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Year : 2019  |  Volume : 5  |  Issue : 4  |  Page : 88-90

What augments nutritional support in acute kidney injury?


Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh, India

Date of Submission02-May-2020
Date of Decision04-May-2020
Date of Acceptance06-May-2020
Date of Web Publication09-Jun-2020

Correspondence Address:
Dr. Anita Saxena
Department of Nephrology, Sanjay Gandhi Post Graduate Institute of Medical Sciences, Lucknow, Uttar Pradesh
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/jrnm.jrnm_8_20

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How to cite this article:
Saxena A. What augments nutritional support in acute kidney injury?. J Renal Nutr Metab 2019;5:88-90

How to cite this URL:
Saxena A. What augments nutritional support in acute kidney injury?. J Renal Nutr Metab [serial online] 2019 [cited 2020 Jul 14];5:88-90. Available from: http://www.jrnm.in/text.asp?2019/5/4/88/286281



Acute kidney injury (AKI) is a common complication affecting approximately 5% of hospitalized patients and 10%–30% of patients managed in intensive care units (ICUs). It may present as sudden decline in glomerular filtration rate, which causes accumulation of metabolic waste products, toxins, and drugs and eventually causes abnormalities in protein, lipid, and carbohydrate metabolism, insulin resistance, and body composition. AKI is summarized by the acronym RIFLE enumerating three stages of kidney injury stratified by severity (risk, injury, and failure) and two outcomes, that is, loss and end-stage renal disease. In prerenal and postrenal injury, there is no change in the nutritional requirements of patients; however, in intrarenal injury, AKI nutritional requirements of the patient are altered. Protein-energy wasting (PEW) is the negative metabolic consequence of acute loss of kidney function on the nutritional state. Severe malnutrition is present in approximately 40% of patients with AKI in the ICU.

AKI is best identified as a triad of hypercatabolism, hyperglycemia, and hypertriglyceridemia.[1],[2],[3] There are several causes of AKI such as sepsis, critical illness, circulatory shock, burns, trauma, cardiac surgery (especially with cardiopulmonary bypass), major noncardiac surgery, nephrotoxic drugs, radiocontrast agents, venom (plants and animals) dehydration or volume depletion, chronic diseases, and cancer.


  What Augments Nutritional Support in Acute Kidney Injury? Top


AKI induces proinflammatory state; interferes with metabolism, thereby inducing protein catabolism, peripheral glucose intolerance, or increased gluconeogenesis; inhibits lipolysis and alters fat clearance; increases oxidative stress by the activation of reactive oxygen species (ROS) and depletion of antioxidant system; and impairs immunocompetence and endocrine abnormalities (hyperparathyroidism, insulin resistance, erythropoietin resistance, resistance to growth factors, and anabolic hormones). It affects hydration status, electrolyte, and acid–basic balance. The causes of hypercatabolism which lead to PEW are insulin resistance, gluconeogenesis inflammatory mediators' academia, catabolic hormones, and activation of muscle–protein catabolism. Metabolic abnormalities caused by proinflammatory state in AKI are listed in [Table 1].
Table 1: Metabolic abnormalities caused by proinflammatory state in acute kidney injury

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Nutritional evaluation is a prerequisite for nutritional intervention; patients with AKI may present with preexisting poor nutritional status due to inadequate dietary intake spanning days to weeks, which is aggravated by further losses during extracorporeal circulation (blood and nutrients), leading to loss of lean body mass. In AKI, the conventional nutritional markers are not reliable indicators of nutritional status due to hypercatabolic state. Catabolism is attributable to underlying disease and its complications rather than the AKI per se. Nutrient requirement is determined based on extent of catabolic state. Studies have documented catabolism of skeletal muscle proteins with increased amino acid turnover and negative nitrogen balance. Dialysis is responsible for a 133% increase in muscle protein degradation and sustained degradation of total body protein even after the end of the dialysis.[3] Both plasma and intracellular components of the amino acid pool are altered, and tissue utilization of exogenously infused amino acids is impaired; in fact, amino acid oxidation is stimulated, but amino acid transport into the muscle is reduced.[2]


  Acute Renal Failure Patients Despite Different Top


In AKI, the nitrogen balance is negative and urea production is increased, indicating that muscle protein catabolism is accelerated. Imbalance in amino acid profile is perceived as decline in serum valine, leucine, and glutamine and elevation in phenylalanine, methionine, taurine, and cysteine are elevated. Nonessential amino acids (tyrosine and arginine) become conditionally essential. During dietary protein restriction or inadequate intake, metabolic mechanisms to reduce the oxidative degradation of the essential amino acids are activated to conserve branched-chain amino acids (BCAAs), leucine, isoleucine, and valine for protein synthesis.[4] Leucine and its ketoacid, alpha-ketoisocaproate, are known to suppress protein degradation in muscles.[3],[4],[5]

This can also have an impact on protein turnover because leucine and its ketoacid, alpha-ketoisocaproate, suppress protein degradation in muscles. Consequently, any stimulus that prevents suppression of BCAA degradation could increase essential amino acid requirements and contribute to muscle atrophy. In chronic renal failure, the stimulus for increased BCAA oxidation is metabolic acidosis.[3],[4],[5],[6] Even though there is increased activity of the muscle degradation rate-limiting branched-chain ketoacid dehydrogenase enzyme for BCAA, metabolic acidosis still remains an important stimulus for muscle catabolism that impairs the ability to adapt to dietary protein restriction.

Changes in amino acid metabolism coupled with inadequate delivery of nutritional substrates cause nutritional depletion and consequently decline in nutritional status. Most of the studies have shown that the average mean daily calorie intake of patients admitted in the ICU is as low as 11 kcal/kg/day.[6],[7] However, studies have shown that permissive underfeeding, trophic feeding, or delayed parenteral feeding is superior in terms of preventing mortality on account of refeeding syndrome.[7],[8],[9],[10],[11] Hence, poor nutrient intake along with high catabolic rate results in negative nitrogen balance which is associated with worse outcomes.[7],[8],[9],[10]

Albumin, the marker of malnutrition, loses its accuracy in AKI patients, as reduction in its levels is not always a consequence of limited energy and protein substrate intake, but it is also due to the presence of inflammation. However, its use as a predictor of mortality has been described in patients with AKI. Hypoalbuminemia is a predictor of mortality in patients with acute tubular necrosis. Each 1 g/dL increase in the serum albumin levels reduces the risk of mortality and dialysis by 44%. A retrospective study has shown that in the absence of multiple organ failure, patients with serum albumin levels lower than 3.5 g/dL had a relative risk of death of 3.6, regardless of the presence of sepsis. There is 50% reduction in the survival of AKI patients who had cholesterol levels lower than 150 mg/dL on admission.[5],[6],[7],[8],[9],[10],[11],[12],[13] Prealbumin of 11 mg/dL is associated with greater mortality[11] However, it has been shown that a 5 mg/dL increase of prealbumin is associated with a 29% reduction in hospital mortality. Survival of patients admitted to the ICU with cholesterol levels below 96 mg/dL significantly reduced.[13] Yet, low serum levels of albumin, low serum levels of prealbumin, and low serum levels of cholesterol are not truly diagnostic, transferrin and prealbumin have low specificity, and nitrogen balance is difficult to do. In critically ill AKI patients, insulin-like growth factor 1 (IGF-1) has been shown to have a good correlation with nutritional status. Reduction in IGF-1 is associated with lower survival in AKI patients; therefore, the short half-life of IGF-1 allows its use as an early and sensitive marker of mortality. Studies have shown that IGF-1 levels lower than 50.6 ng/mL are significantly associated with decreased survival, regardless of the presence of sepsis.

Nutritional strategies aim at avoiding development of deficiency states and of “hospital-acquired malnutrition” and progression from oliguric to anuric state. Nutrition support guidelines National Institute of Clinical Excellence (NICE 2006)[14],[15],[16],[17] recommend that all hospital inpatients on admission and all outpatients at their first clinic appointment should be screened for malnutrition. Screening should be repeated weekly for inpatients and when there is clinical concern for outpatients. The NICE recommends use of the Malnutrition Universal Screening Tool (MUST) to screen for malnutrition in hospital. Sensitivity of MUST is unreliable in patients with kidney impairment because of rapid fluid changes which affect body weight. Screening tool NUTRIC score is used for identifying adverse events for modifying nutrition therapy in the ICU patients. In this issue nutritional management of AKI, patient is given article “practical approach to a patient with AKI.”


  Conclusion Top


AKI is best identified as a triad of hypercatabolism, hyperglycemia, and hypertriglyceridemia. Catabolism is attributable to underlying disease and its complications rather than the AKI per se. AKI induces proinflammatory state and interferes with the metabolism of macronutrients and micronutrients. It increases oxidative stress by activation of ROS and depletion of antioxidant system and impairs immunocompetence and endocrine abnormalities. Nutritional evaluation is a prerequisite for patients with AKI not only to identify preexisting malnutrition which can be treated with appropriate intervention but also to prevent hospital-acquired malnutrition in the absence of preexisting malnutrition.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Druml W, Metnitz B, Schaden E, Bauer P, Metnitz PG. Impact of body mass on incidence and prognosis of acute kidney injury requiring renal replacement therapy. Intensive Care Med 2010;36:1221-8.  Back to cited text no. 1
    
2.
Druml W. Nutritional management of acute renal failure. Am J Kidney Dis 2001;37 Suppl 1:S89-94.  Back to cited text no. 2
    
3.
Berbel MN, Rodrigues Pinto MP, Ponce D, Balbi AL. Nutritional aspects in acute kidney injury. Rev Assoc Med Bras 2011;57:600-6.  Back to cited text no. 3
    
4.
Ikizler TA, Pupim LB, Brouillette JR, Levenhagen DK, Farmer K, Hakim RM, et al. Hemodialysis stimulates muscle and whole body protein loss and alters substrate oxidation. Am J Physiol Endocrinol Metab 2002;282:E107-16.  Back to cited text no. 4
    
5.
Woodrow G, Turney IH. Cause of death in acute renal failure. Nephrol Dial Transplant 1992;7:230-4.  Back to cited text no. 5
    
6.
Rice TW, Mogan S, Hays MA, Bernard GR, Jensen GL, Wheeler AP. Randomized trial of initial trophic versus full-energy enteral nutrition in mechanically ventilated patients with acute respiratory failure. Crit Care Med 2011;39:967-74.  Back to cited text no. 6
    
7.
Arabi YM, Tamim HM, Dhar GS, Al-Dawood A, Al-Sultan M, Sakkijha MH, et al. Permissive underfeeding and intensive insulin therapy in critically ill patients: A randomized controlled trial. Am J Clin Nutr 2011;93:569-77.  Back to cited text no. 7
    
8.
Schetz M, Casear MP, Van den Berghe G. Does artificial nutrition improve outcome of critical illness? Crit Care 2013;17:302. Casaer MP, Mesotten D, Hermans G, Wouters PJ, Schetz M, Meyfroidt G, et al. Early versus late parenteral nutrition in critically ill adults. N Engl J Med 2011;365:506-17.  Back to cited text no. 8
    
9.
Chertow GM, Lazarus JM, Paganini EP, Allgren RL, Lafayette RA, Sayegh MH. Predictors of mortality and the provision of dialysis in patients with acute tubular necrosis. The Auriculin Anaritide Acute Renal Failure Study Group. J Am Soc Nephrol 1998;9:692-8.  Back to cited text no. 9
    
10.
Obialo CI, Okonofua EC, Nzerue MC, Tayade AS, Riley LJ. Role of hypoalbuminemia and hypocholesterolemia as copredictors of mortality in acute renal failure. Kidney Int 1999;56:1058-63.  Back to cited text no. 10
    
11.
Perez Valdivieso JR, Bes-Rastrollo M, Monedero P, de Irala J, Lavilla FJ. Impact of prealbumin levels on mortality in patients with acute kidney injury: An observational cohort study. J Ren Nutr 2008;18:262-8.  Back to cited text no. 11
    
12.
Bauer P, Charpentier C, Bouchet C, Nace L, Raffy F, Gaconnet N. Parenteral with enteral nutrition in the critically ill. Intensive Care Med 2000;26:893-900.  Back to cited text no. 12
    
13.
Guimarães SM, Lima EQ, Cipullo JP, Lobo SM, Burdmann EA. Low insulin-like growth factor-1 and hypocholesterolemia as mortality predictors in acute kidney injury in the intensive care unit. Crit Care Med 2008;36:3165-70.  Back to cited text no. 13
    
14.
Acute Kidney Injury: Prevention, Detection and Management Up to the Point of Renal Replacement Therapy. National Clinical Guideline Centre (UK). London: Royal College of Physicians (UK); 2013.  Back to cited text no. 14
    
15.
National Clinical Guideline Centre (UK). Acute Kidney Injury: Prevention, Detection and Management Up to the Point of Renal Replacement Therapy. London: Royal College of Physicians (UK); 2013.  Back to cited text no. 15
    
16.
National Institute for Health and Clinical Excellence. Acutely Ill Patients in Hospital: Recognition of and Response to Acute Illness in Adults in Hospital. (Clinical Guideline 50); 2007. Available from: http://guidance.nice.org.uk/CG50.  Back to cited text no. 16
    
17.
Kalaiselvan MS, Renuka MK, Arunkumar AS. Use of nutrition risk in critically ill (NUTRIC) score to assess nutritional risk in mechanically ventilated patients: A prospective observational study. Indian J Crit Care Med 2017;21:253-6.  Back to cited text no. 17
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