1. Description of the problem

What every clinician needs to know

AKI is a systemic disease process affecting all physiologic functions and organ systems and exerts a profound impact on the morbidity and mortality of the critically ill patient. Within this context, AKI is a catabolic, pro-oxidative and inflammatory syndrome per se and in addition augments any inflammatory signal of non-renal sources, such as in pneumonia or sepsis. Thus, concomitant renal dysfunction alters the course of any underlying disease process. Moreover, all types of renal replacement therapy (RRT) induce a broad range of metabolic/nutritional consequences.

It must be noted that metabolic factors can play a crucial role in the prevention and therapy of AKI and nutrition support must present a mandatory element in the care of any critically ill patient with AKI.

Unfortunately, there are very few studies available in which the problem of metabolic/nutritional management of patients with AKI has been investigated systematically. As a result, many statements are based rather on the experience in nutritional support of critically ill patients in general and most recommendations present expert opinion only rather than being based on controlled studies.

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Clinical features

The complex systemic consequences of AKI together with RRT modalities have a profound impact on the metabolic environment. However, in the patient with AKI, metabolism is not only affected by acute renal dysfunction/RRT therapy:

Metabolic environment of a patient with AKI:

  • Acute kidney injury per se.

  • Acute disease process (acute phase reaction, SIRS).

  • Underlying disease process.

  • Associated complications (infections, sepsis).

  • AND the consequences of RRT.

Beyond volume overload and electrolyte derangements, AKI per se induces specific metabolic alterations:

  • Stimulation/augmentation of protein catabolism.

  • Insulin resistance.

  • Impairment of lipolysis.

  • Altered hormone secretion/action.

  • Hyperparathyroidism/inadequate vitamin D activation.

  • Altered potassium disposal (altered membrane ion transport).

  • Augmentation of formation of reactive oxygen species.

  • Augmentation of non-renal inflammation.

It must be noted that in addition renal replacement therapies (RRT) exert a profound impact on metabolism and nutrient balances:

Metabolic consequences of renal replacement therapies

Intermittent hemodialysis (HD)

Loss of water soluble molecules: amino acids, water soluble vitamins, L-carnitine, etc.

Activation of protein catabolism by: loss of amino acids, proteins and blood; induction of cytokine-release (TNF-a, etc.), which inhibits protein synthesis and increases ROS production.

The consequences of bioincompatiblity include: induction/activation of blood cells, coagulation, mediator-cascades of an inflammatory reaction

Continuous renal replacement therapies (CRRT)

Consequences include heat loss, excessive load of substrates (lactate, citrate, glucose, etc.), loss of nutrients (amino aciddes, vitamins, selenium etc.), loss of electrolytes (phosphate, magnesium), elimination of peptides/proteins (hormones, mediators, albumin). Consequences of bioincompatibility include induction/activation of (a) mediator-cascades, (b) inflammatory reaction, and (c) stimulation of protein catabolism.

2. Emergency Management


3. Diagnosis


4. Specific Treatment

Nutrition support in patients with AKI is not fundamentally different from that in other critically ill patients but has to take into account the specific metabolic alterations associated with AKI and has to be coordinated/ adapted to the type and intensity of renal replacement therapy (RRT).

Nutrient requirements

Nutrient requirements differ between individual patients but may also vary considerably during the course of disease (acute phase versus recovery phase). The recommendations on nutrient requirements are in accordance with those in other critically ill patients but must also consider the increased nutrient losses during RRT.

Energy intake should never exceed actual energy expenditure of the patient. Excess energy provision is associated with a broad pattern of well defined side effects and increases the risk of infections. Consider the energy intake associated with lactate or citrate content of substitution fluids/ anticoagulation.

Because of RRT associated nutrient losses, protein/amino acid intake should be as high as 1.7 g/kg b.w./day. Despite some controversial evidence intake should not exceed this limit.

Because of RRT associated losses, intake of water soluble vitamins should be higher than in other critically ill patients. The optimal intake of selenium remains to be defined.

Nutrient requirements in patients with AKI

Energy intake: 20-25 (max.30) kcal/kg b.w./day

Glucose: 3-5 g/kg b.w./day

Lipids: 0.8-1.2 (max. 1.5) g/kg b.w./day

Amino acids/protein:

conservative therapy 0.8-1.2 g/kg b.w./day + RRT 1.3-1.5 g/kg b.w./day

+ hypercatabolism (max. 1.7) g/kg b.w./day

Vitamins (combination products proving RDA):

Water-soluble 2 x RDA/ day

(Cave: Vitamin C <250 mg/day)

Lipid-soluble 1-2 x RDA/day

(higher for vitamin D? and E?)

Trace elements (combination products proving RDA):

1 x RDA/day

(higher for selenium >300µg/day?)

Electrolytes: requirements must be assessed individually.

(Cave: refeeding hypokalemia and/or hypophosphatemia)

RDA = recommended dietary allowances

Nutrition support in critically ill patients with AKI

Enteral diets

Clinical practice worldwide is to use standard high molecular enteral diets designed for critically ill patients in general also in subjects with AKI.

Alternatively, enteral diets designed for patients on chronic hemodialysis therapy (higher protein content, reduced electrolyte content, various additions such as carnitine and histidine) can also be used in patients with AKI (no proven benefits).

Whether enteral “immune-enhancing” diets containing specific immunomodulating substrates such as glutamine, selenium, fish-oil or nucleotides may exert advantages in critically ill patients with AKI remains to be demonstrated.

Parenteral solutions

Total nutritional admixtures containing all nutrients have become standard worldwide. Usually, the basic solution is provided by the pharmaceutical industry as a three chamber bag (containing the three macronutrients in each section) and must be completed by additions of vitamins, trace elements and electrolytes as required before use. Please note that the final solution must be complete and contain macronutrients (amino acids, glucose, lipid emulsion), micronutrients (water and lipid soluble vitamins, trace elements) and electrolytes.

In most patients such standardized solutions can be used. Custom designed solutions made by the hospital pharmacy may become necessary in the presence of severe metabolic derangement or severe hyperlipidemia, during concomitant high-dose propofol sedation (which is dissolved in a 10% lipid emulsion).

Specific parenteral “renal failure fluids” which have been used in earlier days of nutrition support are no longer recommended.

5. Disease monitoring, follow-up and disposition


Nutrition support should be viewed as an obligatory component in the care of any critically ill patients and thus also in those with AKI.

At what stage of AKI should nutrition support be adapted to the altered metabolism/ requirements for nutrients?

RIFLE stage R and I/AKIN stage I and II:

In these early stages of AKI preventive measures to avoid progression to a more severe stage are outmost importance and must also include metabolic/nutritional factors such as electrolyte balance, avoidance of hyperglycemia and prevention of malnutrition.

In this more advanced stage of AKI, RRT usually are employed early in order to minimize the systemic consequences of acute renal dysfunction, to maintain volume and electrolyte balances, and to support hemodynamic and respiratory management. In this stage of AKI the metabolic consequences of renal dysfunction plus the effects of RRT have to be considered.

Clinical practice of nutrition support in patients with AKI

Enteral nutrition

As in any other patient group enteral nutrition must present the first and most important route of nutrition support and should be initiated whenever possible.

Enteral nutrition should be initiated early (i.e. within 24 after admission/hemodynamic stabilization).

Buildup of enteral nutrition should be slow. Start with 20-30 ml/h to allow an adequate monitoring of nutrient utilization and to avoid the evolution of gastrointestinal/metabolic side effects.

However, in many patients with AKI the following obstacles to a quantitatively sufficient enteral nutrition may be present in addition to factors seen in other critically ill subjects:

  • Aggravation of impairment of GI-motility by renal dysfunction.

  • Aggravation of hyperglycemia (impairment of gastric emptying).

  • Hypertriglyceridemia (impairment of gastric emptying).

  • Volume overload – increase in abdominal pressure.

  • Altered absorption of nutrients.

If gastrointestinal tolerance to enteral nutrition is impaired prokinetics (early/even preventive) should be used to stimulate intestinal motility.

If intestinal motility cannot be restored by prokinetics alone consider the placement of a postpyloric (jejunal) tube (can also be placed in a reasonable time frame without endoscopy).

Even when a quantitatively sufficient enteral nutrition is not possible try to provide a minimal enteral nutrient supply (“trickle nutrition”; i.e. 50 ml of a high molecular diet 4-6 times/day).

Parenteral nutrition

Parenteral nutrition should be considered only when enteral nutrition is not or not quantitatively possible. However, as detailed above in many patients with AKI there are severe limitations to enteral nutrition so that a supplementary or even total parenteral nutrition can become necessary.

There have been conflicting results from recent studies regarding the optimal timing of parenteral nutrition. One should keep in mind that patients with AKI often have evidence of malnutrition (the severity of which is a major determinant of outcome) and in these patients there are pronounced persistent nutrient losses induced by RRT.

Therefore, many patients with ARF parenteral supplementation will require additional parenteral nutrient supplementation to achieve an adequate nutrient supply and avoid hospital acquired nutrient deficiencies.

Buildup of supplementary or total parenteral nutrition also should be slow. Start at a rate of about 50% of final infusion goal and increase infusion rate, observing an adequate monitoring during 3 days. Make sure that the total energy intake (enteral plus parenteral calories) never should exceed the recommended goal.


Tolerance to administered excessive volumes is impaired. Overhydration has been recognized recently as an important factor associated with outcome. In contrast to common belief, overhydration also impairs renal function. Careful fluid balance must be observed and any infusion of volume associated with nutrition support must be considered in the management of fluid removal by RRT.

Moreover, electrolyte imbalances are frequent in patients with AKI. It should be noted however, that not only an electrolyte excess but also deficiencies, especially in the case of phosphate and potassium, frequently are seen in these patients.

Metabolic complications frequently occur in patients with AKI because utilisation of essentially all nutrients is altered or impaired. An exaggerated protein or amino acid intake results in a high BUN (and waste product) level. Glucose intolerance and decreased fat clearance can cause hyperglycemia and hypertriglyceridemia, respectively.


Because of the limited tolerance to various nutrients and the high risk of inducing metabolic derangements in patients with AKI nutritional therapy requires a tighter schedule of monitoring than in other patient groups.

One reason for gradually increasing the infusion rate of nutrition solution is to allow monitoring and avoid evolution of side effects and complications associated with nutrition support.







Special considerations for nursing and allied health professionals.

Nutrition support in patients with AKI poses a specific challenge also for nursing staff. Because of the impairment of intestinal tolerance, gastrointestinal side effects of enteral nutrition are frequent. Moreover, the altered utilization of various nutritional substrates often causes electrolyte and metabolic derangements which require close monitoring of nutrition support by the nursing staff.

What's the evidence?

Cano, NJ, Aparicio, M, Brunori, G. “ESPEN Guidelines on Parenteral Nutrition: adult renal failure”. Clin Nutr. vol. 28. 2009. pp. 401-14..

Casaer, MP, Mesotten, D, Hermans, G. “Early versus late parenteral nutrition in critically ill adults”. N Engl J Med. vol. 365. pp. 506-17..

Druml, W. “Nutritional management of acute renal failure”. J Ren Nutr. vol. 15. 2005. pp. 63-70.

Druml, W, Mitch, W, RH, R. “Enteral nutrition in renal disease”. Clinical nutrition: Enteral and tube feeding. 2004.

Druml, W. “Metabolic aspects of continuous renal replacement therapies”. Kidney Int Suppl. 1999. pp. S56-61.

Fiaccadori, E, Lombardi, M, Leonardi, S, Rotelli, CF, Tortorella, G. “Prevalence and clinical outcome associated with preexisting malnutrition in acute renal failure: a prospective cohort study”. J Am Soc Nephrol. vol. 10. 1999. pp. 581-93..

Fiaccadori, E, Maggiore, U, Giacosa, R. “Enteral nutrition in patients with acute renal failure”. Kidney Int. vol. 65. 2004. pp. 999-1008..

Kalantar-Zadeh, K, Cano, NJ, Budde, K. “Diets and enteral supplements for improving outcomes in chronic kidney disease”. Nat Rev Nephrol. vol. 7. pp. 369-84..

Martindale, RG, McClave, SA, Vanek, VW. “Guidelines for the provision and assessment of nutrition support therapy in the adult critically ill patient: Society of Critical Care Medicine and American Society for Parenteral and Enteral Nutrition: Executive Summary”. Crit Care Med. vol. 37. 2009. pp. 1757-61..

Metnitz, GH, Fischer, M, Bartens, C, Steltzer, H, Lang, T. “Impact of acute renal failure on antioxidant status in multiple organ failure”. Acta Anaesthesiol Scand. vol. 44. 2000. pp. 236-40..