin can alter protein levels and weight.  Alternative markers have been suggested to help identify when nutrition support should be considered.  IGF-1 has been shown as a specific mark for malnutrition in patients receiving hemodialysis.  C-reactive protein, an indicator of inflammation can be used along with other l protein markers to improve the patients overall assessment.  Nitrogen balance can help assess the patient’s protein breakdown but only if the creatinine clearance is greater than 50, making this difficult with AKI patients.  Gervasio etal suggests that urea nitrogen appearance may be more accurate. 

Controlling blood sugar levels in critically patients can be a challenge to say the least, especially in those with AKI.  The kidneys contribute 15% – 25% of gluconeogenesis, about 10% -20% of glucose uptake and 30% of insulin catabolism.  AKI can clearly be linked as one more contributor to altered carbohydrate metabolism in critically ill patients. 

Energy Expenditure

The kidneys are responsible for nearly 10% of the resting energy expenditure.  AKI without critical illness, however, does not appear to have a direct effect on energy expenditure.   Nutrition support should be based on estimated metabolic stress and protein energy requirements.  Stage 1 AKI has limited effects on energy expenditure.  Stages II and III, however, will generally have greater caloric requirements because it indicates underlying disease progression.  Higher caloric delivery has been studied but does not appear to improve patient outcomes.  Energy delivery in patients with AKI is recommended from 25-35 kcal/kg/d.       

Protein

Patients with AKI and critical illness are in an intense state of catabolism.  Parenteral amino acid administration is often insufficient to correct catabolism but it can decrease overall loss.  Clearance of amino acids in these patients is as high as 1.3 to 1.8 gm/kg.  Protein delivery may sometimes need to be decreased to avoid azotemia.  Yet please note, restricting protein or providing inadequate amounts can contribute to protein malnutrition and other complications.  Advanced AKI in acutely ill patients usually require renal replacement therapy (RRT).  Patients receiving continuous RRT demonstrate positive nitrogen balance when dosages of 1.8 -2.5g/kg/d of protein are delivered and protein dosages from 1.5-2.0 g/kg/d may be sufficient for patients receiving IHD.  Currently, the international and national guidelines do not support use of specialty renal amino acid products. 

Lipids

Impaired lipolysis in AKI results in an increase in plasma triglycerides, very low density lipoproteins, and low density lipoproteins, in turn total circulating cholesterol and high density lipoproteins are decreased.  Administration of parenteral lipids in critically ill patients with AKI has shown reduced clearance.  This lipid metabolism dysfunction can be decreased with administration of amino acids and glucose.   It is also important to keep in mind that lipids are an important energy source in this population and fatty acid oxidation is preserved.

Gervasio JM, Garmon WP, Holowatyj MR.  Nutrition support in acute kidney injury.  Nutr clin Pract.  2011;26:374-381)

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Stephanie Hofhenke

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