You are on page 1of 8

ORIGINAL RESEARCH

Protein Feeding in Pediatric Acute Kidney


Injury Is Not Associated With a Delay
in Renal Recovery
Ursula G. Kyle, MS, RD/LD,* Ayse Akcan-Arikan, MD,*, Jaime C. Silva, MD,*
Michelle Goldsworthy, MSN,* Lara S. Shekerdemian, MD,* and Jorge A. Coss-Bu, MD*

Objective: Critically ill children with acute kidney injury (AKI) are at high risk of underfeeding. Newer guidelines for nutrition support
recommend higher protein intake. Therefore, the study evaluated the effects of protein feeding on the resolution of AKI and compared
energy and protein intake in patients with and without AKI after implementation of Nutrition Support guidelines.
Design: Retrospective study.
Subjects: Five hundred twenty critically ill children from October 2012 to June 2013 and October to December 2013.
Main Outcome Measure: Energy and protein intake in patients with no AKI, resolved, or persistent AKI. Energy and protein intake was
documented for days 1-8 of Pediatric Intensive Care Unit stay and in the postimplementation versus preimplementation period of nutri-
tion support guidelines. AKI was defined by modified pRIFLE. Persistent AKI was defined as patients who did not resolve their AKI during
the study period.
Results: A higher percentage of patients with resolved and persistent AKI met $ 80% of protein needs versus no AKI. After adjustment
for Pediatric Risk of Mortality Score, the odds ratio for protein intake of $ 80% compared to ,80% of estimated protein needs was not
significant, which suggests that higher protein intake was not associated with nonresolution of AKI. There were significant improvements
in the cumulative protein gap in patients with no AKI in the postimplementation (21.0 [21.7 to 20.6] g/kg/day) compared to preimple-
mentation period (21.3 [21.7 to 20.9] g/kg/day, P 5 .001) and persistent AKI in the postimplementation (20.8 [21.4 to 20.1] g/kg/day)
compared to preimplementation (21.3 [21.7 to 20.9] g/kg/day, P 5 .03).
Conclusions: Higher protein intake was not associated with a delay in renal recovery in patients with AKI after adjustment for severity
of illness. Protein intake was improved in critically ill children with no AKI, resolved, and persistent AKI after implementation of Nutrition
Support Guidelines, but underfeeding persisted in these patients.
2016 by the National Kidney Foundation, Inc. All rights reserved.

Introduction their Pediatric Intensive Care Unit (PICU) stay,6 and this

H OSPITAL UNDERNUTRITION IS a known risk


factor for morbidity and mortality in children, ado-
lescents, and adults,1-3 and malnutrition has been shown to
may contribute to worse outcome.
Acute kidney injury (AKI) occurs in 10% of all PICU ad-
missions and in up to 3/4 of patients with cardiorespiratory
adversely affect patient outcome. In addition, suboptimal failure.7 The risk of acute and chronic malnutrition is high
nutrient provision contributes to the deterioration of in patients with AKI, and the presence of malnutrition
nutritional status and has been shown to increase the risk in the context of AKI has been associated with more
of multiorgan failure, length of stay (LOS), and severe clinical deterioration and organ dysfunction.8-11
mortality.4,5 Critically ill children are underfed early in Derangements in substrate metabolism and body
composition12 as a result of physiological changes due to
AKI can lead to hypercatabolism,13 hypoalbuminemia,
*
Section of Critical Care Medicine, Department of Pediatrics, Baylor College
loss of lean body mass, and depletion of adipose tissue,
of Medicine/Texas Childrens Hospital, Houston, Texas. even with adequate ingestion of nutrients.14 Maintenance

Section of Nephrology, Department of Pediatrics, Baylor College of Medicine/ of protein balance in such conditions requires that at least
Texas Childrens Hospital, Houston, Texas. adequate energy and protein intake be provided during
Financial Disclosure: All authors of this research have no conflict of interest to acute illness.
declare related with employment, consultancies, stock ownership, honoraria, and
grants or funding.
Nutrition support is often deferred in critically ill chil-
Support: See Acknowledgments on page XXX. dren, until they are medically stabilized, which delays
Address correspondence to Jorge A. Coss-Bu, MD, Section of Critical Care adequate nutrition support for several days due to fluid re-
Medicine, Department of Pediatrics, Baylor College of Medicine/Texas Chil- striction, digestive intolerance, and interruption of feeding
drens Hospital, 6621 Fannin WT6-006, Houston, TX 77030. E-mail: for diagnostic and therapeutic procedures.15 Pediatric pa-
jorgec@bcm.edu, jacossbu@texaschildrens.org
2016 by the National Kidney Foundation, Inc. All rights reserved.
tients are highly dependent on nutritional support due to
1051-2276/$36.00 their intrinsic high anabolic drive and lower nutrient re-
http://dx.doi.org/10.1053/j.jrn.2016.09.009 serves, when compared to adults. AKI patients are at higher

Journal of Renal Nutrition, Vol -, No - (-), 2016: pp 1-8 1


2 KYLE ET AL

risk due to fluid restriction and concerns about protein Control growth charts29 for children ,2 and $2 years,
loading leading to worsening uremia. In fact, due to the respectively. Severity of illness was assessed on the day of
catabolic nature of the illness associated with AKI, it is admission with the Pediatric Risk of Mortality Score
now suggested that standard recommendations for energy (PRISM III)30,31 and organ dysfunction with the
and protein are appropriate for intensive care patients Pediatric Logistic Organ Dysfunction score (PELOD).32,33
with AKI.16-18 Nutrition Support Guidelines were Estimated energy and protein needs were determined ac-
developed and implemented for Texas Childrens PICU cording to the Schofield prediction equation (basal meta-
because of previous reports6,19-21 of underprescription bolic rate)34 (without correction factors) and American
and underdelivery of nutrition support among critically ill Society for Parenteral and Enteral Nutrition guidelines
children, including patients with AKI.22 for critically ill children,35 respectively (protein recommen-
There is evidence that increased protein provision might dations 0-2 years: 2-3 g/kg; 2-13 years: 1.5-2 g/kg;
protect the kidney from ischemic injury and may preserve .13 years: 1.5 g/kg).
glomerular filtration rate in critical illness23 and may lead Enteral, parenteral nutrition, and IV-glucose containing
to faster recovery from severe AKI.24-26 Studies linking solutions were collected. For enteral nutrition, enteral for-
achievement of protein requirements to outcome are mula provided and the volume given for each 24 hours was
lacking in children with AKI. The purpose of this study collected for each day. For IV and parenteral nutrition, the
was to evaluate the effect of protein feeding on the volume and concentration of all IV fluids were collected.
resolution of AKI and to compare energy and protein Continuous renal replacement therapy (CRRT) fluids
intake in AKI compared to no AKI patients after were not included in the calorie and protein calculations.
implementation of Nutrition Support Guidelines. The actual energy and protein intakes were calculated in a
spreadsheet for each 24 hours for the first 8 days or until
Subjects and Methods oral intake was initiated. The cumulative gap or deficit
Five hundred ninety patients aged 0-18 years admitted to was defined as the differences between actual energy
the Texas Childrens Hospital PICU for .48 hours be- (kcal/kg/day) or protein (g/kg/day) intake minus recom-
tween October 2012-June 2013 (preimplementation) and mended intake based on Schofield equation3 or American
October-December 2013 (postimplementation) were Society for Parenteral and Enteral Nutrition guidelines,4
eligible. Patients were excluded if they were admitted to respectively, for the time the patients remained in the
the PICU more than 72 hours after hospital admission PICU.
(n 5 51), had more than one PICU admission (n 5 18), In July and August 2013, the Texas Childrens Hospital
or had a diagnosis of end-stage renal disease, requiring renal Nutrition Support Team implemented Nutrition Support
replacement therapy or had received a kidney transplant Guidelines to improve feeding practices in our PICU.
(n 5 10). The implementation of Nutrition Support Guidelines con-
Data collected included age, sex, height, admission sisted of a 45-minute training session for all PICU clinical
weight, admission diagnosis, duration of mechanical venti- practitioners as well as written guidelines, made available
lation, medications, intravenous (IV) fluids, duration of on the hospital intranet. The changes in energy and protein
time in PICU and hospital LOS, severity of illness, and sur- intakes were also evaluated in the postimplementation
vival. Recumbent length of children younger than compared to preimplementation of Nutrition Support
24 months was measured using a length board. For patients Guidelines. In order to assess the effects of the energy and
who were unable to stand due to severity of illness, knee/ protein intake on the resolution of AKI, a cutoff of $
heel measurements were obtained by using knee/heel cal- 80% was used.
ipers and converted to height using the previously validated The study was approved by the Baylor College of Med-
formulas.27 Weight was obtained with digital scales (hoist if icine Institutional Review Board, with a waiver of consent.
nonambulatory; Scaletronix Inc, Wheaton, IL) and digital
infant scales. Statistics
Patients were classified as AKI, and further stratified as Continuous variables were classified as normally or non-
risk (R), injury (I), and failure (F) by pRIFLE creatinine normally distributed based on an analysis of frequency dis-
criteria.7 Urine output data were not available. Resolution tribution graph. Normally distributed continuous
of AKI was defined as any stage of AKI present during the variables, reported as mean (standard deviation), were
period of observation and subsequently transitioning to no compared using paired and unpaired t test. Nonnormally
AKI. Persistent AKI was defined as patients who did not distributed variables were expressed as median with inter-
resolve their AKI during the first 8 days of PICU stay. quartile ranges. For dependent samples, Wilcoxon Signed
Weight wasting (moderate/severe) was defined as Rank tests and for independent samples Mann-Whitney
weight-for-height $ 22 z-scores and height stunting U nonparametric tests were performed. Pearsons chi-
(moderate/severe) as height-for-age $ 22 z-scores, using square or Fishers exact test was used for independent obser-
World Health Organization28 and 2000 Center for Disease vations to determine differences between groups of
PROTEIN FEEDING IN CHILDREN WITH AKI 3

categorical variables. Odds ratios with 95% confidence in-


terval were determined by simple and multiple logistic
regression models.
Statistical significance was established a priori P , .05.
Statistical analysis was performed with Statview version
5.0.1 (SAS Institute Inc, Inc, Cary, NC).

Results
One hundred fifty-six of 511 patients (30%) had AKI
(Table 1). Of the AKI patients, 72% of patients had R,
19% had I, and 9% had F. AKI burden was highest on day
2 with 15% (79) of patients classified as AKI, which Figure 1. Incidence of risk (R), injury (I), or failure (F) in critically
ill children by admission day to the Pediatric Critical Care Unit,
decreased to 6% (30) of patients by day 8 (Fig. 1). Nine pa- as determined by modified pRIFLE (Akcan-Arikan, 2007).
tients received CRRTat sometime during the first 8 days of
PICU stay.
Patients with AKI were significantly shorter and weighed P 5 .41) did not have a higher incidence of AKI during
less than no AKI patients. Weight-for-age and weight-for- the PICU stay. In patients with persistent AKI during the
height z-scores were not significantly different. However, observation period, there was a significant association
height-for-age z-scores were significantly lower in AKI with moderate/severe height stunting, PRISM score $
compared to non-AKI patients (Table 1), which suggests 11, PELOD score $ 20, PICU LOS $ 10 days, hospital
that they had more height stunting or chronic malnutrition. LOS $ 20 days, and decreased survival compared to pa-
There were no significant differences in diagnostic cate- tients with no AKI (Table 2).
gories between no AKI and AKI patients, with 46% and Median energy and protein intake was less than recom-
42% having a respiratory diagnosis, 20% and 25% sepsis/ mended in the first 8 days of PICU stay in all patient
septic shock/infection, 6% and 10% cancer, 6% and 5% groups (Table 3). Patients with no AKI, resolved AKI,
seizure disorders, respectively. AKI patients had higher and persistent AKI received 73%, 80%, and 80% of rec-
PELOD and PRISM scores and longer PICU and hospital ommended energy needs, but only 39%, 42%, and 51%
LOS than no AKI (Table 1). of protein needs, respectively. There was no significant
AKI resolved after 1 (1-2.5) days (median [interquartile difference in energy and protein intake between patients
range]) in 72% (n 5 112) of patients. Patients with persis- with resolved and persistent AKI. The energy gap be-
tent AKI (n 5 44/156) had a median duration of AKI of tween the patients with resolved and persistent was signif-
4.5 (2.5-6) days of the first 8 days of PICU stay. Patients icantly smaller AKI compared to no AKI. In addition, the
with chronic disease (AKI 55.8%, no AKI 44.2%, protein gap between patients with persistent versus no
P 5 .41) versus acute disease (AKI 44.2%, no AKI 48.1%, AKI was also significantly smaller. However, the protein

Table 1. Characteristics of Patients Without and With Acute Kidney Injury (AKI)
Basic Characteristics No AKI AKI P

Gender (male/female) % (n) 54.6/45.4 (194/161) 57.1/42.9 (89/67) .615*


AKI (R/I/F) % (n) 72.4/18.6/9.0 (113/29/14)
Age (y) 1.5 (0.4-6.2) 1.2 (0.2-5.8) .100
Height (cm) 81.0 (64.1-116.7) 76.3 (58.0-109.5) .023
Height-for-age z-score 20.34 (2.0) 20.86 (2.3) .009
Weight (kg) 11.0 (6.6-21.3) 9.3 (4.8-20.9) .049
Weight-for-age z-score 20.47 (1.75) 20.72 (1.99) .157
Weight-for-height z-score 20.22 (1.7) 20.0 (2.00) .253
PELOD score 11 (1-11) 11 (2-12) .010
PRISM score 4 (1-8) 7 (3-12.5) ,.001
PICU length of stay (d) 5 (4-9) 7 (3.5-12) ,.002
Hospital length of stay (d) 11 (8-19) 15 (10-24) ,.003
Survival (survived/died) % (n) 95.8/4.2 (340/15) 91.7/8.3 (143/13) .060*
F, failure; I, injury; R, risk; PELOD, Pediatric Logic Organ Dysfunction Score, score 0-71; PICU, Pediatric Critical Care Unit; PRISM, Pediatric
Risk of Mortality score, score 1-76 points; SD, standard deviation.
Median (25-75th percentile) or mean 6 SD; AKI versus non-AKI.
*Chi-square.
Median (25-75th percentile) MannWhitney rank test.
Mean 6 SD, unpaired t test.
4 KYLE ET AL

Table 2. Odds Ratio (OR) in Patients With Resolved and Persistent Acute Kidney Injury (AKI) Compared To No AKI
Basic Characteristics % (n) % (n) OR (CI) P

Weight wasting No/mild Moderate/severe


No AKI 87.0 (309) 13.0 (46) 1
AKI resolved 92.0 (103) 9.0 (9) 0.6 (0.3-1.2) .428
AKI persistent 77.3 (34) 22.7 (10) 1.9 (0.9-4.3) .083
Height stunting No/mild Moderate/severe
No AKI 82.0 (291) 18.0 (64) 1
AKI resolved 78.6 (88) 21.4 (24) 1.2 (0.7-2.1) .422
AKI persistent 65.9 (29) 34.1 (15) 2.4 (1.2-4.6) .014
PRISM score ,10 $11
No AKI 84.0 (274) 16.0 (52) 1
AKI resolved 77.8 (74) 28.2 (29) 2.1 (1.2-3.5) .050
AKI persistent 55.5 (24) 41.5 (17) 3.7 (1.9-7.4) ,.001
PELOD score ,20 $21
No AKI 86.7 (281) 13.3 (43) 1
AKI resolved 83.0 (83) 17.0 (17) 1.1 (0.5-2.2) .351
AKI persistent 65.9 (27) 34.1 (14) 3.3 (1.1-9.4) ,.001
PICU LOS (d) ,10 $10
No AKI 76.9 (273) 23.1 (55) 1
AKI resolved 69.6 (78) 30.4 (34) 1.5 (0.9-2.3) .651
AKI persistent 52.3 (3) 47.7 (21) 3.0 (1.6-5.8) ,.001
Hospital LOS (d) ,15 $15
No AKI 64.5 (229) 35.5 (126) 1
AKI resolved 53.6 (60) 46.4 (52) 1.6 (1.0-2.4) .039
AKI persistent 38.6 (17) 61.4 (27) 2.9 (1.5-5.5) .001
Survival Alive Died
No AKI 95.8 (340) 4.2 (15) 1
AKI resolved 96.8 (105) 6.2 (7) 1.5 (0.6-3.8) .381
AKI persistent 86.4 (38) 13.6 (6) 3.6 (1.3-9.8) .013
CI, confidence interval; LOS, length of hospital stay; PELOD, pediatric logistic organ dysfunction; PICU, Pediatric Critical Care Unit; PRISM,
Pediatric Risk of Mortality Score.
Moderate/severe stunting: height-for-age .2 z-scores below normal, 2000 CDC growth charts; moderate/severe wasting: weight of height .2
z-scores below normal.

and energy gaps were not significant between patients tion period. For the period of observation, there were sig-
with resolved and persistent AKI. nificant improvements in the cumulative protein gap in
Patients (n 5 9) who required CRRT during the PICU patients with no AKI and persistent AKI, but not in the cu-
stay received 64.1% (16.6-80.5) of recommended energy mulative energy gap in the postimplementation compared
needs and 49.8% (10.1-86.3) of recommended protein to preimplementation period for any of the patient groups
needs compared to patients (n 5 147) with AKI without (Table 5). Furthermore, significantly more patients
CRRT: 80.8% (56.6-112.0, P 5 .06) and 43.3% (23.3- received $ 80% compared to ,80% of protein in the post-
67.9, P 5 .91), respectively. Patients with AKI requiring implementation compared to preimplementation period:
CRRT were sicker than those without AKI as shown by no AKI patients: 16% versus 9%, P 5 .045; persistent
higher PRISM and PELOD scores and longer PICU and AKI: 38% versus 11%, P 5 .045; and resolved AKI: 24%
hospital LOS. Energy and protein provided by CRRT versus 14%, P 5 .232. Thus, in general, the actual energy
was not included in the calculations. and protein intakes were improved in all patient groups after
A higher percentage of patients with resolved and persis- implementation of Nutrition Support Guidelines. For all
tent AKI met $ 80% of protein needs than patients with no patients, there were significant improvements in the actual
AKI (Table 4). However, after adjustment for PRISM protein, percentage of protein intake of recommended
score, the odds ratio for protein intake of $ 80 compared needs and protein gap in the postimplementation compared
to ,80% of estimated protein needs was not significant, to preimplementation period.
which suggests that higher protein intake was not associated
with nonresolution of AKI. Discussion
There were significant differences in the actual energy The cumulative energy and protein gap in patients with
and protein intakes in the postimplementation compared persistent AKI and the energy gap in patients with resolved
to preimplementation period (Table 5) in all groups, except AKI were significantly lower than in patients with no AKI;
in patients with persistent AKI, which suggests that patients and the actual protein intake, although not significant, was
with persistent AKI were better fed in the postimplementa- higher in resolved and persistent AKI than no AKI. A
PROTEIN FEEDING IN CHILDREN WITH AKI 5

Table 3. Recommended and Actual Energy and Protein Intake and Gap in Patients With No Acute Kidney Injury (AKI) and With
Resolved and Persistent AKI in the First 8 Days of PICU Stay
AKI Persistent
Basic Characteristics No AKI (n 5 355) AKI Resolved (n 5 112) P* (n 5 44) P P

BMR kcal/kg/d 51.2 (43.0-57.7) 48.9 (41.8-54.1) 49.2 (37.6-56.1)


Actual energy intake kcal/kg/d 35.7 (21.6-50.5) 41.3 (24.2-53.4) .18 38.9 (24.0-54.1) .46 .98
% BMR 73.1 (50.2-100.3) 80.0 (52.0-110.6) .05 79.8 (57.2-119.3) .11 .82
Cumulative energy gap kcal/kg/d 213.0 (224.2 to 0.1) 29.5 (220.0-4.8) .02 26.9 (219.1 to 8.9) .05 .66
Recommended protein intake g/kg/d 2.5 (1.8-2.5) 2.5 (1.8-2.5) 2.5 (1.8-2.5)
Actual protein intake g/kg/d 0.81 (0.4-1.3) 0.96 (0.4-1.4) .29 1.02 (0.5-1.9) .04 .20
% protein needs 39.0 (19.0-62.6) 42.4 (21.2-64.8) .54 51.3 (25.6-82.8) .07 .17
Cumulative protein gap g/kg/d 21.3 (21.8 to 20.8) 21.3 (21.6 to 0.8) .47 21.1 (21.6 to 20.4) .04 .15
BMR, basal metabolic rate, estimated by Schofield; IQR, interquartile range; PICU, Pediatric Critical Care Unit.
Energy or protein gap 5 actual minus recommended intake; MannWhitney test.
Values are median (IQR).
*AKI resolved versus no AKI.
AKI persistent versus no AKI.
AKI persistent versus resolved.
Wilcoxon Signed Rank test between actual and recommended energy and protein intake, P , .05.

higher percentage of patients with AKI met $ 80% of pro- and underprescription of energy and protein. They also had
tein needs. However, protein intake $ 80% of estimated longer PICU and hospital LOS and lower survival.
needs, after adjustment for severity of illness, was not signif- Overall, energy and protein intake did not reach the feeding
icantly associated with persistent AKI. This suggests that goals. Mehta et al.36 reported an association between higher
higher protein intake was not associated with a delay in protein intake (.60% of prescribed) and lower mortality.
renal recovery in patients with AKI. Overall, there was a The current study suggests that higher protein intake was
significant improvement in the protein intake in the post- not associated with a delay in renal recovery in patients with
implementation period. AKI. These two studies suggest that protein intake of at least
It is well known that children with chronic disease are half of recommended intake may have had beneficial effects
more likely to have chronic malnutrition/stunting without associated negative outcome. Prospective random-
(height-for-age z-score). Although patients with chronic ized studies are necessary to determine the benefits of higher
disease did not have a higher incidence of AKI during protein intake in critically ill children with and without AKI.
PICU stay, patients with AKI had lower height-for-age z- Because recommendations for nutrition support were
score (chronic malnutrition/stunting), and there was a sig- recently updated, the Nutrition Support Team at Texas
nificant association in patients with persistent AKI with Childrens Hospital PICU decided to implement the new
moderate/severe height stunting. It is likely that height recommendations. The implementation of Nutrition Sup-
stunting and AKI are related, but no causality can be in- port Guidelines improved feeding practices in the PICU,
ferred in this retrospective study. but underfeeding persisted in critically ill children. The
Patients with persistent AKI were sicker as assessed by percentage of protein intake increased significantly in no
PRISM III and PELOD, which might have lead to delayed AKI, but not in patients with AKI, but the intake remained
enteral feeding but does not fully explain the underfeeding insufficient after the implementation of the Nutrition

Table 4. Odds Ratio (OR) in Patients With Resolved and Persistent Acute Kidney Injury (AKI) Compared To No AKI
Basic Characteristics % (n) % (n) P* OR (CI) P

Calorie intake ,80% $80%


No AKI 57.7 (205) 42.3 (150) 1
AKI resolved 50.0 (56) 50.0 (56) 1.3 (0.8-2.1) .238
AKI persistent 54.5 (24) 45.5 (20) .350 1.2 (0.6-2.3) .633
Protein intake ,80% $80%
No AKI 88.2 (313) 11.8 (42) 1
AKI resolved 83.0 (93) 17.0 (19) 1.1 (0.6-2.1) .820
AKI persistent 72.7 (32) 27.3 (12) .014 1.9 (0.8-4.2) .135
CI, confidence interval; PRISM, Pediatric Risk of Mortality Score.
*Unadjusted chi-square.
Adjusted for PRISM score.
6 KYLE ET AL

Table 5. Recommended and Actual Energy and Protein Intake and Gap in Patients With No AKI and With Resolved or Persistent
AKI in the First 8 Days of PICU Stay
All Patients No AKI
Implementation Pre (n 5 328) Post (n 5 183) Pre (n 5 227) Post (n 5 128)

BMR kcal/kg/d 50.1 (42.6-56.1) 50.7 (42.1-57.6) 51.3 (43.0-57.6) 51.1 (43.1-57.9)
Actual energy intake kcal/kg/d 36.6 (22.9-50.3) 40.3 (21.9-54.9) 35.3 (21.8-48.6)* 38.1 (21.5-53.0)*
% BMR 73.9 (49.9-102.1) 79.2 (52.4-106.8) 69.3 (48.8-97.4) 77 (51.6-105.4)
Energy gap kcal/kg/d 212.2 (222.9 to 1.1) 210.1 (222.7 to 3.4) 214.0 (224.2 to 21.4) 211.0 (224.7 to 1.9)
Recommended protein 2.5 (1.8-2.5) 2.5 (1.8-2.5) 2.5 (1.8-2.5) 2.5 (1.8-2.5)
intake g/kg/d
Actual protein intake g/kg/d 0.8 (0.4-1.2) 1.1 (0.5-1.6) 0.74 (0.4-1.2)* 0.96 (0.5-1.6)*
% protein needs 35.6 (18.9-54.4) 52.3 (23.4-75.4) 34.5 (18.7-53.2) 48.6 (20.7-71.1)
Protein gap g/kg/d 21.3 (21.8 to 20.9) 21.0 (21.6 to 20.5) 21.3 (21.7 to 20.9) 21.0 (21.7 to 20.6)
Resolved AKI Persistent AKI
Pre (n 5 83) Post (n 5 29) Pre (n 5 18) Post (n 5 26)
BMR 48.9 (41.9-53.6) 49 (38.2-58.1) 50.3 (41.4-55.4) 46.9 (34.3-57.4)
Actual energy intake 40.8 (24.8-53.4)* 41.8 (19.5-52.1)* 32.9 (24.5-49.2)* 45.8 (23.7-66.2)
% BMR 80.9 (53.8-111.3) 77.2 (37.9-103.4) 72.8 (49.8-90.3) 90.4 (74.5-120.0)
Energy gap 29.1 (218.7 to 25.0) 212.4 (220.9 to 1.7) 213.1 (220.7 to 25.3) 22.8 (211.9 to 12.1)
Recommended protein intake 2.5 (1.8-2.5) 2.5 (1.8-2.5) 2.5 (1.8-2.5) 2.5 (1.8-2.5)
Actual protein intake 0.89 (0.4-1.3)* 1.25 (0.4-1.5)* 0.8 (0.4-1.4)* 1.39 (0.6-2.1)*
% protein needs 40.6 (21.5-59.1) 50 (18.7-79.2) 33.8 (18.6-54.4) 61.5 (32.3-96.1)
Protein gap 21.3 (21.7 to 20.9) 21.2 (21.5 to 20.4) 21.3 (21.7 to 20.9) 20.8 (21.4 to 20.1)
AKI, acute kidney injury; BMR, basal metabolic rate, estimated by Schofield; IQR, interquartile range.
Values are median (IQR).
Energy or protein gap 5 actual minus recommended intake.
*Wilcoxon Signed Rank test between actual and recommended energy and protein intake; MannWhitney test.
Postimplementation versus preimplementation, P , .05.
AKI resolved versus no AKI.

Support Guidelines. In addition, the cumulative energy and in children37 and adults,40 with a higher risk for infection,
protein gap for the 8-day period improved in the poor wound healing, longer dependency on mechanical
postimplementation compared to preimplementation, ventilation, and increased length of hospital stay in
with protein and energy provision remaining below adults,41,42 adequate nutrition support, especially protein
recommended intakes. The implementation of Nutrition provision, is essential for improving patient outcomes.
Support Guidelines did decrease the gap between energy Furthermore, adequate protein feeding seems to be
and protein delivery and needs. beneficial in AKI as systemic administration of protein in
Previous studies have shown that critically ill children the form of amino acids early in the course of
who received better nutritional support had significant experimental AKI in small animal models of nephrotoxic
improvement in physiological stability and outcome.37 and septic AKI had anti-inflammatory and antiapoptotic ef-
Furthermore, recent studies have shown that higher protein fects in the renal tubular epithelium.43,44 Renal recovery
intake might protect the kidney from injury and may pre- was faster and survival higher in adults with oliguric AKI
serve glomerular filtration rate in critically ill patients23 who were given IV amino acid infusions than in patients
and could decrease the time to recovery from AKI.24-26 who were given isocaloric carbohydrates alone.24
Studies linking achievement of protein requirements to Several studies have shown beneficial effects of higher
outcome are lacking in children with AKI. protein provision.23-26 The current study was not able to
The goals of nutrition support in AKI are identical to demonstrate a beneficial effect of protein feeding on renal
those suggested for other critically ill patients in the function. Although the amount of protein provided was
PICU17,38 and include prevention of protein energy suboptimal and less than recommended in critically ill
wasting, preservation of lean body mass and nutritional children, the higher protein intake was not associated
status, avoidance of metabolic derangements and with a delay in renal recovery in patients with AKI.
complications, improvement of wound healing, and Limitations of this study were several; data were collected
support of immune function.11,38 Protein restriction with retrospectively from patient charts and were limited single
the goal of delaying the need for renal replacement center and, therefore, may not be generalized to other
therapy should be avoided.39 Since protein energy malnu- PICUs. Fluid overload and oliguria are both well-
trition is associated with increased mortality and morbidity recognized risk factors in the PICU.45-47 There was no
PROTEIN FEEDING IN CHILDREN WITH AKI 7

data available on the fluid balance and urine volume of ill children: a two-center retrospective cohort study. Crit Care.
patients. PRISM and PELOD scores were obtained on 2011;15:R146.
9. Wooley JA, Btaiche IF, Good KL. Metabolic and nutritional aspects of
PICU admission day only, which might not reflect the acute renal failure in critically ill patients requiring continuous renal replace-
progression of organ dysfunction during the entire study ment therapy. Nutr Clin Pract. 2005;20:176-191.
period. Another limitation of this study was that energy 10. Fiaccadori E, Lombardi M, Leonardi S, et al. Prevalence and clinical
expenditure was calculated from prediction equations outcome associated with preexisting malnutrition in acute renal failure: a pro-
instead of using indirect calorimetry. spective cohort study. J Am Soc Nephrol. 1999;10:581-593.
11. Fiaccadori E, Cremaschi E, Regolisti G. Nutritional assessment
In conclusion, higher protein intake ($80% of estimated and delivery in renal replacement therapy patients. Semin Dial.
needs) was not associated with a delay in renal recovery in 2011;24:169-175.
patients with AKI after adjustment for severity of illness. 12. Maursetter L, Kight CE, Mennig J, Hofmann RM. Review of the
Protein intake was improved in critically ill children with mechanism and nutrition recommendations for patients undergoing contin-
no AKI, resolved, and persistent AKI after implementation uous renal replacement therapy. Nutr Clin Pract. 2011;26:382-390.
13. National Kidney Foundation. KDOQI Clinical Practice Guidelines
of Nutrition Support Guidelines, but underfeeding per- and Clinical Practice Recommendations for Anemia in Chronic Kidney Dis-
sisted in these patients. ease. Am J Kidney Dis. 2006;47(Suppl 3):S11-S146.
14. Berbel MN, Pinto MP, Ponce D, Balbi AL. Nutritional aspects in acute
kidney injury. Rev Assoc Med Bras. 2011;57:600-606.
Practical Application 15. Lambe C, Hubert P, Jouvet P, Cosnes J, Colomb V. A nutritional sup-
Adequate nutrition support has been shown to improve port team in the pediatric intensive care unit: changes and factors impeding
outcome in critically ill children. Higher protein intake was appropriate nutrition. Clin Nutr. 2007;26:355-363.
not associated with a delay in renal recovery in patients with 16. Kalista-Richards M. The kidney: medical nutrition therapyyesterday
AKI after adjustment for severity of illness. The implemen- and today. Nutr Clin Pract. 2011;26:143-150.
17. McClave SA, Martindale RG, Vanek VW, et al. Guidelines for the Pro-
tation of Nutrition Support Guidelines improved feeding vision and Assessment of Nutrition Support Therapy in the Adult Critically Ill
practices in the PICU, but underfeeding persisted in criti- Patient: Society of Critical Care Medicine (SCCM) and American Society for
cally ill children with AKI. Parenteral and Enteral Nutrition (A.S.P.E.N.). JPEN J Parenter Enteral Nutr.
2009;33:277-316.
18. Kyle UG, Akcan-Arikan A, Orellana RA, Coss-Bu JA. The adequacy
Acknowledgments of nutritional support in critically ill children with acute kidney injury. In:
Support: The study was carried out at Texas Childrens Hospital, with Rajendram R, Preedy VR, Patel VB, eds. Diet and nutrition in critical care. Lon-
internal funding by Baylor College of Medicine. don, UK: Springer; 2015:885-896.
U.G.K. designed and carried out the study, carried out the data ana- 19. Briassoulis G, Zavras N, Hatzis T. Malnutrition, nutritional indices,
lyses, and drafted the manuscript. A.A.-A. conceived and J.C.S., M.G., and early enteral feeding in critically ill children. Nutrition. 2001;17:
and L.S.S. assisted with the data analysis and the draft of the manuscript. 548-557.
J.A.C.-B. participated in the design of the study, contributed to the data 20. Mehta NM, McAleer D, Hamilton S, et al. Challenges to optimal
analysis, and helped to draft the manuscript. All authors read and enteral nutrition in a multidisciplinary pediatric intensive care unit. JPEN J
approved the final manuscript. Parenter Enteral Nutr. 2010;34:38-45.
21. Taylor RM, Preedy VR, Baker AJ, Grimble G. Nutritional support in
critically ill children. Clin Nutr. 2003;22:365-369.
References 22. Kyle UG, Akcan-Arikan A, Orellana RA, Coss-Bu JA. Nutrition sup-
1. Coss-Bu JA, Klish WJ, Walding D, et al. Energy metabolism, nitrogen port among critically ill children with AKI. Clin J Am Soc Nephrol.
balance, and substrate utilization in critically ill children. Am J Clin Nutr. 2013;8:568-574.
2001;74:664-669. 23. Doig GS, Simpson F, Bellomo R, et al. Intravenous amino acid therapy
2. Delgado AF, Okay TS, Leone C, et al. Hospital malnutrition and inflam- for kidney function in critically ill patients: a randomized controlled trial.
matory response in critically ill children and adolescents admitted to a tertiary Intensive Care Med. 2015;41:1197-1208.
intensive care unit. Clinics (Sao Paulo). 2008;63:357-362. 24. Abel RM, Beck CH Jr, Abbott WM, et al. Improved survival from
3. Kyle UG, Genton L, Pichard C. Low phase angle determined by acute renal failure after treatment with intravenous essential L-amino acids
bioelectrical impedance analysis is associated with malnutrition and nutri- and glucose. Results of a prospective, double-blind study. N Engl J Med.
tional risk at hospital admission. Clin Nutr. 2013;32:294-299. 1973;288:695-699.
4. Cahill NE, Dhaliwal R, Day AG, Jiang X, Heyland DK. Nutrition ther- 25. Singer P. High-dose amino acid infusion preserves diuresis and im-
apy in the critical care setting: what is best achievable practice? An interna- proves nitrogen balance in non-oliguric acute renal failure. Wien Klin Wo-
tional multicenter observational study. Crit Care Med. 2010;38:395-401. chenschr. 2007;119:218-222.
5. Bartlett RH, Dechert RE, Mault JR, et al. Measurement of metabolism 26. Doig GS, Simpson F, Finfer S, et al. Effect of evidence-based feeding
in multiple organ failure. Surgery. 1982;92:771-779. guidelines on mortality of critically ill adults: a cluster randomized controlled
6. Kyle UG, Jaimon N, Coss-Bu JA. Nutrition support in critically ill chil- trial. JAMA. 2008;300:2731-2741.
dren: underdelivery of energy and protein compared with current recommen- 27. Chumlea WC, Guo SS, Steinbaugh ML. Prediction of stature from
dations. J Acad Nutr Diet. 2012;112:1987-1992. knee height for black and white adults and children with application to
7. Akcan-Arikan A, Zappitelli M, Loftis LL, et al. Modified RIFLE criteria mobility-impaired or handicapped persons. J Am Diet Assoc. 1994;94:1385-
in critically ill children with acute kidney injury. Kidney Int. 2007;71:1028- 1388. 1391; quiz 1389-1390.
1035. 28. World Health Organization Multicentre Growth Reference Study
8. Alkandari O, Eddington KA, Hyder A, et al. Acute kidney injury is Group. WHO Child Growth Standards: length/height-for age, weight-for-age,
an independent risk factor for pediatric intensive care unit mortality, weight-for-length, weight-for-height and body mass index-for-age: methods and devel-
longer length of stay and prolonged mechanical ventilation in critically opment. Geneva, Switzerland: World Health Organization; 2006.
8 KYLE ET AL

29. Kuczmarski RJ, Ogden CL, Guo SS, et al. 2000 CDC Growth Charts 39. Sabatino A, Regolisti G, Maggiore U, Fiaccadori E. Protein/energy
for the United States: Methods and Development. Vital Health Stat 11. debt in critically ill children in the pediatric intensive care unit: acute kidney
2002;246:1-190. injury as a major risk factor. J Ren Nutr. 2014;24:209-218.
30. De Le on AL, Romero-Gutierrez G, Valenzuela CA, Gonzalez- 40. Biolo G. Can we increase protein synthesis by anabolic factors? Am J
Bravo FE. Simplified PRISM III score and outcome in the pediatric intensive Kidney Dis. 2001;37(1 Suppl 2):S115-S118.
care unit. Pediatr Int. 2005;47:80-83. 41. Pichard C, Kyle UG, Morabia A, et al. Nutritional assessment: lean
31. Pollack MM, Patel KM, Ruttimann UE. PRISM: an updated pediatric body mass depletion at hospital admission is associated with increased length
risk of mortality score. Crit Care Med. 1996;24:743-752. of stay. Am J Clin Nutr. 2004;79:613-618.
32. Leteurtre S, Duhamel A, Grandbastien B, Lacroix J, L F. Paediatric logistic 42. Heyland DK. Making inferences from scientific research. Nutr Clin
organ dysfunction (PELOD) score. Lancet. 2006;367:897. author reply 900-902. Pract. 1998;13:S1-S7.
33. Leteurtre S, Martinot A, Duhamel A, et al. Validation of the paediatric 43. Hu YM, Pai MH, Yeh CL, Hou YC, Yeh SL. Glutamine administra-
logistic organ dysfunction (PELOD) score: prospective, observational, multi- tion ameliorates sepsis-induced kidney injury by downregulating the high-
centre study. Lancet. 2006;362:192-197. mobility group box protein-1-mediated pathway in mice. Am J Physiol Ren
34. Schofield WN. Predicting basal metabolic rate, new standards and re- Physiol. 2011;302:F150-F158.
view of previous work. Hum Nutr Clin Nutr. 1985;39 Suppl 1:5-41. 44. Kim YS, Jung MH, Choi MY, et al. Glutamine attenuates tubular cell
35. Mehta NM, Compher C. A.S.P.E.N. Clinical Guidelines: nutrition apoptosis in acute kidney injury via inhibition of the c-Jun N-terminal kinase
support of the critically ill child. JPEN J Parenter Enteral Nutr. phosphorylation of 14-3-3. Crit Care Med. 2009;37:2033-2044.
2009;33:260-276. 45. Macedo E, Malhotra R, Bouchard J, Wynn SK, Mehta RL. Oliguria is
36. Mehta NM, Bechard LJ, Zurakowski D, Duggan CP, Heyland DK. an early predictor of higher mortality in critically ill patients. Kidney Int.
Adequate enteral protein intake is inversely associated with 60-d mortality 2011;80:760-767.
in critically ill children: a multicenter, prospective, cohort study. Am J Clin 46. Arikan AA, Zappitelli M, Goldstein SL, et al. Fluid overload is associ-
Nutr. 2015;102:199-206. ated with impaired oxygenation and morbidity in critically ill children. Pediatr
37. Pollack MM, Ruttimann UE, Wiley JS. Nutritional depletions in crit- Crit Care Med. 2011;13:253-258.
ically ill children: associations with physiologic instability and increased quan- 47. Sutherland SM, Zappitelli M, Alexander SR, et al. Fluid overload and
tity of care. JPEN J Parenter Enteral Nutr. 1985;9:309-313. mortality in children receiving continuous renal replacement therapy: the
38. Cano NJ, Aparicio M, Brunori G, et al. ESPEN Guidelines on Paren- prospective pediatric continuous renal replacement therapy registry. Am J Kid-
teral Nutrition: adult renal failure. Clin Nutr. 2009;28:401-414. ney Dis. 2010;55:316-325.

You might also like