Recent reports have demonstrated a link between acute kidney injury (AKI) and chronic kidney disease (CKD). Individuals with AKI are more likely to have CKD and eventually progress to end-stage renal disease.
Conversely, patients with CKD are more susceptible to having AKI (Am J Physiol Renal Physiol 2011;300:F602-F610). AKI results in multiple metabolic derangements that eventually lead to severe loss of lean body mass and energy reserve depletion. These losses culminate in protein-energy wasting that is strongly associated with mortality (J Am Soc Nephrol 1999;10:581-593).
Prevalence of PEW
Fiaccadori et al (J Am Soc Nephrol 1999;10:581-593) used subjective global assessment (SGA) to assess the prevalence of protein-energy wasting in patients with AKI and found 40% had a score of C, reflecting severe malnourishment. The causes of these extreme nutritional losses are similar to those of any patient in a highly stressed and catabolic state.
High concentrations of stress hormones, pro- and anti-inflammatory or oxidative stress mediators, uremia, insulin resistance, and metabolic acidosis trigger a cascade of actions resulting in the production of quick energy in the form of glucose, and preservation of vital organs potentially at the expense of peripheral lean body mass, and fluid retention (Semin Dial 2011;24:169-175). To complicate matters, many of these patients have comorbidities—congestive heart failure, chronic obstructive pulmonary disease, and diabetes mellitus—all of which increase energy and protein needs.
Challenges in assessment
Rapid assessment and intervention must occur, in order to ameliorate the loss of lean body mass and energy reserves in patients with AKI. However, thorough assessment has some inherent challenges. Due to the inflammation present in AKI, many of the traditional visceral serum markers are difficult to use and interpret accurately.
For example, both serum albumin and serum pre-albumin are negative-phase proteins; therefore, they are reduced in a catabolic condition such as AKI. Furthermore, noting that the goal is to retain body fluid and that AKI patients often are hypervolemic, weight and anthropometric measures such as mid-arm muscle circumference are unreliable.
Multiple evaluative factors
It is for this reason that clinicians familiar with AKI use either a composite method of assessment, such as the SGA, or other diagnostic panels to assess nutritional status. Such a panel should include biochemical, weight loss, muscle mass, and protein and energy intake parameters.
Furthermore, functional markers such as handgrip strength, rate of wound healing, or physical exams similar to those found at the end of SGA may be extremely valuable indicators of nutritional status. The clinician must look at all available data to determine status, as one marker is incapable of defining protein energy wasting.
To prescribe optimal nutrition intervention, a reasonable estimation of energy and protein needs should be made. The gold standard for estimating energy needs is indirect calorimetry. In a more recent review by Fiaccadori and colleagues (J Nephrol 2008;5:645-656), the researchers state that energy needs are rarely greater than 1.3 times basal energy expenditure in AKI.
Therefore, it is important to monitor the diet of the AKI patient and whereas diet must not be insufficient, overfeeding should also be avoided.
Specified protein content
Nutrition support, in the form of enteral or parental nutrition, is a key therapy used to offset the previously mentioned metabolic derangements in AKI. The goals of nutritional intervention are to provide an adequate substrate while ameliorating the systemic inflammatory effects.
Protein content in nutrition support should be at least 1.5g/kg if the patient is receiving renal replacement therapy (RRT) (Clin Nutr 2009;28:401-414). Additionally, if the patient is on RRT, there is a need to compensate for protein losses. Increases of 0.2-0.3 g/kg/day have been recommended.
To allow for protein sparing effects while avoiding overfeeding of the AKI patient, 25 non-protein kcal/kg/day or an indirect calorimetry measurement is recommended (Clin Nutr 2009;28:401-414). To prevent hyperglycemia and hypertriglyceridemia while in a catabolic state, glucose should be infused at <5g/kg/day. Thirty-five percent of these non-protein kcals should be from lipids or approximately 1.0-1.5 g/kg/day. It has been suggested that a combination of medium and long-chain lipids are preferable; however, the data on this combination are not strong. Finally, micronutrients are an important consideration and may be needed at higher than the typical multivitamin preparation provides.
In summary, patients with AKI are highly catabolic and require strong nutritional assessment and intervention to prevent protein-energy wasting. Composite methods of assessment are preferable as no one marker can accurately determine status nor reflect improvement. Nutritional intervention should be high in protein with adequate energy to promote protein sparing.
Dr. Steiber is Coordinator of the Dietetic Internship/Master’s Degree Program at Case Western Reserve University in Cleveland.