Abstract
Acute kidney injury (AKI) in critically ill children is frequently a component of the multiple organ failure syndrome. It occurs within the framework of the severe catabolic phase determined by critical illness and is intensified by metabolic derangements. Nutritional support is a must for these children to improve outcomes. Meeting the special nutritional needs of these children often requires nutritional supplementation by either the enteral or the parenteral route. Since critically ill children with AKI comprise a heterogeneous group of subjects with varying nutrient needs, nutritional requirements should be frequently reassessed, individualized and carefully integrated with renal replacement therapy. This article is a state-of-the-art review of nutrition in critically ill children with AKI.
Similar content being viewed by others
Introduction
Acute kidney injury (AKI) is common in pediatric intensive care unit (PICU) patients. The risk of protein-energy wasting is high in this patient group because of the metabolic derangements, the difficulties in nutrient requirement estimation, and the possible negative effects of AKI and renal replacement therapy (RRT) itself on nutrient balance [1–3]. No specific guidelines on nutritional support in PICU patients with AKI are currently available. Current evidence suggests that protein/energy debt, a widely accepted concept in the literature on adult ICU patients with negative implications for patients’ major outcomes, is also likely to develop in critically ill pediatric patients and that AKI represents a key factor for its development [1, 4, 5]. The nutritional management of these children is based on knowledge acquired from adult literature, concepts of alterations in nutrient utilization known to be present in AKI, and the limited data available on critically ill children without AKI.
This article is a state-of-the-art review on nutrition guidelines in critically ill children with AKI. The objectives of this review are: (1) to review the pathological mechanisms underlying protein-energy wasting in an AKI setting; (2) to understand the importance of nutrition in critically ill children with AKI; (3) to understand the nutritional challenges in treating a child with AKI in the PICU; (4) to review the methods of assessing nutritional status in a sick child; (5) to review the dietary requirements of a critically ill child with AKI (including those on RRT), including protein, energy, vitamins, and minerals; (6) to review the evidence for the benefit of enteral and intradialytic parenteral nutrition.
Protein-energy wasting in acute kidney injury: pathogenesis
“Protein-energy wasting” in children with AKI refers to the wasting of lean body mass and depletion of fat mass. This proposed concept is thought to be the result of multiple mechanisms, in addition to decreased nutrient intake in these children.
General factors
General factors which contribute to protein-energy wasting include factors related to the critical illness (sepsis, trauma), associated acute and chronic morbidities, pre-existing nutritional status. Metabolic acidosis and uremic state are additional factors leading to wasting.
Derangement in the hormonal and metabolic pathways in AKI
The neuroendocrine axis response to acute critical illness mediates hormonal and metabolic changes that favor hepatic shift away from anabolic metabolism towards acute phase proteins and altered fuel utilization. Table 1 shows the metabolic derangements which can occur in a pediatric patient with AKI. These derangements in protein, carbohydrate, and lipid metabolism lead to a general disruption in the “internal milieu” [1–3]. The disruption in metabolism is primarily due to increased catabolism of the skeletal muscle proteins, negative nitrogen balance and increased amino acid turnover, and insulin resistance, hyperglycemia, and altered lipid metabolism.
Nutritional status of a critically ill child with AKI
Of the children admitted to the ICU, more than 20 % have protein-energy wasting, and it is likely to worsen during the stay. Protein-energy wasting is an independent risk factor for poor outcomes and increased mortality risk; moreover, pediatric patients are highly dependent on nutrition due to their high anabolic drive and lower nutrient reserves as compared to adults. In critically ill children, nutritional support is often deferred until the patient is medically stable, which delays the provision of adequate nutrition due to fluid restriction, gut intolerance, and interruption of feed due to diagnostic and therapeutic procedures [1, 2].
Limited data are currently available on the nutritional status in children admitted to the PICU with AKI. Recent studies [one on patients not on RRT; another on children on continuous RRT (CRRT)] showed a high prevalence of acute and chronic malnutrition among this population. It is important to note that fluid overload might lead to underdiagnosis of protein-energy wasting [1, 2].
Multiple studies on critically ill children in the PICU confirm the high risk of protein/energy debt, especially in the first few days of the patient’s stay in the PICU, and protein debt appears to be the more common and important disorder [1, 4–6]. In their retrospective analysis of 167 critically ill children, Kyle et al. showed that underfeeding was accentuated in the children with AKI and that protein underfeeding was greater than energy underfeeding in the first 5 days of ICU stay [4]. On almost 87 % of the patient-days, <90 % of protein needs were met in all patients. These authors showed that <68 % of energy needs and <35 % of protein needs were covered by the current nutrition practices in the ICU [4]. Using prospective data collected on 174 children treated with CRRT, Castillo et al. showed that children with AKI who were malnourished had a higher mortality risk than well-nourished children (51 vs. 33 %, respectively; p = 0.03) and that protein-energy wasting was the only factor associated with mortality (odds ratio 2.11; 95 % confidence interval 1.067–4.173; p = 0.03) [5].
Challenges in treating a critically ill child with AKI
Treating a child with AKI in the ICU presents unique challenges.
Worsening of anthropometric variables and fluid overload
During the ICU stay and also after discharge, these children demonstrate a significant decline in anthropometric variables. Children in the ICU commonly develop fluid overload, making dry weight estimation difficult [1, 2, 7, 8]. During critical illness, anasarca may obscure the loss of lean tissue, which may only become apparent following resolution of edema when diuresis is successful. A reliable indicator of global loss of lean body mass and chronic malnutrition can be seen in the wasting of the interosseous and thenar muscles of the hand, which becomes apparent 2 or 3 weeks after hospitalization with the resolution of edema [7, 8].
Underfeeding, a common practice
These children are often underfed in the ICU, as they are medically unstable and do not tolerate oral feeds; in addition, the feeds are often interrupted due to various diagnostic and therapeutic procedures. Adequate nutritional support takes 4–5 days in the ICU, which places these children in further danger of starvation and underfeeding [1, 2, 7].
Baseline status
These children may have a poor baseline nutritional status due to associated chronic morbidity [9, 10].
Growth requirements
The requirement for continued nutritional support in these growing children is always important. The inverse relationship between energy expenditure and body weight leads to higher needs in younger children with lower body weight [11–14].
Losses during RRT
Renal replacement therapy leads to additional nutritional losses, requiring additional support, especially in terms of higher protein needs to account for the losses in dialysis.
Assessment of nutritional status
Assessment of the nutritional status is a very important part of the clinical evaluation in these children, but nutritional status is difficult to assess accurately and correct nutritional support is difficult to achieve. A comprehensive assessment should evaluate all available parameters with ongoing monitoring and serial measurements.
History
A careful medical history interview which takes into account previous weight gain, diet, recent illness, and medications can help a clinician in understanding the risk factors of undernutrition at the time of admission [1, 2, 7].
Anthropometry
A baseline height-for-age and weight-for-height of <10th percentile at the time of hospital admission may suggest poor baseline nutritional status. Weight at the time of hospital admission should be documented, but a history of pre-illness weight should be obtained since the critically ill child may present with fluid overload and weight gain [15].
Triceps skin-fold thickness and mid-arm circumference may be used in children when weight or age data are not reliable. Mid-arm circumference has been used as an age-independent criterion in malnourished children between the ages of 1 and 5 years and can be a helpful tool because it is not affected by altered fluid status as are other anthropometric parameters. Anthropometric assessments are extremely operator dependent and lack precision, with high intra- and inter-observer variability. However, they can be used at centers with extensive experience of making such measurements, preferably by the same member of staff [16, 17].
Clinical examination
A general physical examination, including examination of hair, skin, mouth, and extremities, with the focus on signs of malnutrition, specific vitamin, and mineral deficiencies should be conducted.
Thin hair, yellowish teeth lacking in enamel, a pale, furrowed tongue with scattered papillae on the surface, thin pale skin, occasionally in association with a bronze complexion, a smelly fishy breath, and loss of muscle mass are specific to severe cachexia. However, although important, these are all subjective diagnostic markers and should be considered late indicators of cachexia. Signs of edema or dehydration should be looked for in order to assess the hydration status. In acute wasting, hair changes are most evident at the root of the hair. The hairs are also sparse and easily pluckable. When nutrition status is regained, the root becomes pigmented, leading to a typical ‘flag-sign’.
Nutritional deficiencies of tyrosine, niacin, zinc, and vitamins may contribute to abnormalities of skin pigmentation. Glossitis, stomatitis, and cheilosis are due to underlying vitamin B complex deficiency. During the examination, the medical doctor should also look for rickets and examine the eyes for xerophthalmia and the nervous system for vitamin B6 and B12 deficiency.
Follow-up in the ICU: weight changes
Data on body weight are not always available in the pediatric ICU, and often the pediatric intensivist has to depend on pre-illness weight. Weight changes in the ICU should be interpreted in the context of fluid balance, which occur due to fluid overload, fluid administered, diuretics given to the child, and water losses. Bed scales, if available, can provide a useful estimate of daily weight changes.
A pre-existing chronic kidney disease
A detailed history and examination should be conducted to exclude an underlying chronic kidney disease (CDK) and its complications, especially anemia, growth retardation, and deformities due to mineral bone disease.
The presence of co-morbidities
A thorough search should be done to exclude other co-morbidities, especially serious underlying infections, such as tuberculosis, and other chronic disorders, such as hypertension and obesity.
Laboratory parameters
Various biochemical parameters have been proposed as markers of nutritional status, including serum albumin and total protein, pre-albumin, transferrin and creatinine levels, hemoglobin, total lymphocyte counts, cholesterol, triglycerides, and retinol binding protein. Relatively shorter half-life serum proteins, such as pre-albumin [half-life (t1/2) = 2–3 days] and transferrin (t1/2 = 8–9 days), also reflect nutrition status and respond more quickly to changes in anabolic state. However, none of these can be considered to be sufficiently sensitive or specific to be to be used as single diagnostic markers for protein-energy wasting.
Serum albumin may be considered a poor marker of nutrition but may be a useful marker of disease severity [18]. The 2006 International Society of Renal Nutrition and Metabolism (ISRNM) panel proposed that low serum albumin level be one of the criteria required to diagnose the complex clinical picture of protein-energy wasting in adults [19]. The presence of low serum albumin levels should suggest that a further evaluation of nutritional status is needed, also in children with CKD or on dialysis, unless it is caused by nephrotic proteinuria.
However, longitudinal determination of specific plasma proteins, including albumin, transferrin, and pre-albumin, may have some value in terms of assessing the response of patients to nutritional support. Serum protein levels frequently decrease during acute critical illness without reflecting any preceding malnutrition. This phenomenon occurs with capillary leak syndrome and is seen in the first hours following pediatric ICU admission in patients with sepsis, cardiopulmonary bypass operations, ischemia–reperfusion injury, and stresses.
Limited data on changes in growth hormone/insulin-like growth factor axis status in critically ill patients in the ICU are available for used in clinical practice [20–22].
Body composition and mass parameters
Bioelectrical impedance analysis (BIA), a noninvasive technique, has been proposed for measuring fat-free mass, total body water, percentage fat, body cell mass, intracellular water, and extracellular water. BIA and bioimpedance spectroscopy have both been proposed as tools to assess body composition in various patient populations, including children and adults, but have been mostly used in patients with CKD [23, 24]. A drawback of BIA is its inaccuracy in the presence of abnormalities in body fluid distribution: i.e., poor sensitivity to changes in fluid volume in the trunk compared with the limbs. In patients with an abnormal hydration status [such as children on peritoneal dialysis (PD)], it is often difficult to distinguish whether the changes in bioelectrical values are due to alterations in the amount of water or the amount of body cell mass. The little data on the use of BIA in children which have been published to date have far from demonstrated its true usefulness in identifying patients with protein-energy wasting. In addition, the major guidelines do not recommend it as an essential tool to assess nutritional status in CKD patients [23–27].
Dual energy X-ray absorptiometry scanning can be used to estimate fat mass, lean body mass, and bone mineral density. However, lean body mass assessment based on this type of scanning is often confounded by fluid overload in patients with CKD [28]. Thus, this tool should not be used for day-to-day assessment in critically ill children. More sophisticated tools for the measurement of body composition, such as neutron activation analysis, total body nitrogen, and total body potassium, are not practical for everyday clinical use [29, 30].
Table 2 shows the markers of nutritional status in a critically ill child in the PICU according to clinical, laboratory, and body mass and composition parameters.
Nutritional assessment using an assessment tool has been used in practice for children who are nutritionally at risk, facilitating early detection of subsequent nutrition deterioration and finally adequate therapy. Assessment tools consist of clinical assessment of nutritional status, including several steps with detailed medical and dietary history and physical examination, comprised of anthropometric, body composition measurement, and laboratory data. The process is lengthy and time-consuming, making it impossible to evaluate every child admitted to the hospital. Various assessment tools used in practice, especially for hospitalized children, include: the Subjective Global Nutritional Assessment in Children (SGNA) [31], the Paediatric Yorkhill Malnutrition Score (PYMS) [32], the Screening Tool for the Assessment of Malnutrition in Paediatrics (STAMP) [33], and the Screening Tool for Risk on Nutritional Status and Growth (STRONG-kids) [34].
Goals of nutrition
The primary goals of treating a critically ill child with AKI in the ICU are to ensure the energy and protein delivery to prevent protein energy wasting and to ensure optimal—and not only adequate—dialysis dose in patients requiring dialysis [1, 2, 7].
Factors affecting the estimate of energy provision
A child with AKI is hypercatabolic, with increased serum counter-regulatory hormones inducing insulin and growth hormone resistance. This state leads to further catabolism of endogenous stores of protein, carbohydrate, and fat in order to provide essential substrate intermediates and energy necessary to support the ongoing metabolic stress response. Failure to provide adequate energy during this phase may result in loss of critical lean body mass and may make existing malnutrition even worse [1–3]. On the other hand, critically ill children on dialysis who are sedated and mechanically ventilated may have a significant reduction in true energy expenditure due to multiple factors, including decreased activity, decreased insensible fluid losses, and absence of growth during the acute illness. These patients may in fact be at a higher risk of overfeeding when estimates of energy requirements are based on age-appropriate equations, which are actually developed for healthy children [1–3].
To account for dynamic alterations in energy metabolism during the critical illness course, resting energy expenditure (REE values) remain the only true guide for energy intake. Estimating energy expenditure needs based on standard equations has been shown to be inaccurate and can significantly underestimate or overestimate the REE in critically ill children [13, 35]. Such under/overestimates expose the critically ill child to potential underfeeding or overfeeding during the ICU stay, with significant morbidity associated with each scenario.
Literature data on energy intake in AKI
There is a paucity of literature on energy and protein provision in pediatric patients with AKI. A review of data in the Prospective Pediatric Continuous Renal Replacement Therapy Registry focused on current protein and caloric prescription practices for critically ill children and young adults diagnosed with AKI and undergoing CRRT. Data from 195 patients (median age 8.1 years, interquartile range 12.8 years) were analyzed. The authors of the study assessed prescribed protein intake and prescribed versus recommended energy intakes; REE was estimated using the Caldwell–Kennedy equation. A tendency to restrict protein in patients with AKI not on dialysis was documented (around 1 g/kg per day); however, after CRRT was started, protein intake was increased to approximately 1.3 (±1.5) g/kg per day, with a mean maximum protein prescription during CRRT of approximately 2.0 (±1.5) g/kg per day. The prescribed energy intake was 150 % of the estimated REE in many patients, suggesting an increased risk of overfeeding in this clinical setting [36].
The inadequacy of nutritional support in pediatric patients with AKI was also confirmed in another study which focused on comparing estimated needs [Schofield equation for energy and AmericanSociety of Enteral and Parenteral Nutrition (A.S.P.E.N.) recommendations for proteins] with actual nutrient intake in 167 patients (53 %; age <2 years) during the first 5 days of PICU stay. The relationships between severity of AKI and nutritional support adequacy were also evaluated. The results showed a high prevalence of underfeeding, with patients receiving on average <68 % of their estimated energy needs and <35 % of their estimated protein needs; by day 5 patients classified as I/F (injury/failure according to the RIFLE criterion) were significantly more likely to be underfed than patients with no AKI [4].
There is no evidence that intakes for children on dialysis [including PD and hemodialysis (HD)] should exceed those for normal children, although dietary energy intake may need to be reduced for children on PD to compensate for the energy derived from dialysate glucose, estimated at 8–12 kcal/kg/day [37, 38]. The estimated caloric load from a single 1.5–4.25 % glucose-based exchange can range from 50 to 300 kcal and can supply 30 % of the total daily energy intake of an adult patient undergoing PD [39]. Glucose balance during CRRT is dependent on the glucose concentration of the substitution fluid. Solutions designed for PD should no longer be used for CRRT because they promote excessive glucose uptake. Dialysate glucose concentrations should range between 1 and 2 g/dL to maintain a zero glucose balance.
Estimating energy needs
The gold standard to quantify energy needs in children and in adults is the measurement of actual energy consumption by indirect calorimetry [13, 35]. When large endotracheal tube leaks are present, alternative isotope methods may be used that are not affected by air leaks or the fraction of inspired oxygen (FiO2) [40, 41]. There are concerns regarding the validity of measuring REE in patients receiving CRRT. These concerns are related to bicarbonate fluxes that occur at the level of the HD membrane, namely, that the use of bicarbonate-based dialysis solutions may lead to “bicarbonate enrichment” in the patient, which converts to CO2, leading to a false elevation of expired CO2, with a consequent overestimation of REE [42, 43]. Suggested criteria for selecting pediatric patients who might benefit from indirect calorimetry in the PICU is provided in Table 3. It is important to remember that if indirect calorimetry is not feasible or available, energy provision may be based on published equations or normograms. A recent review comparing predictive equations in children with indirect calorimetry to measure energy expenditures reported a wide correlation. For ease of application, the Schofield equation is frequently used, with reasonable correlation (21–45 % of ICU children) to the measured expenditures by calorimetry. The Schofield equation can be calculated from the weight, height, and age of the patient. The product of this calculation can be initially used for prescribing nutritional supplements for energy support until adjustments based on measured energy expenditure (MEE) can be done [45].
Metabolic carts are available at institutions performing research, but these are often not available for widespread clinical use. The Vmax® Encore metabolic cart (Viasys Healthcare, Loma Linda, CA) has become one of the more frequently used systems in place of the Deltatrac metabolic monitor that is no longer manufactured. Current studies are evaluating the use of the ventilator-derived CO2 removal (VCO2) measurement, as measured through an existing ventilator adapted with a CO2 sensor or by stand-alone VCO2 monitors in-line to generate the MEE. This developing technology should improve access for the clinician to an accurate means of measuring and balancing the metabolic support of the ill child [46, 47]. It is also important to remember that as the phase of critical illness changes so do the energy requirements. It has also been demonstrated that early on in critical illness, a lower body metabolic rate is present. The REE calculated from predictive formulas does not need to be met fully on day 1 of the critical illness [48].
Normal range of REE in critically ill children
Reports of REE in critically ill children vary, with various authors reporting REE values as high as 25 % above the expected basal metabolic needs and others reporting no change in REE in critical illness or sepsis [49–52]. The range of mean REE values reported in critically ill pediatric patients has been between 35 and 65 kcal/kg per day (0.15 and 0.27 MJ/kg per day), owing to differences in severity of illness and patient populations. Since no data on REE in critically ill children with AKI are available, the REE values for a critically ill child in an ICU can be used in such settings.
Energy prescription
It has been suggested that a caloric intake of 20–30 % above the estimated requirement will provide adequate calories in most children with AKI without causing a significant risk of overfeeding and associated complications [53]. There is a close relationship between carbohydrate and protein metabolism. Excess carbohydrate loads may induce lipogenesis. Providing an adequate energy supply ensures that nitrogen does not get retained (unless the amino acid supply is adequate; conversely, an increased amino acid supply will not be useful if energy is limited) [54]. Thus, the energy provision should consist of approximately 20–25 % carbohydrates (with insulin if required). A tight glucose control is recommended, since insulin resistance is common in these children; in addition, there is strong evidence linking hyperglycemia with poor clinical outcomes.
Patients with AKI have an increased lipid oxidation rate and reduced glucose oxidation rate. Thus, due to increased lipid demands and limited stores, critically ill children are susceptible to a deficiency of essential fatty acids. Lipid supplementation, in the form of 20 % lipid emulsions, providing 30–40 % of total energy needs should be provided, as in other critically ill children, if they are unable to be enterally fed. The remainder of the energy needs should be provided by protein [53].
Protein
There are multiple hormonal changes in AKI due to the critical illness (including increased hepatic gluconeogenesis, relative insulin resistance, metabolic acidosis, reduced renal synthesis of amino acids, and elevated stress hormones). Protein turnover is highest in younger children and is associated with increased REE. High protein turnover involves the redistribution of amino acids from the skeletal muscle to the liver and other tissues involved in the inflammatory response. This hypercatabolic state leads to a high rate of urea nitrogen production (180–250 mg/kg per day) and a net negative nitrogen balance [1, 55].
Even critically ill children who do not have AKI have a negative nitrogen balance despite protein supplementation as high as 2.5 g/kg/day. The provision of sufficient dietary protein to optimize protein synthesis and the inflammatory response, as well as to preserve skeletal muscle mass, is the most important nutritional intervention in these critically ill children with AKI. It is difficult to maintain a positive nitrogen balance in these children, especially in the presence of RRT.
The recommendations issued by the A.S.P.E.N. suggest the following age-adjusted intakes for critically ill children in the PICU: 0–2 years, 2–3 g/kg per day; 2–13 years, 1.5–2 g/kg per day; 13–18 years, 1.5 g/kg per day. However, specific studies are needed to validate these recommendations in critically ill children with AKI, either on RRT or not. During RRT, 10–20 % of amino acid intake should be added to the diet to account for losses in the dialysate. It has been recommended that target serum urea nitrogen levels should fall in the range of 40–80 mg/dL as a guide to determine the adequacy of protein intake [44].
Clearance of amino acids in children on CRRT falls in the range of 20–40 ml/min/1.73 m2. Various pediatric studies have reported that glutamine losses during CRRT accounted for 25 % of all amino acid losses [1, 55–57].
In adults on HD, there is a loss of small water-soluble molecules and, thus, also of amino acids, which accounts for about 2 g/h dialysis session. Protein catabolism during dialysis is caused by amino acid losses; by the activation of protein breakdown, as mediated by the release of leukocyte-derived proteases and inflammatory mediators (tumor necrosis factor-alpha and interleukins) induced by blood membrane interactions; or by endotoxin. Usually, such protein catabolism will account for a loss of approximately 0.2 g/L filtrate and, depending on the filtered volume, will result in a total loss of 10–15 g amino acid per day, representing about 10–15 % of total amino acid intake. Amino acid losses during continuous hemofiltration and continuous HD are of a comparable magnitude. However, CRRTs are associated with protein loss, depending on the type of therapy and the membrane material used [58–61].
In children undergoing PD, protein intake must provide at least 100 % of the recommended nutrient intake plus provide for an allowance for both the replacement of transperitoneal losses and replacement of daily nitrogen losses in order to achieve a positive nitrogen balance. Only a few studies describe the optimal amount of protein for children on acute PD and HD, and current data do not include all age groups. Recommended protein intakes for children on PD should be generous [37, 38, 62].
Recommendations for protein in patients on acute PD and acute HD can be extrapolated from chronic dialysis. For chronic HD patients, the Kidney Disease Outcomes Quality Initiative (K/DOQI) recommends the recommended dietary allowance for age plus an increment of 0.4 g/kg/day to achieve positive nitrogen balance [63]. This recommendation is based on work done in adults on HD who failed to maintain nitrogen balance on 1.1 g protein/kg/day [64].
It is well recognized that infants and small children on PD can suffer excessive losses of both protein and sodium via PD. Current guidelines recommend an allowance for protein of 1.8 g/kg/day for the first 6 months of life, 1.5 g/kg/day for months 7–12, and 1.3 g/kg/day for 1–3 years, taking into account the dietary reference intakes and peritoneal losses [63].
Electrolytes
Complications of AKI, including hyperkalemia, hyponatremia, hypocalcemia, hyperphosphatemia, hypermagnesemia, and metabolic acidosis, require close monitoring and replacement, as necessary. Underlying etiologies, such as cystic dysplasia, may require sodium supplementation since these children are non-oliguric [65, 66]. The same can be said for all infants on PD therapy, many of whom can become salt depleted as a result of high ultrafiltration requirements, with subsequent severe clinical manifestations, such as hypotension [67].
Children treated with acute PD generally do not require potassium restriction in the diet if the dialysis prescription is adequate (after the first few cycles of PD). However, closer monitoring should be performed in the following patient groups: anuric patients, patients treated with angiontension-converting enzyme inhibitors, patients receiving potassium supplements, and children aged <2 years. Infants may be able to tolerate breast milk or regular infant formula.
Vitamins and trace elements
No published data are available on vitamin and trace element metabolism in a critically ill pediatric child with AKI. Deficiencies in water-soluble and fat-soluble vitamins and trace elements have been found in adults, with the exception of vitamin K [68].
Losses of water-soluble vitamins are likely in children managed by CRRT. Thus, serum water-soluable vitamin levels should be monitored in children receiving CRRT for prolonged periods to determine whether additional supplementation is required. As vitamin C has the potential to worsen renal injury (concern for oxalosis), it is recommended not to exceed 100 mg per day in patients not requiring CRRT; supplementation up to 200 mg per day (in adults) for patients requiring CRRT is allowed.
Tappy et al. evaluated the clearance of five trace elements—manganese, copper, selenium, chromium, and zinc—in 14 critically ill children receiving CRRT and found that prior to CRRT initiation approximately 50 % of the patients had low serum zinc levels and 25 % had low serum copper levels, whereas the serum levels of the other three trace elements were in the normal range [54]. Serum zinc and copper levels, however, are difficult to interpret owing to their association with other factors, such as serum albumin (zinc) and the presence of inflammation (copper and zinc). Most of the patients in this study had been receiving parenteral nutrition solutions with standard additional trace element pediatric preparations at the time of CRRT initiation; thus, the presence of normal serum selenium and chromium concentrations suggests that the prescribed supplementation was adequate. With respect to zinc, selenium, copper, manganese, and aluminum, extraordinary losses during CRRT are uncommon; consequently, any losses which do occur can usually be replaced with a standard multiple trace element preparation, with the exception of selenium, for which an additional 100 mcg/day (in adults) appears to be necessary to offset cumulative losses from CRRT [54]. Based on folate levels in the patients of the Tapy et al. study [54], it is possible that additional folate supplementation is needed in children who are receiving CRRT for prolonged periods. It has been suggested that the recommended daily allowances should be provided and that water-soluble vitamin, trace element and folate levels be strictly monitored in children receiving prolonged RRT [57, 69].
In patients on PD, the blood concentrations of only a few water-soluble vitamins (C, B6, folic acid) have been reported to be low due to a combination of inadequate intake, increased transperitoneal losses, and increased needs [70, 71]. Supplements of these vitamins should also be provided to children. There are no reported specific micronutrient requirements for children on acute PD and HD, and 100 % of the recommended nutrient intake can be considered to be the goal for these children.
Specific aspects
Phosphorus and magnesium
Due to very efficient removal of small molecular weight substances, patients undergoing CRRT or intermittent extended daily dialysis are at increased risk of hypophosphatemia, which is to be carefully monitored during RRT. Hypophosphatemia can be prevented by timely and adequate phosphate supplementation. By the same mechanism, patients are also likely to be at increased risk of magnesium depletion [1].
Glutamine
Glutamine has been studied extensively in humans and is best known for its cell protective effects through modulation of insulin resistance during stress, induction of heat shock proteins, and enhancement of chaperone proteins. Glutamine also has a specific role in attenuating the oxidative stress in renal tubular cells and downregulating inflammatory pathways. There are large losses of glutamine in the ultrafiltrate of CRRT, which would suggest that replacement is indicated, depending on its availability, when employing this type of dialysis [1, 72, 73].
Omega-3 fatty acids
Animal models of ischemia–reperfusion injury have demonstrated a protective effect of docosahexenoic acid, an omega-3 polyunsaturated fatty acid from fish oil, by decreasing polymorphonuclear leukocyte recruitment and cytokine levels in the kidney, while enhancing anti-inflammatory proteins [1, 72, 73] There is clearly a paucity of literature in the field of immuno-nutrition and other elements in humans with AKI. More research is needed in the field of immuno-nutrition to warrant its use in clinical practice.
Route and timing of nutritional support
Once energy expenditure and requirement in a critically ill child with AKI have been calculated, the next major step is to select the appropriate route and start nutritional support. If feasible, the enteral route should always be preferred over the parenteral route. Enteral feeding has been shown to promote gut mucosal integrity, restore immune responses, reduce catabolic activity, and prevent gut atrophy. There is also emerging data showing the favorable effect of enteral nutrition on the phenotype of lymphocytes in the gut mucosa. The enteral route also reduces the added risk of nosocomial infection, as compared to using the parenteral route, and is, moreover, cost-effective. There are no systematic studies on route or timing of nutritional supplementation in these pediatric patients [1–3, 6, 7, 44, 74].
At the present time most centers would start enteral nutrition within 48–72 h of patient admission. Recent studies have confirmed the benefits of using enteral and parenteral nutrition in a complementary manner as opposed to an exclusive manner, with experts recommending the combined approach if energy intake targets are not met after 3–5 days; this is especially relevant to AKI patients receiving RRT [1–3, 6, 7, 44].
Insufficient data are available to recommend the appropriate site (gastric vs. post-pyloric/ transpyloric) for enteral feeding in critically ill children. Post-pyloric or transpyloric feeds may improve caloric intake when compared to gastric feeds. Post-pyloric feeding may be considered in children at high risk of aspiration or in those who have failed a trial of gastric feeding. Post-pyloric or transpyloric feeding may be limited by the ability to obtain small bowel access, as well as by the expertise and resources in individual PICUs.
Intradialytic parenteral nutrition (IDPN) has the advantage of providing proteins and calories to patients during HD without the need for a separate central venous catheter. The carbohydrate content prevents protein catabolism rather than just meeting caloric needs. Numerous studies of adults have demonstrated the efficacy of this method [75, 76]. There are only four studies of IDPN during chronic HD in children, so it is difficult to draw conclusions about its effectiveness and, moreover, these studies were done in children on maintenance HD. In these studies the weight of patients did improve, which might help in long-term improvement of outcomes [76–78]. Table 4 shows the suggested nutritional guidelines for feeding critically ill children with AKI.
Conclusions
Protein-energy wasting is common in children with AKI and is a major negative prognostic factor for mortality. A protein/energy debt (i.e., a negative cumulative balance of macronutrients) is likely to occur in PICU patients, especially during the first days of the PICU stay, thereby worsening nutritional status and patient prognosis. Nutritional support (as in parenteral and/or enteral nutrition) is often required in this clinical setting. The main targets of nutritional support in children with AKI are very similar to those of critically ill children with normal renal function, but with additional nutrient repletion of losses from RRT. The enteral route is the preferred initial route for nutrient delivery in patients with AKI, although it is often necessary to combine enteral and parenteral nutrition to reach nutritional targets. Nutritional requirements should be frequently reassessed on a regular basis by a registered dietitian. Nutrition needs can differ widely between patients, as well as in the same patient during different phases of the critical illness. Patients with renal failure require an individualized approach in nutrition support. Due to the altered metabolism of many nutrients and intolerances for electrolytes and volume, the nutrition support in pediatric patients with AKI requires much closer monitoring to avoid under/overfeeding and to exploit the potential pharmacologic benefits of nutrients. Multidisciplinary efforts by physicians, dieticians, psychologists, nurses, and parents are needed in an attempt to optimize every aspect of care. Such a common effort alone could prevent children from losing muscle mass and protein stores and thus allow for reduced morbidity and a better quality of life.
Summary points
-
“Protein-energy wasting” in children with AKI is a result of multiple mechanisms, including derangement in hormonal and metabolic pathways.
-
There is a high risk of protein/energy debt in critically ill children, especially during the first few days of the ICU stay.
-
It is important to assess nutritional status in all critically ill children with AKI.
-
The gold standard to quantify energy needs in children and in adults is the measurement of actual energy consumption by indirect calorimetry. For ease of application, the Schofield equation is frequently used, with reasonable correlation.
-
For protein intake, the A.S.P.E.N. guidelines for critically ill children may be followed, with added allowances for children on RRT.
-
Special attention should also be made for the electrolyte and micronutrient requirements in these children.
Questions (answers are provided following the reference list)
-
1.
All of the following are metabolic derangements in AKI except:
-
a.
increased secretion of catabolic hormones
-
b.
decreased secretion of anabolic hormones
-
c.
reduced peripheral lipoprotein lipase
-
d.
increased hepatic triglyceride levels.
-
2.
Which of the following statements about markers of nutritional status in AKI is false?
-
a.
anthropometric variables may be interfered with by the fluid status of the critically ill child
-
b.
laboratory markers such as albumin and transferrin are negative markers of inflammation
-
c.
body composition parameters are always helpful in the clinical setting of AKI
-
d.
limited data are available on growth hormone/insulin-like growth factor axis changes in critically ill patients in the ICU to be used in clinical practice.
-
3.
Which of the following statements is true about energy needs in critically ill children?
-
a.
the gold standard to quantify energy needs in children and in adults is the measurement of actual energy consumption by indirect calorimetry
-
b.
resting energy expenditure calculations in patients receiving continuous RRT are always reliable
-
c.
the Schofield equation should not be used in children as it has no correlation with indirect calorimetry
-
d.
The Schofield equation can be calculated from the weight, mid-arm circumference, and age.
-
4.
Which of the following statements is true about protein losses in dialysis?
-
a.
in a pediatric study, glutamine losses during CRRT accounted for 25 % of all amino acid losses
-
b.
during RRT, there is no need to account for protein losses in the dialysate
-
c.
clearance of amino acids in children on CRRT is in the range of 60–100 ml/min/1.73 m2
-
d.
AKI is a state of low protein turnover.
-
5.
Which of the following statement is not true?
-
a.
for children receiving CRRT for prolonged periods, serum levels of water soluble vitamins should be monitored, and additional supplementation may be required
-
b.
additional folate supplementation is needed in children who are receiving CRRT for prolonged periods
-
c.
for children on acute PD and HD, 100 % of the recommended nutrient intake of micronutrients can be considered the target
-
d.
there is evidence to prove that all patients on CRRT should receive glutamine supplements.
References
Sabatino A, Regolisti G, Maggiore U, Fiaccadori E (2014) Protein/energy debt in critically ill children in the pediatric intensive care unit: acute kidney injury as a major risk factor. J Ren Nutr 24:209–218
Fiaccadori E, Parenti E, Maggiore U (2008) Nutritional support in acute kidney injury. J Nephrol 21:645–656
Fiaccadori E, Cremaschi E (2009) Nutritional assessment and support in acute kidney injury. Curr Opin Crit Care 15:474–480
Kyle UG, Akcan-Arikan A, Orellana RA, Coss-Bu J (2013) Nutritional support among critically ill children with AKI. Clin J Am Soc Nephrol 8:568–574
Castillo A, Santiago MJ, López-Herce J, Montoro S, López J, Bustinza A, Moral R, Bellón JM (2012) Nutritional status and clinical outcome of children on continuous renal replacement therapy: a prospective observational study. BMC Nephrol 13:125
Silva FM, Bermudes AC, Maneschy IR, Zanatta Gde A, Feferbaum R, Carvalho WB, Tannuri U, Delgado AF (2013) Impact of early enteral nutrition therapy on morbimortality reduction in a pediatric intensive care unit: a systematic review. Rev Assoc Med Bras 59:563–570
McCarthy MS, Phipps SC (2014) Special nutrition challenges: current approach to acute kidney injury. Nutr Clin Pract 29:56–62
Hulst JM, van Goudoever JB, Zimmermann LJ, Tibboel D, Joosten KF (2006) The role of initial monitoring of routine biochemical nutritional markers in critically ill children. J Nutr Biochem 17:57–62
Akcan-Arikan A, Zappitelli M, Loftis LL, Washburn KK, Jefferson LS, Goldstein SL (2007) Modified RIFLE criteria in critically ill children with acute kidney injury. Kidney Int 71:1028–1035
Vazquez Martinez JL, Martinez-Romillo PD, Diez Sebastian J, Ruza Tarrio F (2004) Predicted versus measured energy expenditure by continuous, online indirect calorimetry in ventilated, critically ill children during the early postinjury period. Pediatr Crit Care Med 5:19–27
Franz M, Hörl WH (1997) Protein catabolism in acute renal failure. Miner Electrolyte Metab 23:189–193
Coss-Bu JA, Jefferson LS, Walding D, David Y, Smith EO, Klish WJ (1998) Resting energy expenditure in children in a pediatric intensive care unit: comparison of Harris-Benedict and Talbot predictions with indirect calorimetry values. Am J Clin Nutr 67:74–80
Coss-Bu JA, Jefferson LS, Walding D, David Y, Smith EO, Klish WJ (1998) Resting energy expenditure and nitrogen balance in critically ill pediatric patients on mechanical ventilation. Nutrition 14:649–652
Coss-Bu JA, Klish WJ, Walding D, Stein F, Smith EO, Jefferson LS (2001) Energy metabolism, nitrogen balance, and substrate utilization in critically ill children. Am J Clin Nutr 74:664–669
Bettler J, Roberts KE (2000) Nutrition assessment of the critically ill child. AACN Clin Issues 11:498–506
National Kidney Foundation Kidney Disease Quality Outcome Initiative (K/DOQI) (2009) Clinical practice guideline for nutrition in children with CKD: 2008 update. Am J Kidney Dis 53[Suppl 2]:S1–S123
World Health Organization (2015) Management of severe malnutrition. World Health Organization, Geneva, Switzerland. Available at: http://www.who.int/nutrition/publications/severemalnutrition/9789241598163_eng.pdf. Accessed 15 Dec 2015
Friedman AN, Fadem SZ (2010) Reassessment of albumin as a nutritional marker in kidney disease. J Am Soc Nephrol 21:223–230
Fouque D, Kalantar-Zadeh K, Kopple J, Cano N, Chauveau P, Cuppari L, Franch H, Guarnieri G, Ikizler TA, Kaysen G, Lindholm B, Massy Z, Mitch W, Pineda E, Stenvinkel P, Trevinho-Becerra A, Wanner C (2008) A proposed nomenclature and diagnostic criteria for protein-energy wasting in acute and chronic kidney disease. Kidney Int 73:391–398
Bartz S, Mody A, Hornik C, Bain J, Muehlbauer M, Kiyimba T, Kiboneka E, Stevens R, Bartlett J, St Peter JV, Newgard CB, Freemark M (2014) Severe acute malnutrition in childhood: hormonal and metabolic status at presentation, response to treatment, and predictors of mortality. J Clin Endocrinol Metab 99:2128–2137
Schuetz P, Müller B, Nusbaumer C, Wieland M, Christ-Crain M (2009) Circulating levels of GH predict mortality and complement prognostic scores in critically ill medical patients. Eur J Endocrinol 160:157–163
Balcells J, Moreno A, Audí L, Roqueta J, Iglesias J, Carrascosa A (2001) Growth hormone/insulin-like growth factors axis in children undergoing cardiac surgery. Crit Care Med 29:1234–1238
Schaefer F, Georgi M, Zieger A, Scharer K (1994) Usefulness of bioelectric impedance and skinfold measurements in predicting fatfree mass derived from total body potassium in children. Pediatr Res 35:617–624
Wuhl E, Fusch C, Scharer K, Mehls O, Schaefer F (1996) Assessment of total body water in paediatric patients on dialysis. Nephrol Dial Transplant 111:75–80
Woodrow G (2009) Body composition analysis techniques in the aged adult: indications and limitations. Curr Opin Clin Nutr Metab Care 12:8–14
Woodrow G (2011) Volume status in peritoneal dialysis. Perit Dial Int 31[Suppl 2]:S77–S82
Piers LS, Soares MJ, Frandsen SL, O’Dea K (2000) Indirect estimates of body composition are useful for groups but unreliable in individuals. Int J Obes Relat Metab Disord 24:1145–1152
Rees L, Shaw V (2007) Nutrition in children with CRF and on dialysis. Pediatr Nephrol 22:1689–1702
Shypailo RJ, Ellis KJ (2011) Whole body counter calibration using Monte Carlo modeling with an array of phantom sizes based on national anthropometric reference data. Phys Med Biol 56:2979–2997
Manning EM, Shenkin A (1995) Nutritional assessment in the critically ill. Crit Care Clin 11:603–634
Secker DJ, Jeejeebhoy KN (2007) Subjective global nutritional assessment for children. Am J Clin Nutr 85:1083–1089
Gerasimidis K, Macleod I, Maclean A, Buchanan E, McGrogan P, Swinbank I, McAuley M, Wright CM, Flynn DM (2011) Performance of the novel Paediatric Yorkhill Malnutrition Score (PYMS) in hospital practice. Clin Nutr 30:430–435
McCarthy H, Dixon M, Crabtree I, Eaton-Evans MJ, McNulty H (2012) The development and evaluation of the Screening Tool for the Assessment of Malnutrition in Paediatrics (STAMP ©) for use by healthcare staff. J Hum Nutr Diet 25:311–318
Hulst JM, Zwart H, Hop WC, Joosten KFM (2010) Dutch national survey to test the STRONGkids nutritional risk screening tool in hospitalized children. Clin Nutr 29:106–111
White MS, Shepherd RW, McEniery JA (2000) Energy expenditure in 100 ventilated, critically ill children: Improving the accuracy of predictive equations. Crit Care Med 28:2307–2312
Zappitelli M, Goldstein SL, Symons JM, Somers MJ, Baum MA, Brophy PD, Blowey D, Fortenberry JD, Chua AN, Flores FX, Benfield MR, Alexander SR, Askenazi D, Hackbarth R, Bunchman TE, Prospective Pediatric Continuous Renal Replacement Therapy Registry Group (2008) Protein and calorie prescription for children and young adults receiving continuous renal replacement therapy: a report from the prospective pediatric continuous renal replacement therapy registry group. Crit Care Med 36:3239–3245
Salusky I, Fine RN, Nelson P, Blumenkrantz MJ, Kopple JD (1983) Nutritional status of children undergoing CAPD. Am J Clin Nutr 38:599–611
Edefonti A, Picca M, Damiani B, Loi S, Ghio L, Giani M, Consalvo G, Grassi G (1999) Dietary prescription based on estimated nitrogen balance during peritoneal dialysis. Pediatr Nephrol 13:253–258
Grodstein GP, Blumenkrantz MJ, Kopple JD, Moran JK, Coburn JW (1981) Glucose absorption during continuous ambulatory peritoneal dialysis. Kidney Int 19:564–567
Garza JJ, Shew SB, Keshen TH, Dzakovic A, Jahoor F, Jaksic T (2002) Energy expenditure in ill premature neonates. J Pediatr Surg 37:289–293
Shew SB, Beckett PR, Keshen TH, Jahoor F, Jaksic T (2000) Validation of a [13C]bicarbonate tracer technique to measure neonatal energy expenditure. Pediatr Res 47:787–791
AARC clinical practice guideline (1994) Metabolic measurement using indirect calorimetry during mechanical ventilation. American association for respiratory care. Respir Care 39:1170–1175
Ruzicka J, Novak I, Rokyta R, Matejovic M, Hadravsky M, Nalos M, Sramek V (2001) Effects of ultrafiltration, dialysis, and temperature on gas exchange during hemodiafiltration: a laboratory experiment. Artif Organs 25:961–966
Mehta NM, Compher C, A.S.P.E.N. Board of Directors (2009) A.S.P.E.N. Clinical Guidelines: nutrition support of the critically ill child. JPEN J Parenter Enteral Nutr 33:260–276
Carpenter A, Pencharz P, Mouzaki M (2015) Accurate estimation of energy requirements of young patients. J Pediatr Gastroenterol Nutr 60:4–10
Mehta NM, Smallwood CD, Joosten KF, Hulst JM, Tasker RC, Duggan CP (2015) Accuracy of a simplified equation for energy expenditure based on bedside volumetric carbon dioxide elimination measurement-a two center study. Clin Nutr 34:151–155
Kerklaan D, Augustus ME, Hulst JM, Rosmalen J, Verbruggen SC, Joosten KF (2016) Validation of ventilator-derived VCO2 measurements to determine energy expenditure in ventilated critically ill children. Clin Nutr. doi:10.1016/j.clnu.2016.01.001
Meyer R, Kulinskaya E, Briassoulis G, Taylor RM, Cooper M, Pathan N, Habibi P (2012) The challenge of developing a new predictive formula to estimate energy requirements in ventilated critically ill children. Nutr Clin Pract 27:669–676
Verhoeven JJ, Hazelzet JA, van der Voort E, Joosten KF (1998) Comparison of measured and predicted energy expenditure in mechanically ventilated children. Intensive Care Med 24:464–468
Joosten KF, Verhoeven JJ, Hazelzet JA (1999) Energy expenditure and substrate utilization in mechanically ventilated children. Nutrition 15:444–448
Briassoulis G, Venkataraman S, Thompson AE (2000) Energy expenditure in critically ill children. Crit Care Med 28:1166–1172
Turi RA, Petros AJ, Eaton S, Fasoli L, Powis M, Basu R, Spitz L, Pierro A (2001) Energy metabolism of infants and children with systemic inflammatory response syndrome and sepsis. Ann Surg 233:581–587
Agus MS, Jaksic T (2002) Nutritional support of the critically ill child. Curr Opin Pediatr 14:470–481
Tappy L, Schwarz JM, Schneiter P, Cayeux C, Revelly JP, Fagerquist CK, Jéquier E, Chioléro R (1998) Effects of isoenergetic glucose-based or lipid-based parenteral nutrition on glucose metabolism, de novo lipogenesis, and respiratory gas exchanges in critically ill patients. Crit Care Med 26:860–867
Butler BA (1991) Nutritional management of catabolic acute renal failure requiring renal replacement therapy. ANNA J 18:247–254, 257–259
Kuttnig M, Zobel G, Ring E, Grubbauer HM, Kurz R (1991) Nitrogen and amino acid balance during total parenteral nutrition and continuous arteriovenous hemofiltration in critically ill anuric children. Child Nephrol Urol 11:74–78
Zappitelli M, Juarez M, Castillo L, Coss-Bu J, Goldstein SL (2009) Continuous renal replacement therapy amino acid, trace metal and folate clearance in critically ill children. Intensive Care Med 35:698–706
Yoon JW, Pahl MV, Vaziri ND (2007) Spontaneous leukocyte activation and oxygen-free radical generation in end-stage renal disease. Kidney Int 71:167–172
Druml W (1999) Metabolic aspects of continuous renal replacement therapies. Kidney Int Suppl 72:S56–S61
Mokrzycki MH, Kaplan AA (1996) Protein losses in continuous renal replacement therapies. J Am Soc Nephrol 7:2259–2263
Morgera S, Slowinski T, Melzer C, Sobottke V, Vargas-Hein O, Volk T, Zuckermann-Becker H, Wegner B, Müller JM, Baumann G, Kox WJ, Bellomo R, Neumayer HH (2004) Renal replacement therapy with high-cutoff hemofilters: Impact of convection and diffusion on cytokine clearances and protein status. Am J Kidney Dis 43:444–453
Quan A, Baum M (1996) Protein losses in children on continuous cycler peritoneal dialysis. Pediatr Nephrol 10:728–731
National Kidney Foundation (2000) Kidney Disease Outcomes Quality Initiative (K/DOQI) Clinical practice guidelines for nutrition in CRF. Am J Kidney Dis 35[Suppl 2]:S1–S40
Slomowitz LA, Monteon FJ, Grosvenor M, Laidlaw SA, Kopple JD (1989) Effect of energy intake on nutritional status in maintenance hemodialysis patients. Kidney Int 35:704–711
Wassner SJ, Kulin HE (1990) Diminished linear growth associated with chronic salt depletion. Clin Pediatr 29:719–721
Parekh RS, Flynn JT, Smoyer WE, Milne JL, Kershaw DB, Bunchman TE, Sedman AB (2001) Improved growth in young children with severe chronic renal insufficiency who use specified nutritional therapy. J Am Soc Nephrol 12:2418–2426
Paulson WD, Bock GH, Nelson AP, Moxey-Mims MM, Crim LM (1989) Hyponatremia in the very young chronic peritoneal dialysis patient. Am J Kidney Dis 14:196–199
Druml W, Schwarzenhofer M, Apsner R, Horl WH (1998) Fat-soluble vitamins in patients with acute renal failure. Miner Electrolyte Metab 24:220–226
Pasko D, Churchwell M, Btaiche I, Jain J, Mueller B (2009) Continuous venovenous hemodiafiltration trace element clearance in pediatric patients: a case series. Pediatric Nephrol 24:807–813
Kriley M, Warady BA (1991) Vitamin status of pediatric patients receiving long-term peritoneal dialysis. Am J Clin Nutr 53:1476–1479
Warady, Kriley M, Alon U, Hellerstein S (1994) Vitamin status in infants receiving long-term peritoneal dialysis. Pediatr Nephrol 8:354–356
Honoré PM, De Waele E, Jacobs R, Mattens S, Rose T, Joannes-Boyau O, De Regt J, Verfaillie L, Van Gorp V, Boer W (2013) Nutritional and metabolic alterations during continuous renal replacement therapy. Blood Purif 35:279–284
Berg A, Norberg A, Martling CR, Gamrin L, Rooyackers O, Wernerman J (2007) Glutamine kinetics during intravenous glutamine supplementation in ICU patients on continuous renal replacement therapy. Intensive Care Med 33:660–666
Fivez T, Kerklaan D, Mesotten D, Verbruggen S, Wouters PJ, Vanhorebeek I, Debaveye Y, Vlasselaers D, Desmet L, Casaer MP, Garcia Guerra G, Hanot J, Joffe A, Tibboel D, Joosten K, Van den Berghe G (2016) Early versus late parenteral nutrition in critically Ill children. N Engl J Med 24:1111–1122
Korzets A, Azoulay O, Chagnac A, Weinstein T, Avraham Z, Ori Y, Zevin D, Gafter U (1999) Successful intradialytic parenteral nutrition after abdominal “catastrophes” in chronically hemodialysed patients. J Ren Nutr 9:206–213
Smolle KH, Kaufmann P, Holzer H, Druml W (1995) Intradialytic parenteral nutrition in malnourished patients on chronic haemodialysis therapy. Nephrol Dial Transplant 10:1411–1416
Goldstein SL, Baronette S, Gambrell TV, Currier H, Brewer ED (2002) nPCR assessment and IDPN treatment of malnutrition in pediatric hemodialysis patients. Pediatr Nephrol 17:531–534
Orellana P, Juarez-Congelosi M, Goldstein SL (2005) Intradialytic parenteral nutrition treatment and biochemical marker assessment for malnutrition in adolescent maintenance hemodialysis patients. J Ren Nutr 15:312–317
Acknowledgments
We acknowledge the help provided by Dr. Reema Gulati (MD, Division-Director, Pediatric Gastroenterology, Metrohealth Drive, Cleveland, USA) and Victoria Vitale (MS, RD, LD., Pediatric Clinical Dietitian, Akron Children’s Hospital, Cleveland, USA) for reviewing this manuscript.
Author information
Authors and Affiliations
Corresponding author
Ethics declarations
Conflict of interest
None
Additional information
Answers
1. d; 2. c; 3 a; 4. a; 5. d
Rights and permissions
About this article
Cite this article
Sethi, S.K., Maxvold, N., Bunchman, T. et al. Nutritional management in the critically ill child with acute kidney injury: a review. Pediatr Nephrol 32, 589–601 (2017). https://doi.org/10.1007/s00467-016-3402-9
Received:
Revised:
Accepted:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s00467-016-3402-9