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Table of Contents
EDITORIAL
Year : 2019  |  Volume : 5  |  Issue : 4  |  Page : 77-78

How aggressive are we in providing nutritional support to patients with acute kidney injury?


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

Date of Submission08-May-2020
Date of Acceptance09-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_10_20

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How to cite this article:
Saxena A. How aggressive are we in providing nutritional support to patients with acute kidney injury?. J Renal Nutr Metab 2019;5:77-8

How to cite this URL:
Saxena A. How aggressive are we in providing nutritional support to patients with acute kidney injury?. J Renal Nutr Metab [serial online] 2019 [cited 2020 Aug 9];5:77-8. Available from: http://www.jrnm.in/text.asp?2019/5/4/77/286277



Hippocrates wrote “Declare the past, diagnose the present, foretell the future: practice these acts. As to diseases, make a habit of two things – to help, or at least to do no harm.”[1] English Medical Cookbook published in 1390 ends with “'Explicit de coquina quae est optima medicina,” which means “food is the best medicine,”[2] and it was in 1859 that Florence Nightingale wrote “thousands of patients are annually starved in the midst of plenty.”[3],[4] It was that in the early 1970s, a publication entitled, “The skeleton in the hospital closet” highlighted the medical profession's ignorance regarding disease-related undernutrition and the profession's practice habits, which contributed to and sustained the problem. Did these words of wisdom imply renal disease and speak of the plight of renal patients?

Acute kidney injury (AKI) is a metabolic disaster which begins with sudden decline of glomerular filtration rate accompanied by the accumulation of metabolic wastes, translating into uremic intoxication, altering milieu interior of the body. This upheaval destroys acid–base equilibrium, fluid and electrolyte balance, and most of the regulated metabolic activities of macro- and micro-nutrients. Protein catabolism, a hallmark of AKI, is worse with underlying illness, leading to prolonged intense state of catabolism,[5],[6],[7] and therefore, mortality is tightly interwoven with nutritional status and pro-inflammatory and pro-oxidative milieu. Hypercatabolism is identified at four levels: nutrition, endocrine (clinical trials with IGF-I and rHGH have been disappointing), mediators of inflammation, and interventions to block catabolic pathways. Yet, no, the so-called effective methods reduce or stop hypercatabolism in clinical situation. Poor nutrient intake coupled with high catabolic rate creates negative nitrogen balance, which is associated with worse outcomes. Special considerations have to be given to malnourished critically ill patients who are hemodynamically unstable and who have not had their intravascular volume fully resuscitated. The requirements of energy (glucose and fat) protein (essential and nonessential amino acids) differ corresponding to the extent of catabolism. Therefore, the goals for nutritional support exceed conventional interventions considered in a patient with renal disease without AKI, without inducing dumping and refeeding syndromes. Despite elevated plasma insulin levels, critically ill patients have decreased insulin-dependent glucose utilization in the skeletal muscle and adipose tissue, which contributes to insulin resistance and hyperglycemia (not to forget accelerated hepatic gluconeogenesis). This factor can be a determinant of prolonged hospital stay, hence heeds considerable attention.[8]

Nutritional therapy in AKI patients requires frequent monitoring to avoid metabolic complications. However, how aggressive are we in proposing nutritional support to these patients in view of volume, metabolic abnormalities, gastroparesis, fear of increased bloodstream infectious complications in the setting of sepsis, and eventually the cost? How well do we preserve splanchnic flow, prevent mucosal breakdown, and lower stress hormone concentrations? Malnutrition is invariably undertreated which hampers speedy recovery.

Nutrition support guidelines of the National Institute of Clinical Excellence (2006[9]) recommend “… all hospital inpatients on admission and all outpatients at their first clinic appointment should be screened for malnutrition, and screening should be repeated weekly for inpatients and when there is clinical concern for outpatients.” Whatever be the case, the first and the foremost question that one needs to answer is “how does the journey to recovery begin in a patient with AKI knowing that the conventional markers of nutritional status, such as low serum levels of albumin, low serum levels of prealbumin, and low serum levels of cholesterol, are not truly diagnostic of malnutrition?” Which nutritional screening tool scores highest on criterion of validity? Is it the NUTRIC score?[10]

This issue of JRNM has two articles on AKI under categories: classroom reading “what augments nutritional support in acute kidney injury?” and clinical practice “practical approach to a patient with acute kidney injury,” with intent to simplifying understanding basics and management of AKI from nutritional perspective for trainees. The Journal invites articles under these two categories, which will help trainees understand important areas of renal nutrition in a simplified way.



 
  References Top

1.
Kamien M. Declare the past, diagnose the present, foretell the future: Rural health for all Australians by 2000? Aust J Rural Health 1997;5:178-83.  Back to cited text no. 1
    
2.
Beck AM, Balknäs UN, Fürst P, Hasunen K, Jones L, Keller U, et al. Food and nutritional care in hospitals: How to prevent undernutrition – Report and guidelines from the Council of Europe. Clin Nutr 2001;20:455-60.  Back to cited text no. 2
    
3.
Nightingale F. Notes on Nursing: What it is and what it is not. London: Harrison and Sons; 1859.  Back to cited text no. 3
    
4.
Holder H. Starving amidst plenty: Malnutrition is still a problem. Br J Nurs 2009;18:1158.  Back to cited text no. 4
    
5.
Fiaccadori E, Regolisti G, Cabassi A. Specific nutritional problems in acute kidney injury, treated with non-dialysis and dialytic modalities. NDT Plus 2010;3:1-7.  Back to cited text no. 5
    
6.
Biolo G, Grimble G, Preiser JC, Leverve X, Jolliet P, Planas M, et al. Position paper of the ESICM Working Group on Nutrition and Metabolism. Metabolic basis of nutrition in intensive care unit patients: Ten critical questions. Intensive Care Med 2002;28:1512-20.  Back to cited text no. 6
    
7.
Casaer MP, Mesotten D, Schetz MR. Bench-to-bedside review: Metabolism and nutrition. Crit Care 2008;12:222.  Back to cited text no. 7
    
8.
Biolo G, Grimble G, Preiser JC, Leverve X, Jolliet P, Planas M, et al. Position paper of the ESICM Working Group on Nutrition and Metabolism. Metabolic basis of nutrition in intensive care unit patients: Ten critical questions. Intensive Care Med 2002;28:1512-20.  Back to cited text no. 8
    
9.
National Institute for Health and Care Excellence: Clinical Guidelines. London: National Institute for Health and Care Excellence (UK); 2006.  Back to cited text no. 9
    
10.
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.  Back to cited text no. 10
    




 

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