Acute kidney injury (AKI), the preferred nomenclature to replace acute renal failure (ARF), is defined as an abrupt and sustained decrease in renal function. The definition of AKI is interpreted broadly and encompasses different degrees of severity.(1) The three mechanisms of AKI are pre-renal (a pre-decline in renal blood flow), intrinsic (or tubular cell injury) and post–renal (or obstructive).
The majority of AKI in intensive care units (ICUs) is associated with pre-renal and intrinsic renal failure.(2) Often multifactorial, the condition can include sepsis, trauma, hypotension, contrast dye, medications and pre-existing chronic kidney disease (CKD). AKI is associated with crude mortality rates ranging 50% to 60%, with the majority of deaths occurring in the ICU. AKI may be treated with continuous renal replacement therapy (CRRT).(3)
Nutrition and Metabolic Considerations in AKI
During AKI, the physiologic and metabolic functions of the kidneys are disrupted, including excreting metabolic end-products, toxins, and drugs, maintaining acid-base balance, regulating fluids and electrolytes, as well as degrading proteins and converting amino acids. These disruptions can lead to fatal electrolyte imbalances and metabolic acidosis.
Malnutrition is common in AKI patients, aided by conditions such as anorexia, impaired protein metabolism and transport, oxidative stress, metabolic acidosis, or nutrient losses through the hemodiafilter and ileus. Moreover, nutritional and metabolic changes in these patients are the result of underlying conditions such as surgery, trauma, burns, organ failure, sepsis and other comorbidities.
Consequences of these metabolic derangements include the loss of body energy reserves (glycogen, protein and fat stores), azotemia, hyperglycemia, hypertriglyceridemia and electrolyte abnormalities (hyponatremia, hyperkalemia, hyperphosphatemia and hypermagnesemia). Metabolic intervention is vital in this patient population, and proper nutrition support is aimed at minimizing the effects of hypermetabolism and hypercatabolism and improving patient recovery.
CRRT in the Critically Ill
About 5% to 10% of ICU patients with AKI are treated with CRRT, the emerging therapy of choice for patients with severe AKI in some institutions. Potential advantages of CRRT include its ability to provide dialysis more physiologically, to enhance cytokine removal and to allow for more aggressive nutrition therapy. CRRT also is ideal for patients who are bedridden, acutely ill, hemodynamically unstable and/or intolerant of major fluid shifts. Increased cost and staffing requirements, as well as a general lack of dosing guidance and supporting evidence, are among the potential disadvantages. The therapeutic goals in CRRT include:
- Limiting further renal injury
- Supporting the patient until kidney function recovers
- Correcting azotemia and fluid, electrolyte, and acidbase abnormalities
- Preventing systemic complications
- Permitting nutrition and other supportive therapies to be provided with minimal limitation(2)
It is important to consider that these patients are highly catabolic and likely ill before the AKI diagnosis and that poor nutrition may affect treatment and outcome. Thus, nutritional goals during CRRT are to:
- Maintain or improve nutritional status without exacerbating metabolic derangements
- Enhance wound healing, support host defense and recovery
- Reduce morbidity and mortality rates
CRRT is an attractive option from a nutrition standpoint because it facilitates improved, continuous nutrition support (i.e., a full-protein diet, effective control of uremia and electrolytes) as well as acid base balance.
Although clinical research related to the metabolic implications of AKI and CRRT are still lacking, several key studies have helped guide therapy. Nutrition. Scheinkestel et al measured energy and protein needs in 50 critically ill patients requiring CRRT in order to assess compliance of actual feeding with target feeding, correlate predictive energy requirements with the actual energy expenditure and determine if feeding regimens affect outcome. Patients were given protein 2 g/kg/day for six days vs. protein 1.5, 2, 2.5 g /kg/day, escalated every two days. The authors found that nitrogen equilibrium was attained only at a protein dose of 2.5 g/kg/day, and the probability of survival increased by 21% (P =0.03) for each 1 g/day increase in nitrogen balance. The authors concluded that nitrogen balance was directly associated with hospital outcome (P=0.03) and ICU outcome (P=0.02), and that enteral feeding benefits patient outcome (P=0.04).(4)
Journal of Parenteral and Enteral Nutrition. Mirtallo et al conducted a prospective, randomized, double-blind, controlled trial to evaluate comparable concentrations of essential amino acid solution (EAA) and general amino acid solution (GAA) and to determine their effects on renal function and nutritional status. Twenty-one patients received GAA vs. 24 patients who received EAA. All patients also received parenteral nutrition (PN). The authors found that mortality rates, serum creatinine (Scr), blood urea nitrogen (BUN) and nitrogen balance were similar between the two groups, and that no difference was found between EAA vs. GAA protein formulations. The authors concluded that there was no advantage demonstrated in using EAA as the only protein component of PN, and that the combination of EAA/GAA should be used until positive data using EAA are established. This is the last published study on this topic to date.(5)
Journal of Parenteral and Enteral Nutrition. In a prospective, observational, randomized, controlled trial of 12 trauma patients, Klein et al attempted to quantify calcium, magnesium, zinc and nitrogen losses during CRRT vs. control. Patients received daily total parenteral nutrition (TPN) providing 30 kcal/kg/day and 1.5 g protein/kg/ day. The authors found that patients receiving CRRT lost 23.9 ± 3.1 mmol/day Mg and 69.8 ± 2.7 mmol/day Ca. Patients not receiving CRRT (not in AKI) lost 10.2 ± 1.2 mmol/ day and 2.9 ± 2.5 mmol/ day. These differences are both statically significant with P<0.01. The zinc intake also was greater than the loss in both groups (P<0.03). Nitrogen equilibrium was attained only at a protein dose of 2.5 g/kg/day. Survival rates improved for each 1 g/day increase in nitrogen balance. Scr excretion did not differ between groups. Magnesium was 0.75 ± 0.04 mmol/L for CRRT vs. 0.90 ± 0.03 mmol/L for control (P<0.01). Also, calcium was below normal in both groups, and ionized calcium below normal in the CRRT group. The authors concluded that the nutritional requirements for magnesium and calcium during CRRT were higher than presently provided amounts, and that CRRT necessitates administration of more magnesium and calcium than provided in standard PN. Furthermore, protein requirements are minimally altered, which indicates that protein intake does not need to be overly restricted during CRRT. Zinc requirements are lower or unchanged.(6)
Critical Care Medicine. The American Society for Parenteral and Enteral Nutrition (A.S.P.E.N.) and the Society of Critical Care Medicine recently published guidelines for nutrition support,(7) offering specific recommendations for this unique patient population including:
- Patients with renal disease should undergo formal nutrition assessment, including evaluation of inflammation, with development of a nutrition care plan.
- Standard amino acid PN formulations should be used in acute kidney injury.
- Patients with renal failure who require nutrition support therapy should receive enteral nutrition if intestinal function permits.
- Energy requirements in patients with renal disease should be evaluated using indirect calorimetry when possible. If indirect calorimetry is not possible, individualized assessment of energy intake goals (as with other nutrition support patients) is recommended.
- To promote positive nitrogen balance in patients with acute kidney injury, protein intake should be adjusted according to catabolic rate, renal function, and dialysis losses.
- Electrolyte intake in patients should be adjusted by monitoring serum concentrations of potassium, magnesium, phosphorus, and calcium.
Role of the Healthcare Provider
In managing nutrition support for patients with AKI and/ or receiving CRRT, members of the multiprofessional team should monitor electrolytes frequently, especially magnesium and calcium, and supplement intravenously as needed. Patient response to feeding should be assessed regularly and nutritional support altered quickly and appropriately to avoid complications and promote recovery. Healthcare providers should also be prepared to recognize signs and symptoms of nutritional toxicities and deficiencies and monitor mineral, protein and fluid intake while patients are beginning or weaning from CRRT, as therapy becomes intermittent, and in other therapy changes.
In conclusion, AKI is very common in the critically ill and more patients are receiving CRRT; the multiprofessional team can help recognize and meet these patients’ nutritional needs. Patients with AKI should receive a balanced mixture of both essential and non-essential amino acids. Though many questions remain unanswered regarding nutritional support in CRRT patients, data suggest they should receive at least 2 g /kg/day to 2.5 g /kg/day of protein. They also require close electrolyte and trace element monitoring and appropriate replacement.
1. Ostermann M, Chang RW. Acute kidney injury in the intensive care unit according to RIFLE. Crit Care Med. 2007; 35(8):1837-1843.
2. Wooley JA, Btaiche IF, Good KL. Metabolic and nutritional aspects of acute renal failure in critically ill patients requiring continuous renal replacement therapy. Nutr Clin Pract. 2005; 20(2):176-191.
3. Ympa YP, Sakr Y, Reinhart K, et al. Has mortality from acute renal failure decreased? A systematic review of the literature. Am J Med. 2005; 118(8):827-832.
4. Scheinkestel CD, Kar L, Marshall K, et al. Prospective randomized trial to assess caloric and protein needs of critically Ill, anuric, ventilated patients requiring continuous renal replacement therapy. Nutrition. 2003; 19(11-12):909-916.
5. Mirtallo JM, Schneider PJ, Mavko K, et al. A comparison of essential and general amino acid infusions in the nutritional support of patients with compromised renal function. JPEN J Parenter Enteral Nutr. 1982; 6(2):109-113.
6. Klein CJ, Moser-Veillon PB, Schweitzer A, et al. Magnesium, calcium, zinc, and nitrogen loss in trauma patients during continuous renal replacement therapy. JPEN J Parenter Enteral Nutr. 2002; 26(2):77-93.
7. Brown RO, Compher C; American Society for Parenteral and Enteral Nutrition Board of Directors. A.S.P.E.N. clinical guidelines: nutrition support in adult acute and chronic renal failure. JPEN J Parenter Enteral Nutr. 2010; 34(4):366-377.
The author has no disclosures to report.