|Year : 2019 | Volume
| Issue : 1 | Page : 28-31
Why is acute kidney injury more demanding in terms of nutritional support?
Consultant Nephrologist, Department of Nephrology, Lilavati Hospital, Mumbai, Maharashtra, India
|Date of Web Publication||15-Nov-2019|
Dr. Hemant Mehta
Department of Nephrology, Lilavati Hospital, Mumbai, Maharashtra
Source of Support: None, Conflict of Interest: None
Treatment for acute kidney injury (AKI) primarily relies on treating the underlying cause and maintaining the patient until kidney function has recovered. Enteral and parenteral nutrition are commonly used to treat nutritional disorders in AKI patients; however, their efficacy in treating AKI are still debated. This article focuses on nutritional requirements of patients with AKI.
Keywords: Acute kidney injury, nutrition, urea nitrogen appearance
|How to cite this article:|
Mehta H. Why is acute kidney injury more demanding in terms of nutritional support?. J Renal Nutr Metab 2019;5:28-31
|How to cite this URL:|
Mehta H. Why is acute kidney injury more demanding in terms of nutritional support?. J Renal Nutr Metab [serial online] 2019 [cited 2020 Jul 14];5:28-31. Available from: http://www.jrnm.in/text.asp?2019/5/1/28/271045
| Introduction|| |
Acute kidney injury (AKI) is a complex clinical disorder that is associated with severe morbidity and mortality. AKI is associated with complications such as uremia, metabolic abnormalities, bleeding, infections, and malnutrition. It is a syndrome caused by many different diseases and mechanisms. AKI is a complication in critically ill patients and has a persistently high mortality rate in hospitalized patients (40%–60%). International experts established the Acute Dialysis Quality Initiative (ADQI) and devised the RIFLE definition and staging system for AKI. Shortly after this, many of the original members of the ADQI group created the AKI Network (AKIN). The AKIN group modified the RIFLE staging system to refiect the clinical significance of relatively small rises in serum creatinine. Which was followed by yet another international guideline group, Kidney Disease: Improving Global Outcomes (KDIGO) has harmonized the previous definitions and staging systems proposed by both ADQI and AKIN.,,,,,
Over the past 30 years, the survival rate for AKI has not improved, primarily because affected patients are now older and have more comorbid conditions. Treatment for AKI primarily relies on treating the underlying cause and maintaining the patient until kidney function has recovered. Enteral and parenteral nutrition are commonly used to treat nutritional disorders in AKI patients; however, their efficacy in treating AKI is still debated. The optimal nutritional support in AKI still remains an open issue.
| Dietetic Classification of Acute Kidney Injury|| |
Although KDIGO has given definition and staging of AKI, from a nutritional point of view, patients can be divided into two groups:
- Patients with AKI in the noncatabolic state
- Patients with AKI in the catabolic state.
Urea nitrogen appearance (UNA) rate is a measure of net protein degradation in patients with renal failure. Accordingly, the patients are divided as Group I (no excess catabolism, UNA <6 g/day), Group II (moderate hypercatabolism, UNA 6–12 g/day), and Group III (severe hypercatabolism, UNA >12 g/day).
| Normal Energy Expenditure|| |
The human body should be seen as a metabolic engine that needs organic fuels. These fuels (lipids, carbohydrates, and proteins) are combusted in combination with oxygen and produce heat, kcal, and waste. The energy yield differs from 9.1 kcal/g for lipids, 4 kcal/g for protein, and 3.75 kcal/g for glucose., Normal nutritional requirements (daily energy expenditure) can be calculated by different formulas:
Basal energy expenditure (BEE)kcal/24 h
Men = 66 + (13.7 × weight) + (5.0 × height) – (6.7 × age)
Women = 655 + (9.6 × weight) + (1.8 × height) – (4.7 × age)
Resting energy expenditure = 1.2 × BEE
EE in critical illness – EE should always be measured, or calculated, and then corrected depending on the concomitant condition; in most cases, it does not exceed 1.3 × BEE, though it may reach 1.5–1.7 × BEE in some cases.
In practice, we use simplified computations – 25–35 kcal/kg ideal body weight (BW) (in AKI, the dry weight should be used as these patients are often hyperhydrated or have overt edema), depending on activity and stress (more than 40 kcal/kg/day are seldom used and are potentially dangerous).
Caloric requirements –70% from carbohydrates and 30% from fats.
Protein requirements –0.8–1.2 g/kg/day in normal metabolism and 1.2–1.7 (preferably 1.2–1.5) g/kg/day in hypercatabolism.
| Goals of Nutritional Support in Acute Kidney Injury|| |
- To prevent protein–energy wasting (PEW)
- To preserve lean body mass and nutritional status
- To avoid further metabolic derangements
- To avoid complications
- To improve wound healing
- To support immune function
- To minimize infiammation
- To improved antioxidant activity and endothelial function
- To reduce mortality.
| Nutritional Status in Acute Kidney Injury|| |
Owing to the presence of many interfering factors, such as acute illness, alterations in body water distribution, external fiuid balance derangements, etc., the evaluation of nutritional status can be difficult in AKI, especially if they are critically ill.
To better characterize the condition of lean body mass wasting and fat mass depletion occurring in AKI, the term “PEW” has been proposed, along with the recommendation to use four categories of diagnostic criteria: biochemical (such as albumin or prealbumin), BW loss, decreased muscle mass, and low energy and protein intakes.
Protein–energy wasting seems to be a frequent problem in acute kidney injury
Severe malnutrition, as defined by the subjective global assessment, can be observed in ~40% of patients with AKI in the intensive care unit (ICU). Many factors are likely to contribute PEW in these patients, including inadequate nutritional support, preexisting poor nutritional status, superimposed catabolic illnesses (sepsis, trauma, surgery, chemotherapy, etc.), acidosis, blood losses, nutrient losses during extracorporeal circulation, etc.; moreover, a key role is thought to be played by specific derangements in metabolic and hormonal pathways, leading to lean body mass catabolism.
Nutritional status is a major prognostic factor in the patients with AKI. Severe PEW severely impairs patient's outcome, whether defined in term of length of hospital stay, increased risk of complications (sepsis, bleeding, arrhythmia, respiratory failure, etc.), or increased in-hospital mortality.
Factors involved in the pathogenesis of protein catabolism in AKI after given in [Table 1].
|Table 1: Factors involved in the pathogenesis of protein catabolism in acute kidney injury|
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KDIGO guidelines for AKI, on glycemic control and nutritional support in AKI, recommend as follows:
- In critically ill patients, insulin therapy should target plasma glucose 110–149 mg/dl
- Achieve a total energy intake of 20–30 kcal/kg/d in patients with any stage of AKI
- Avoid restriction of protein intake with the aim of preventing or delaying initiation of renal replacement therapy (RRT)
- Administering 0.8–1.0 g/kg/d of protein in noncatabolic AKI patients without need for dialysis, 1.0–1.5 g/kg/d in patients with AKI on RRT, and up to a maximum of 1.7 g/kg/d in patients on continuous RRT (CRRT) and in hypercatabolic patients
- Providing nutrition preferentially via enteral route in patients with AKI.
In 2012, a review on nutritional support for AKI was published by “The Cochrane Collaboration.” The aim was to evaluate effectiveness and safety of nutritional support for patients with AKI. It explored the following potential sources of heterogeneity using subgroup analyses or meta-regression: intervention (essential amino acids [EAA], general amino acids, essential and nonessential amino acid, calories, nitrogen); total parenteral nutrition (TPN), enteral nutrition (EN), placebo, or no nutritional therapy; dose (nitrogen, amino acids, and calories); and patients in and out of ICU. The review concluded that there is no strong evidence to suggest that Essential L-amino acids (ELAA), high-calorie TPN, and high-dose amino acids or nitrogen and fat improves the survival and recovery from AKI in critically ill patients.
A prospective, multicenter, observational study using indirect calorimetry (IC) and protein catabolic rate (PCR) on critically ill patients was conducted to (a) evaluate the validity of conventional predictive formulas and equations for the calculation of energy expenditure and protein needs, by using IC and the normalized PCR as gold standards and (b) compare prescribed and actually received nutrients with estimated and measured needs. The study concluded that use of predictive equations and formulas in order to guide the nutritional approach is not accurate in critically ill patients with AKI in the ICU and should be discouraged. Whenever possible, critically ill patients with AKI should have their feeding regimen tailored by actual measurements of energy and protein needs.
| Nutrient Requirements in Acute Kidney Injury: Carbohydrates, Proteins, Lipids|| |
In patients with AKI, energy expenditure seems to depend more on the severity of the underlying disease, preexisting nutritional status, and acute/chronic comorbidities, than on the presence of the syndrome itself. The optimal protein intake of AKI patients is ill defined; as PCR in this clinical condition varies from 1.4 to 1.8 g/kg/day, an intake of at least 0.25 g of nitrogen/day is required to achieve less negative or nearly positive nitrogen balance.
With 2.5 g/kg/day of protein and 35 kcal/kg/day of energy, only one-third of patients achieved a positive nitrogen balance; in a cross-over study on AKI patients receiving an isocaloricregimen, in most cases through EN, nitrogen balance was positively related to protein intake, with a positive nitrogen balance being more likely to be obtained with intakes >2 g/kg/day (0.3 g nitrogen/kg/day). However, in many patients with AKI, hypercatabolism cannot simply be overcome by increasing protein or amino acid intake much above 0.25–0.3 g nitrogen/kg/day, even when energy intake is optimal. It is likely that above this level of nitrogen intake, any further increase contributes nothing to protein synthesis, simply increasing urea production. Both essential amino acids and non-essential amino acid are recommended in AKI, since a higher provision of EEA only does not appear to be advantageous. Nutritional support is able to significantly increase amino acid levels in AKI patients.
Protein and amino acid losses through the extracorporeal circulation of RRT can be quantified as ~0.2 g amino acids/l of ultrafiltrate (up to 10–15 g amino acids/day) and 5–10 g/day of protein; in order to compensate for these losses, especially when high-fiux filters and/or highly efficient modalities (such as CRRT or sustained low-efficiency dialysis) are used, the protein intake should be increased by ~0.2 g/kg/day. For relatively noncatabolic AKI patients with the milder nonoliguric forms of the syndrome not needing RRT and who are likely to regain renal function in a few days (drug toxicity, contrast nephropathy, etc.), lower protein intakes (up to 0.8 g/kg/day) will suffice for short periods of time, combined with adequate calorie intakes (30 kcal/kg/day).
| What's Optimum?|| |
The optimal energy to nitrogen ratio has not been clearly defined in patients with AKI. In an observational study of patients on CRRT, less negative or weakly positive nitrogen balance values were predicted by linear regression analysis models when protein intakes of 1.5 g/kg BW/day were provided in parallel with nonprotein energy intakes of ~25 kcal/kg BW/day; simply increasing the calorie to nitrogen ratio in this study was not invariably associated with better nitrogen balance. With a protein intake of 1.5 g/kg/day, an increase in energy provision up to 40 kcal/g/day did not improve nitrogen balance compared with lower energy intakes (30 kcal/kg/day); instead, more severe metabolic complications (hypertriglyceridemia and hyperglycemia) ensued.
| Lipids Supplements|| |
Lipids should represent ~30%–35% of total nonprotein energy supply. In the case of parenteral nutrition, this can be obtained by giving the patient 0.8–1.2 g/kg/day of lipid from 10% to 30% lipid emulsions or as a part of the commercially available three-in-one total nutrient admixtures. Lipids should be infused over 18–24 h, and serum triglycerides should be monitored, stopping lipid administration when triglycerides exceed 400 mg/dl. Even though the use of parenteral MCT may result theoretically in lower serum triglyceride levels because of faster oxidation rate, pharmacokinetic studies failed to show any clear advantages, in terms of plasma clearance of triglyceride, of the mixed medium chain triglycerides/long chain triglycerides (MCT/LCT) lipid formulas compared with LCT only emulsions. Lipid losses through the filters do not occur during hemodialysis or hemofiltration.
All patients should be screened for risk of malnutrition within 24 h of admission to ICU, having AKI.
Renal Association Guidelines for AKI (2011), have suggested the following audit measures specifically for AKI Stage 3:
- Proportion of patients with AKI receiving renal replacement therapy reviewed by dietitian within 24 h
- Proportion of patients with AKI receiving renal replacement therapy prescribed the recommended nutritional support.
Financial support and sponsorship
Confiicts of interest
There are no confiicts of interest.
| References|| |
Canaud B, Leray-Moragues H, Leblanc M, Klouche K, Vela C, Béraud JJ. Temporary vascular access for extracorporeal renal replacement therapies in acute renal failure patients. Kidney Int Suppl 1998;66:S142-50.
Storck M, Hartl WH, Zimmerer E, Inthorn D. Comparison of pump-driven and spontaneous continuous haemofiltration in postoperative acute renal failure. Lancet 1991;337:452-5.
Kanagasundaram NS, Greene T, Larive AB, Daugirdas JT, Depner TA, Garcia M, et al.
Prescribing an equilibrated intermittent hemodialysis dose in intensive care unit acute renal failure. Kidney Int 2003;64:2298-310.
Kelber J, Delmez JA, Windus DW. Factors affecting delivery of high-efficiency dialysis using temporary vascular access. Am J Kidney Dis 1993;22:24-9.
KDIGO clinical practice guideline for acute kidney injury. Kidney Int 2012;2.
Li Y, Tang X, Zhang J, Wu T. Nutritional support for acute kidney injury. Cochrane Database Syst Rev 2012;8:CD005426.
Sabatino A, Theilla M, Hellerman M, Singer P, Maggiore U, Barbagallo M, et al.
Energy and protein in critically ill patients with AKI: A Prospective, multicenter observational study using indirect calorimetry and protein catabolic rate. Nutrients 2017;9. pii: E802.
Ftouh S, Thomas M, Acute Kidney Injury Guideline Development Group. Acute kidney injury: Summary of NICE guidance. BMJ 2013;347:f4930.
Koza Y. Acute kidney injury: Current concepts and new insights. J Inj Violence Res 2016;8:58-62.
Lewington A, Kanagasundaram S. Renal association clinical practice guidelines on acute kidney injury. Nephron Clin Pract 2011;118 Suppl 1:c349-90.