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Year : 2019  |  Volume : 2  |  Issue : 1  |  Page : 2-15

Nutritional challenges across the spectrum of chronic kidney disease

Division of Nephrology, Children's National Health System, Washington, DC, USA

Date of Web Publication17-May-2019

Correspondence Address:
Asha Moudgil
1.5.100 West Wing, Division of Nephrology, Children's National Health System, 111 Michigan Avenue NW, Washington, DC 20010
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/AJPN.AJPN_2_19

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Maintenance of optimal nutrition plays a key role in the management of children with chronic kidney disease (CKD) across different stages of CKD, during dialysis and following transplantation. Malnutrition, both under- and over-nutrition, is widely prevalent and negatively impacts short- and long-term outcomes. It leads to growth retardation, increased risk of hospitalization and infections, poor cognition, and decreased quality of life. Understanding of the pathogenesis of malnutrition is crucial for its proper management. This review discusses the definition, prevalence, pathogenesis, and management of malnutrition in different stages of CKD.

Keywords: Altered body composition, end stage renal disease, micronutrients, obesity, protein–energy wasting, uremia

How to cite this article:
Sgambat K, Amatya K, Moudgil A. Nutritional challenges across the spectrum of chronic kidney disease. Asian J Pediatr Nephrol 2019;2:2-15

How to cite this URL:
Sgambat K, Amatya K, Moudgil A. Nutritional challenges across the spectrum of chronic kidney disease. Asian J Pediatr Nephrol [serial online] 2019 [cited 2021 Apr 19];2:2-15. Available from: https://www.ajpn-online.org/text.asp?2019/2/1/2/258560

  Introduction Top

Maintenance of optimal nutrition is important in children across the entire spectrum of chronic kidney disease (CKD), including in the phase prior to initiating renal replacement therapy (RRT), during peritoneal dialysis (PD) and hemodialysis, and after transplantation. Malnutrition includes both undernutrition and overweight. Malnutrition negatively impacts patient outcomes by influencing morbidity and mortality, and contributes to increased risk of hospitalization and infections, poor cognition, reduced growth, decreased quality of life, and increased health-care costs.[1] While undernutrition is widely prevalent in CKD and during dialysis (CKD 5D), being overweight or obese is common after kidney transplantation.

The aim of nutritional management in patients with any stage of CKD is to maintain healthy weight, promote growth and development, ensure adequate intake of macro- and micro-nutrients, and avoid metabolic imbalances or development of mineral bone disease (MBD). The long-term goal is to reduce the risk of chronic morbidities and mortalities, including in adulthood, and to promote cardiovascular health. This review focuses on the pathophysiology of malnutrition in different phases of CKD and strategies to address them.

  Definition of Malnutrition Top

The World Health Organization defines malnutrition as “deficiencies, excesses, or imbalances in a person's intake of energy and/or nutrients,” to signify being either undernourished or overweight. Undernutrition, termed protein and energy malnutrition (PEM), is the result of a cumulative deficit of energy, protein, or micronutrients that negatively affects growth, development, and other health outcomes. PEM in children without CKD is defined as weight-for-height or body mass index (BMI) ≤−1 standard deviation score (SDS), and classified as mild if weight-for-height SDS is <−1 to −1.9; moderate if <−2 to −2.9; and severe if <−3.[2] Further, height-for-age ≤−3 SDS, considered as short stature, denotes chronic PEM. However, caution is advised when applying these criteria to children with CKD. Patients with CKD may have growth failure due to nonnutritional factors such as growth hormone resistance and/or MBD. Therefore, these children may have short stature due to growth failure, but have adequate weight for height and/or even be overweight. In a report of the Chronic Kidney Disease in Children (CKiD) cohort including 799 patients, 46% of the patients with glomerular disease and 32% of those with nonglomerular disease were overweight or obese.[3] Their median height-for-age and weight-for-age SDS were adequate at −0.55 and 0.03, respectively; only 12% had short stature. Children in the cohort appeared to consume excess calories from fast foods.[4] Hence, the diagnosis of PEM should not be made solely on low height-for-age SDS in children with CKD.

Overweight or obesity is the result of cumulative increase in energy stores and excessive fat deposition. Anthropometric measures that define obesity include BMI, waist circumference, and waist-to-height ratio (WHr). BMI for age between the 85th and <95th percentile indicates being overweight, whereas obesity is defined as BMI for age ≥95th percentile.[5] However, evaluating children with CKD using BMI-for-age percentiles underestimates both lean mass and adiposity, due to the high prevalence of short stature and delayed maturation.[6] The Kidney Disease Outcomes Quality Initiative (KDOQI) guidelines recommend using BMI-for-height age (the age at which the child's current height is the 50th percentile) to assess children with CKD to provide a more appropriate comparison to children of similar stature and maturation.[7]

Another limitation of BMI is its inability to differentiate between fat mass and lean mass. Some overweight and obese children have normal BMI with increased waist circumference and/or WHr due to abdominal adiposity. Abnormal waist circumference is reported according to the age- and sex-specific percentiles of Cook et al., with thresholds of >94th percentile in boys and >84th percentile in girls.[8] Waist circumference underestimates the presence of abdominal obesity in persons with short stature, for example, CKD, and should be indexed to height. Based on a study of NHANES III data that linked elevated WHr with increased cardiovascular risk in the pediatric population, a WHr >0.49 is considered overweight and >0.54 as obese.[9]

  Protein–energy Malnutrition Versus Protein–energy Wasting in Chronic Kidney Disease Top

PEM in children without CKD reflects a state of isolated decrease in body stores of protein and energy that is easily corrected by the supplementation of protein and calories. PEM in children with CKD cannot be easily corrected solely by nutritional supplementation due to the presence of additional factors, such as persistent inflammation, metabolic acidosis, endocrine disorders, hypermetabolism, poor physical activity, and frailty, that leads to a breakdown of protein and muscle stores. Therefore, the term “protein–energy wasting (PEW)” is used in children and adults with CKD to differentiate it from PEM[10] The International Society of Renal Nutrition and Metabolism (ISRNM) defines PEW as a syndrome, unique to the CKD population, characterized by a convergence of nutritional and catabolic alterations that results in increased morbidity and mortality. Factors contributing to PEW in adults include anorexia, increased energy expenditure related to uremia, inflammation and acidosis, increased catabolism of muscle and fat due to altered hormonal regulation, reduced physical activity, and frailty. Further, the procedure of dialysis is also implicated in the pathogenesis of PEW in patients on maintenance hemodialysis.[11] Factors contributing to PEW are summarized in [Figure 1].
Figure 1: Pathogenesis of protein–energy wasting in children with chronic kidney disease (CKD)

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  Evaluation for Protein–energy Wasting in Chronic Kidney Disease Top

In adult patients with CKD 3–5D, both the ISRNM[12] and the KDOQI guidelines for Nutrition in Adults with CKD[13] recommend assessing nutrition by Subjective Global Assessment (SGA) to diagnose PEW. The SGA involves evaluating four indicators (weight change, dietary intake, gastrointestinal symptoms, and physical examination for fat and muscle mass), each of which are ranked on a 7-point scale, and combining the ranks in a score indicating the overall nutritional status. While a pediatric version of SGA was developed[14] and tested in a small cohort of children with CKD,[15] there is insufficient evidence to support the routine use of SGA in the evaluation of malnutrition in pediatric CKD population. Nutrition-focused physical examination is a similar but more detailed assessment method that has become a standard practice in the evaluation of malnutrition in the general pediatric population.[16],[17] However, further research is needed to determine the optimal method to assess PEW in children with CKD. Based on an analysis of data from the CKiD study, Abraham et al. have proposed five criteria for the diagnosis of PEW in children with CKD, namely[10] (i) decreased appetite, reported by patient; (ii) serum biochemistry (low cholesterol, albumin and transferrin, and high C-reactive protein [CRP]); (iii) reduced body mass; (iv) reduced muscle mass; and (v) short stature or poor growth, a pediatric-focused criterion. The key criterion for the diagnosis of PEW was poor growth, as it identified more children at risk and was the only indicator associated with the outcome of increased hospitalization.

Hence, in addition to standard parameters such as weight, height, BMI, and waist circumference, nutrition evaluation in children with CKD should include a history of dietary intake and measurement of rate of weight gain or loss, growth velocity, mid-upper arm circumference, WHr, and trunk-to-limb ratio, which is also altered in CKD. [Table 1] and [Table 2] present strategies for the diagnosis and management of PEM in patients with CKD and dialysis.
Table 1: Evaluation and management of protein-energy malnutrition in patients with chronic kidney disease stages 3-5 and dialysis (5D)

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Table 2: Evaluation and management of protein-energy wasting in patients with chronic kidney disease stages 3-5 and dialysis (5D)

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  Global Prevalence of Protein–energy Wasting in Chronic Kidney Disease Top

PEW is highly prevalent in adults with CKD and end-stage renal disease (ESRD), and is associated with increased risk of cardiovascular disease and mortality. Reports of its prevalence vary widely, due in part to lack of standardized criteria to define PEW. A recent meta-analysis reported the prevalence of PEW, synthesizing data from 93 studies, published between 2000 and 2014 each with a minimum of fifty patients with acute kidney injury (AKI), CKD, CKD 5D, or after kidney transplant.[18] The overall average prevalence of PEW across all nations and disease states was 42%. The prevalence of PEW was 28%–54% in patients on maintenance dialysis (n = 16,434), 11%–54% in those with CKD 3–5 (n = 1776), 28%–52% in kidney transplant recipients (n = 1067), and 60%–82% in patients with AKI (n = 189). The prevalence of PEW also varied widely across countries and regions, as illustrated in a heat map derived from studies in adult patients with CKD 5D included in the meta-analysis [Figure 2].[18]
Figure 2: Worldwide prevalence of protein–energy wasting in adults on dialysis, based on published data between 2009 and 2014

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Information on the prevalence of PEW in children with CKD is sparse, and the meta-analysis did not include pediatric studies. Results of the CKiD study indicate a prevalence ranging from 7% to 20%, depending on the criteria used to define PEW in pediatric CKD.[10] The prevalence was 7% when using the standard PEW definition that requires three out of four criteria to be met, but rose to 15% when using a modified definition that included the standard PEW definition plus short stature or poor growth. Overall, 20% of the children met a “minimum” definition of PEW (≥2 out of 4 criteria). In a study of 39 children on chronic PD, Brem et al. reported 35.9% prevalence of “protein malnutrition,” as suggested by hypoalbuminemia (<2.9 g/dL) alone.[19] In other single-center pediatric studies not designed to detect PEW, the prevalence of general malnutrition ranges from 20% to 45% among children with CKD.[20],[21]

  Alterations in Growth and Body Composition Top

In addition to PEW, children with CKD and ESRD have poor growth and alterations in body composition. Factors implicated in causing growth failure include polyuria, salt losses in patients with congenital anomalies of kidneys and urinary tract, metabolic acidosis, and complications of MBD, including adynamic bone disease, hyperparathyroidism, destruction of growth plate, epiphyseal displacement and metaphyseal fractures, and resistance to the action of growth hormone and insulin-like growth factor (IGF)-1. Children with CKD and after kidney transplantation have discordant body composition, characterized by high-fat mass, low lean mass, high trunk: leg fat mass ratio, and increased central adiposity.[22] Short stature with central adiposity leads to increased WHr, which is considered more sensitive than BMI and waist circumference alone in detecting adiposity-related cardiovascular risk factors in children with CKD[23] as well as posttransplantation.[24] As growth hormone is lipolytic and enhances the incorporation of protein into tissue, recombinant growth hormone (rGH) therapy promotes lower fat accretion and increases lean mass, apart from increasing linear growth in children with CKD.

Dual-energy X-ray absorptiometry (DXA) is a validated but expensive method to assess body composition, including fat mass, lean mass, and bone mineral content, in euvolemic children and adults with CKD and ESRD.[7] Its limitations include the inability to distinguish volume status, leading to overestimation of lean mass in fluid-overloaded patients,[25] and poor discrimination between cortical and trabecular bones, causing underestimation of bone mineral density in individuals with short stature.[26] Both factors, apart from cost, are important considerations limiting the use of DXA in children with CKD and ESRD. Bioelectric impedance analysis, while less expensive, has not been validated to evaluate body composition in children with CKD and ESRD. It determines the fluid content of body compartments by measuring the impedance of an electrical current based on its conductance through body water. However, its limitation is that it assumes that water comprises 73% of the total body weight, and is therefore inaccurate in the states of fluid overload, causing overestimation of fat mass and large margins of error in patients with kidney disease.[25],[27] Further research is needed to identify methods to accurately assess fluid, fat mass, and lean mass in children with CKD.

  Contributors to Altered Nutrition Top

The CKD milieu is associated with a cascade of disturbances in the regulation of several physiologic functions that contribute to malnutrition. These factors are summarized below.

Altered taste sensitivity

Patients with CKD have altered and reduced taste sensation that impacts appetite and contributes to malnutrition. Potential contributors include fewer fungiform papillae on the anterior tongue, as compared to healthy controls,[28] altered salt and urea concentration in saliva,[29] and reduced number of taste buds, possibly related to micronutrient deficiencies.[30] Altered taste for salt can lead to either undernutrition or overnutrition.


Factors implicated in causing anorexia in children with CKD include dysregulation of hormones, inflammatory cytokines, and the microbiome. An unpalatable prescribed diet that is low in salt, potassium, and phosphate, and medications such as phosphate binders often reduce intakes. Appetite and intake decline in parallel with decrease in glomerular filtration rate (eGFR) due to release of cytokines, including tumor necrosis factor, interleukin-6, and interleukin-1.[31] Altered balance of orexigenic (appetite stimulating) and anorexigenic (appetite inhibiting) hormones plays a key role in the pathogenesis of anorexia in CKD. As CKD progresses, more insulin and leptin are secreted, while the production of ghrelin declines, thus inhibiting neuropeptide Y, which, in turn, downregulates appetite. Other anorexigenic hormones elevated in CKD include obestatin, visfatin, and cholecystokinin; these promote early satiety and delayed gastric motility.[32] Altered gut microbiome in CKD is associated with increased intestinal absorption of uremic toxins including phenols, indoles, amines, guanidine, phenylacetic acid, and hippuric acid, which suppresses the appetite. Probiotics may be beneficial in restoring intestinal microbial balance and maintaining the health of colonic epithelial cells.[33] Studies investigating the effects of probiotics on uremic toxins, inflammation, and CKD progression have yielded varying results. One recent meta-analysis concluded that evidence does not support beneficial effects of probiotics on eGFR, serum creatinine, inflammation or urea in CKD, however another,[34] meta-analysis reported significant reduction in urea levels in patients receiving probiotics, compared to controls.[35] Large controlled studies are needed to clarify the role of probiotics in retarding the progression of CKD.

Protein loss and altered metabolism

Proteinuria and losses in dialysate affect anabolism in CKD. Protein synthesis is downregulated in polyuric patients with salt wasting. Metabolic acidosis increases protein catabolism.[36],[37] Protein losses in PD are significant, particularly in younger children on PD.[38] Losses in dialysate along with increased catabolism caused by inflammatory reaction to the hemodialysis membrane also affect protein balance negatively.[39]

Micronutrient abnormalities

Several micronutrient abnormalities are reported in children with CKD. Children on dialysis are particularly prone. While toxicities may occur due to repeated exposure to substances in supply water used to prepare hemodialysis dialysate or reduced renal clearance, deficiencies may occur due to inadequate intake and removal of water-soluble vitamins and protein-bound trace elements in the dialysate/effluent. Zinc deficiency, known to affect one-fifth of the global population, particularly young children in developing countries,[40] contributes to erythropoietin-resistant anemia, growth impairment, wasting, and decreased taste perception.[30] Zinc deficiency was present in 43% of children on chronic dialysis, despite receiving daily supplementation,[41] and the levels of zinc and selenium were significantly lower in patients receiving hemodialysis and PD compared to healthy children or those with CKD.[42] Children on chronic dialysis show higher levels of lead compared to healthy children and those with CKD.[42],[43],[44] Because lead affects neurodevelopment in children, its levels should be monitored in patients with CKD 5D. While more clinical research is needed to develop supplementation guidelines for trace minerals in children with CKD,[43] current evidence supports daily supplementation of water-soluble vitamins, as well as periodic monitoring of zinc, selenium, and lead levels in pediatric patients on dialysis. Currently, in the USA, these minerals are not monitored routinely.

Adherence and psychosocial factors influencing intake

Children with CKD are advised dietary restrictions, depending on the stage of disease, modality of dialysis, and/or underlying disease, that may be burdensome and difficult to adhere to. Studies consistently indicate nonadherence to dietary restrictions among children with CKD,[45],[46] with significant differences between actual and recommended intakes of sodium, phosphorus, protein, and calories, particularly in young children[47] and teenagers on dialysis.[48] Adolescents have significant difficulties in adherence, due to hormonal and psychosocial changes related to puberty and transition to adulthood. Adults with CKD report that dietary restrictions interfere with maintaining relationships and in social situations, and make them feel burdened, deprived, and overwhelmed.[49] It is likely that adolescents with CKD feel similar social challenges and feel judged negatively by peers in following restricted diets or taking phosphorus binders at meals. Findings from research on pediatric patients with other chronic diseases and dietary restrictions support this notion. Dietary nonadherence is highly prevalent among patients with type 1 diabetes, due to fear of negative perception by peers.[50] Factors linked to dietary nonadherence in children with CKD include decreased parental monitoring, intrusive parenting, and presence of mental health difficulties, which are considered more common in the diseased than in the general population.[51] Studies on pediatric liver and kidney transplant recipients show that poor mental health negatively impacts adherence to medical therapies,[52],[53] and is associated with poorer quality of life in children with CKD.[54] Other psychosocial constraints that impact dietary adherence include poverty and limited access to food supplies.[55]

Given concerns with adherence to dietary recommendations among pediatric CKD patients, dietary intake and related difficulties should be monitored regularly, and dietary consultations and clinic visits should include education and psychosocial interventions. Interventions targeting understanding of diet and disease and behavioral interventions targeting self-efficacy and self-management are particularly helpful to adults with CKD[56] and might also benefit pediatric patients. Motivational interviewing, which targets intrinsic motivation and improved commitment to behavior-changing goals, was effective in improving dietary adherence among youth with diabetes[57] and might have a similar impact on pediatric CKD patients. Multidisciplinary collaborations in education, interventions, and research are essential to improve our understanding of psychosocial aspects of dietary challenges among children with CKD.

Food insecurity

Food insecurity, referring to uncertain or nonavailability of safe and nutritious foods consistently, was present in 7.7% (2.9 million) of households with children in the USA in 2017.[58] It is more common in developing countries, affecting 42.7% of households in India,[59] 53%–87% in South Africa,[60] 61.8% in Nigeria,[61] and 83.9% of households in Malaysia.[62] These developing countries also have high rates of PEW among patients with CKD [Figure 2]. A longitudinal cohort study of US adults enrolled in the National Health and Nutrition Examination Study (NHANES) showed that patients with CKD and food insecurity had an increased risk of progression to ESRD than those without food insecurity.[63] A pilot study conducted on a pediatric nephrology population in Seattle, Washington, USA,[64] reported food insecurity in 34% of families, significantly higher than the prevalence in general US population (7.7%). Reasons for food insecurity were financial difficulties, lack of access to government benefits or community resources, and inability to obtain foods appropriate for renal dietary restrictions. Given that developing countries have fewer resources and high rates of food insecurity, it can be presumed that children with CKD in these regions are at high risk for food insecurity.

In impoverished regions, food insecurity leads to child hunger and undernutrition due to inadequate intake of macro- and micro-nutrients. However, urban areas of both developing and developed countries show a paradoxical trend, with food insecurity leading to obesity.[65] This is because of increased intake of inexpensive, readily-accessible, energy-dense fast foods and processed foods, which are high in sugars and saturated fats and low in nutritional value, as compared to nutritious fresh proteins and products that are not accessible due to price or geographic unavailability. Hence, both developed and developing countries require interventions to target food insecurity in order to improve child health and nutrition and to lower the risk of disease progression in CKD.

  Challenges in Nutritional Management Top


Nutritional management in children with CKD 3–5 differs by the underlying diagnosis. The leading causes of CKD in children are CAKUT and glomerular disorders. Children with CAKUT have polyuria, and therefore, increased water intake, that compromises the intake of solid foods, resulting in energy deficits. Children with CAKUT may also have salt wasting, leading to decreased protein synthesis.[3] These patients require aggressive salt and fluid supplementation to optimize their nutrition. Conversely, children with glomerular disorders often retain salt and water, leading to hypertension, while proteinuria may cause hypoalbuminemia and dyslipidemia. These patients merit a low sodium, heart-healthy diet and fluid restriction.

Factors affecting bone health and growth, including metabolic acidosis, growth hormone resistance, and MBD, contribute to undernutrition and short stature in children with CKD. Metabolic acidosis decreases the levels of IGF-1 and growth hormone receptors and increases steroid production and protein degradation. Hence, monitoring for and correction of metabolic acidosis is important in optimizing growth and nutrition in these patients. Reduced consumption of animal-based proteins decreases the dietary acid load and prevents metabolic acidosis, which may help slow progression to ESRD.[66] Management of MBD is critical in optimizing growth and minimizing the development of bony deformities and vascular calcifications, which may begin even in CKD Stage 3. Management involves routine monitoring for and correction of abnormalities in levels of phosphorus, vitamin D, calcium, and parathyroid hormone levels [Table 3].
Table 3: Evaluation and management of mineral bone disease in patients with chronic kidney disease stages 3-5 and dialysis (5D

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Children receiving chronic hemodialysis

Children receiving chronic dialysis usually require dietary restriction of sodium, potassium, phosphorus, and fluid. Provision of adequate nutrition is particularly challenging in young anuric children who are volume restricted but depend on formula, as highly concentrated feeds may exacerbate gastrointestinal symptoms. In older children, it may be difficult to meet macro- and micro-nutrient needs due to the elimination of many favorite foods. It may be tough to meet protein requirements, which are higher than the daily recommended intake (DRI) for age by 0.1 g/kg/day, to compensate for losses in dialysate. The normalized catabolic protein rate (nPCR), monitored monthly in patients with CKD 5D, is an important marker of protein and overall nutritional status; an nPCR below 1 indicates decline in nutritional status in this population.[67]

The KDOQI guidelines recommend that children on hemodialysis receive the DRI for B Vitamins, Vitamins A, C, D, E, and K, folic acid, copper, zinc, and fiber.[7] However, oral intake of many key nutrients is inadequate due to dietary restrictions on dairy products, fruits, vegetables, and whole grains that are high in potassium and/or phosphorus. These patients, therefore, require a daily multivitamin supplement specific for patients with ESRD. Reduced fiber intake also compromises bowel health. Patient and family education is necessary to provide knowledge about alternative options to ensure adequate nutritional intake, using simple dietary education materials featuring visual graphics, particularly in areas with low literacy rates and/or limited access to nutrition professionals.[68] Strategies for the management of electrolytes, fiber, vitamins, and minerals in these patients are presented in [Table 4].
Table 4: Management of electrolyte abnormalities, fiber, vitamin, and mineral intake in patients with chronic kidney disease stages 3-5 and dialysis (5D)

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Hemodialysis-related carnitine deficiency

Carnitine is a naturally occurring amino acid derivative required for the transport of fatty acids into the mitochondria and energy production in skeletal muscles and myocardium. Patients receiving chronic hemodialysis may have carnitine deficiency due to reduced intake, losses in dialysis effluent, and lack of endogenous synthesis by kidneys.[69] Carnitine losses during dialysis may lead to concurrent accumulation of long-chain acylcarnitines that may be toxic to myocytes and increased cardiovascular risks.[70] Intravenous carnitine administration during hemodialysis may protect myocytes from oxidative damage by removing excess acylcarnitines. Based on the current evidence, carnitine supplementation during hemodialysis is not part of standard of care and may be considered in patients with erythropoietin-resistant anemia or intractable hypotension.[71]

Infants and children receiving chronic peritoneal dialysis

Infants and children receiving chronic PD commonly have decreased oral intake (<75% of energy needs) due to early satiety, delayed gastric emptying, and gastroesophageal reflux (GER) associated with peritoneal dialysate dwell. Oral motor skills are also delayed, necessitating the need to assess feeding skills and initiate feeding therapy, if indicated. Inadequate dialysis prescription and loss of residual renal function are other contributors to decreased appetite.[72] These, coupled with loss of protein in the PD effluent, contribute to PEM. On the other hand, overweight patients are at risk for obesity or diabetes due to absorption of dextrose from PD fluid. Nutritional support via gastrostomy tube (G-tube) and growth hormone therapy improve growth and nutrition in young children on PD.[73]

  Management of Protein–energy Wasting in Children With Chronic Kidney Disease and End-Stage Renal Disease Top

Nutritional interventions

Nutritional interventions in children with PEW due to CKD aim to enable optimal growth and development by optimizing caloric and protein intake through oral or enteral routes. Enteral regimens must be customized to accommodate volume needs, manage electrolyte and acid–base status, and take into account patient and family preferences, with the ultimate goal of optimizing. Overfeeding should be avoided as it increases fat mass without improving muscle mass or accelerating growth.[10]

Oral nutrition

Breastmilk has ideal nutrient and electrolyte composition for infants with renal failure because it has whey-based protein and low content of phosphorus and potassium. When breastmilk is not available, a low-electrolyte infant formula with a 60:40 whey-to-casein ratio is recommended. For anorexic infants with insufficient intake, either the caloric concentration of formula may be increased or modular carbohydrate, lipid, and/or protein supplements may be added to infant formula or expressed breastmilk to increase the nutritional density of feeds. Older children who are feeding orally can be advised to take calorie-rich food items cooked in heart-healthy oils; calorie-dense (up to 60 cal/oz), renal-specific nutritional shakes; and protein bars or powders to supplement the diet. To maximize patient acceptance, the diet should be designed keeping in mind individual tastes and cultural preferences. To restrict salt intake, food should be seasoned with alternatives, such as herbs, spices, lemon, and vinegars. The primary advantage of oral nutrition intervention is that it is noninvasive as no surgical procedures are required. However, specialized formulas and supplements are expensive and often not palatable; children may also experience taste fatigue, leading to high rates of nonadherence to oral nutrition supplements over time.

Providing oral intradialytic nutrition is another strategy to help improve nutritional status in children receiving hemodialysis. Historically, eating during dialysis has been perceived as associated with the risk of hemodynamic changes such as postprandial hypotension, nausea, and aspiration; however, precise evidence is lacking.[74] Numerous studies have demonstrated that oral intradialytic feeding is safe and improves markers of PEW in adult patients on chronic hemodialysis.[75] A recent prospective pediatric study evaluated the impact of providing protein bars, small meals, or snacks to children during hemodialysis sessions.[76] While 72% of children felt better after eating, only 2% felt worse; hence, oral intradialytic feeding was perceived as being safe and well tolerated in supplementing nutrition in this population.

Enteral nutrition

Most infants and young children with kidney failure require supplemental enteral support in order to meet their nutritional needs. The KDOQI guidelines for CKD and dialysis recommend considering enteral nutrition support for children under 3 years of age with advanced CKD who cannot meet caloric needs orally, and/or are not demonstrating adequate weight gain and growth.[7] Studies show that early intervention with enteral tube feeding in such patients improves nutritional status, including increased weight gain and growth.[73],[77],[78],[79],[80] Options for administration of enteral nutrition include placement of nasogastric (NG) tube and G-tube or by postpyloric routes, such as gastrostomy–jejunostomy (GJ) or jejunostomy (J) tubes. For short-term, temporary nutrition support, NG feeding is ideal, as the tube can be placed without surgical intervention and is easily removed. However, the tube is easily dislodged or pulled out, and may exacerbate gagging, emesis, and GER. In addition, it is associated with an increased risk of posttraumatic feeding disorder in young children, which may slow the development of oral feeding skills.

Enteral nutritional supplementation via G-tube is the preferred method for long-term nutritional supplementation in children with CKD and ESRD. In children who start PD before 2 years of age, the use of enteral nutritional support is associated with consistent increases in BMI, whereas BMI declines in children who are on oral feeds alone.[73] The G-tube offers a secure access for long-term nutritional support and allows the flexibility to give either bolus or continuous feeding. G-tube does, however, require either endoscopic or surgical placement and poses some risk of infection, particularly of peritonitis in children on PD. Evidence suggests that placing the G-tube prior to PD catheter reduces infection risk.[77]

Finally, postpyloric feeding through a GJ or J-tube may be the optimal choice to ensure adequate nutrition in those with severe GER or intractable vomiting related to delayed gastric motility.[81] The jejunal route bypasses the stomach, thus reducing the risk of GER and aspiration in patients who cannot tolerate gastric feedings for the above reasons. Limitations of jejunal feeding include requirement to infuse formula at a slow continuous rate and the risk of dislodgement requiring replacement under fluoroscopy. A surgical J-tube may offer a more secure access if the patient is expected to be J-tube dependent on the long term.[81]

Intradialytic parenteral nutrition

Intradialytic parenteral nutrition (IDPN) is a form of parenteral nutrition support in which dextrose, amino acids, and lipids are infused intravenously during the hemodialysis session. It is shown to be effective in improving nutritional status in both pediatric and adult patients. A recent prospective multicentric randomized controlled trial demonstrated that 16 weeks of IDPN therapy significantly improved nutritional status and increased prealbumin levels in adult hemodialysis patients with PEW and was more effective than nutritional counseling alone.[82] Small studies in pediatric hemodialysis patients have demonstrated nutritional benefits of IDPN, including increases in nPCR, weight, BMI, and serum albumin.[83],[84],[85] Disadvantages of IDPN include its cost; need for close monitoring for side effects of the therapy, such as hyperglycemia, hypokalemia, hypophosphatemia, and hyperlipidemia;[86] and the limited amount of nutrition that can be provided within the volume and time limits of the hemodialysis session.

Increasing physical activity to help ameliorate protein–energy wasting

Physical activity is effective in ameliorating PEW in adults with advanced CKD. A Cochrane systematic review on the effects of >8 weeks of regular exercise training on markers of PEW included 41 prospective randomized controlled trials and 928 adults with CKD Stages 2–5D and posttransplantation.[87] Patients who participated in any type of exercise training had improved aerobic capacity and muscle strength compared to those who do not exercise. Further, aerobic and resistance exercise training was associated with increased mid-thigh muscle area. Various mechanisms explain the anabolic effects of exercise on muscle. Endurance exercise stimulates protein synthesis by mitochondrial biogenesis, whereas resistance training increases the expression and sensitivity of insulin signaling intermediates to increase glycogen synthesis.[88] Given its beneficial effects on aerobic capacity, strength, and muscle building, participation in regular aerobic exercise and strength training may reduce the risk of PEW in patients with CKD and ESRD. A recent study on 19 patients showed that bicycling during hemodialysis sessions decreases myocardial strain, thus reducing the risk of myocardial stunning.[89] More research is needed to investigate the benefits of exercise on nutrition and cardiovascular health in the pediatric CKD population.

  Nutritional Challenges After Transplantation Top

While undernutrition is common before transplantation, different nutritional challenges arise posttransplantation, such as rapid weight gain, obesity, and metabolic syndrome[90],[91] and development of new-onset diabetes after transplant (NODAT).[92] Magnesium wasting and hypophosphatemia are also common. Weight gain is very common in the 1st year after transplantation,[93] and then tends to stabilize. Factors that contribute to this gain include removal of dietary and fluid restrictions and improved appetite due to the reversal of uremia and intake of corticosteroids. Posttransplant obesity is associated with adverse outcomes, including increased risk of allograft failure,[94] surgical complications, and cardiovascular morbidity.[95]

Causes of posttransplant hypophosphatemia include phosphaturia due to persistently elevated levels of fibroblast growth factor-23 and hyperparathyroidism from before transplantation. Immunosuppressive medications may carry nutrition-related adverse effects. Calcineurin inhibitors, particularly tacrolimus, carry the risk for hyperglycemia, NODAT, hypomagnesemia, hyperkalemia, and hypertension. Corticosteroids (prednisone) are associated with hypertension, dyslipidemia, hyperglycemia, NODAT, increased appetite leading to weight gain/obesity, metabolic syndrome, and osteoporosis. Mycophenolate mofetil and azathioprine may have gastrointestinal adverse effects such as nausea, diarrhea, and altered taste acuity.

Posttransplant failure to thrive

Failure to thrive may occur in a subset of children after kidney transplantation. In a single-center study of pediatric kidney transplant recipients, 21.9% and 17.9% of patients had failure to thrive at 1 and 3 years posttransplantation, respectively.[96] Compared to other recipients, patients with failure to thrive were more likely to experience infections and hospitalization in the first 3 years posttransplantation.

Dependence on clean intermittent catheterization (CIC) after transplant was associated with increased risk. Inflammation, either by chronic inflammation or repeated acute inflammatory responses associated with recurrent urinary tract infections, contributes to failure to thrive in children requiring CIC after transplant, by causing hormonal alterations resulting in anorexia, increasing protein catabolism, and decreasing anabolism, thus creating a cycle of negative energy and protein balance, weight loss, muscle wasting, and poor growth.[97] The multicentric Immune Development in Pediatric Transplantation study reported an association between lower BMI at transplant with an increased risk of posttransplant viral infections and failure to thrive.[98] Hence, nutrition should be optimized both before and after transplantation to improve patient health and transplant outcomes.

Management of nutritional issues after transplantation

Posttransplant nutrition and dietary recommendations are summarized in [Table 5]. After transplant, patients and families should receive education and counseling to promote a healthy balanced diet including lean proteins, low fat or nonfat dairy, fruits, vegetables, and unsaturated fats. Intake of carbohydrates, proteins, and unsaturated fats should be maintained within ranges recommended by the acceptable macronutrient distribution range of the DRI to prevent and manage obesity, dyslipidemia, and NODAT.[7] Pediatric transplant recipients are at a high risk of early-onset cardiovascular disease, as categorized by the National Heart, Lung, and Blood Institute expert panel, warranting close monitoring of lipid levels, lifestyle and dietary interventions, and consideration of statin therapy in those who do not respond to dietary intervention.[99] The Dietary Approaches to Stop Hypertension (DASH) eating plan is known to help promote lower blood pressure[100] and help maintain a healthy weight. The principles of the diet include increased intake of foods rich in potassium, calcium, magnesium, fiber, and protein (fruits, vegetables, legumes, nuts, whole grains, and low fat dairy), as well as limiting the intake of sodium, saturated fats, and refined carbohydrates by avoiding foods such as red meats, processed foods, and sugar-sweetened beverages. Following the DASH diet after kidney transplant is independently associated with improved allograft function and lower all-cause mortality.[101]
Table 5: Nutritional management after kidney transplantation

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Mental health has a key role in overall health and nutrition outcomes after transplant. Involvement of a psychologist in posttransplant care is useful in detecting and treating nutrition-related and other mental health disorders. Bariatric surgery may be considered for patients with morbid obesity posttransplant that cannot be corrected by diet intervention, and has been successfully performed in solid organ transplant recipients, resulting in weight loss and reduced comorbidities with stable and therapeutic immunosuppression drug levels.[106]

  Conclusions Top

Nutritional disorders, including malnutrition, PEW, obesity, and metabolic syndrome, affect children across the entire spectrum of CKD, dialysis, and transplant. They negatively impact patient outcomes by increasing morbidity and mortality and increasing the risk of infection, hospitalization, and length of stay, which leads to increased health-care costs, poor cognition, and decreased quality of life. Early intervention is the key to negate the effects of nutritional disorders on health outcomes, and emphasis should be placed to optimize nutrition throughout the journey of child through different phases of CKD.

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Conflicts of interest

There are no conflicts of interest.

  References Top

Corkins MR, Guenter P, DiMaria-Ghalili RA, Jensen GL, Malone A, Miller S, et al. Malnutrition diagnoses in hospitalized patients: United States, 2010. JPEN J Parenter Enteral Nutr 2014;38:186-95.  Back to cited text no. 1
Becker P, Carney LN, Corkins MR, Monczka J, Smith E, Smith SE, et al. Consensus statement of the academy of nutrition and dietetics/American society for parenteral and enteral nutrition: Indicators recommended for the identification and documentation of pediatric malnutrition (undernutrition). Nutr Clin Pract 2015;30:147-61.  Back to cited text no. 2
Rodig NM, McDermott KC, Schneider MF, Hotchkiss HM, Yadin O, Seikaly MG, et al. Growth in children with chronic kidney disease: A report from the chronic kidney disease in children study. Pediatr Nephrol 2014;29:1987-95.  Back to cited text no. 3
Chen W, Ducharme-Smith K, Davis L, Hui WF, Warady BA, Furth SL, et al. Dietary sources of energy and nutrient intake among children and adolescents with chronic kidney disease. Pediatr Nephrol 2017;32:1233-41.  Back to cited text no. 4
Ogden CL, Kuczmarski RJ, Flegal KM, Mei Z, Guo S, Wei R, et al. Centers for disease control and prevention 2000 growth charts for the United States: Improvements to the 1977 National Center for Health Statistics Version. Pediatrics 2002;109:45-60.  Back to cited text no. 5
Gao T, Leonard MB, Zemel B, Kalkwarf HJ, Foster BJ. Interpretation of body mass index in children with CKD. Clin J Am Soc Nephrol 2012;7:558-64.  Back to cited text no. 6
KDOQI Work Group. KDOQI clinical practice guideline for nutrition in children with CKD: 2008 update. Executive summary. Am J Kidney Dis 2009;53:S11-104.  Back to cited text no. 7
Cook S, Auinger P, Huang TT. Growth curves for cardio-metabolic risk factors in children and adolescents. J Pediatr 2009;155:S6.e15-26.  Back to cited text no. 8
Kahn HS, Imperatore G, Cheng YJ. A population-based comparison of BMI percentiles and waist-to-height ratio for identifying cardiovascular risk in youth. J Pediatr 2005;146:482-8.  Back to cited text no. 9
Abraham AG, Mak RH, Mitsnefes M, White C, Moxey-Mims M, Warady B, et al. Protein energy wasting in children with chronic kidney disease. Pediatr Nephrol 2014;29:1231-8.  Back to cited text no. 10
Carrero JJ, Stenvinkel P, Cuppari L, Ikizler TA, Kalantar-Zadeh K, Kaysen G, et al. Etiology of the protein-energy wasting syndrome in chronic kidney disease: A consensus statement from the International Society of Renal Nutrition and Metabolism (ISRNM). J Ren Nutr 2013;23:77-90.  Back to cited text no. 11
Fouque D, Kalantar-Zadeh K, Kopple J, Cano N, Chauveau P, Cuppari L, et al. Aproposed nomenclature and diagnostic criteria for protein-energy wasting in acute and chronic kidney disease. Kidney Int 2008;73:391-8.  Back to cited text no. 12
Clinical practice guidelines for nutrition in chronic renal failure. K/DOQI, National Kidney Foundation. Am J Kidney Dis 2000;35:S1-140.  Back to cited text no. 13
Secker DJ, Jeejeebhoy KN. How to perform subjective global nutritional assessment in children. J Acad Nutr Diet 2012;112:424-31.e6.  Back to cited text no. 14
Secker D, Cornelius V, Teh J. Validation of subjective global (Nutritional) assessment (SGNA) in children with CKD (abstract). J Renal Nutr 2011;21:207.  Back to cited text no. 15
Academy Quality Management Committee and Scope of Practice Subcommittee of Quality Management Committee. Academy of nutrition and dietetics: Revised 2012 standards of practice in nutrition care and standards of professional performance for registered dietitians. J Acad Nutr Diet 2013;113:S29-45.  Back to cited text no. 16
Green Corkins K. Nutrition-focused physical examination in pediatric patients. Nutr Clin Pract 2015;30:203-9.  Back to cited text no. 17
Carrero JJ, Thomas F, Nagy K, Arogundade F, Avesani CM, Chan M, et al. Global prevalence of protein-energy wasting in kidney disease: A Meta-analysis of contemporary observational studies from the international society of renal nutrition and metabolism. J Ren Nutr 2018;28:380-92.  Back to cited text no. 18
Brem AS, Lambert C, Hill C, Kitsen J, Shemin DG. Prevalence of protein malnutrition in children maintained on peritoneal dialysis. Pediatr Nephrol 2002;17:527-30.  Back to cited text no. 19
Apostolou A, Printza N, Karagiozoglou-Lampoudi T, Dotis J, Papachristou F. Nutrition assessment of children with advanced stages of chronic kidney disease-A single center study. Hippokratia 2014;18:212-6.  Back to cited text no. 20
Sozeri B, Mir S, Kara OD, Dincel N. Growth impairment and nutritional status in children with chronic kidney disease. Iran J Pediatr 2011;21:271-7.  Back to cited text no. 21
Rashid R, Neill E, Smith W, King D, Beattie TJ, Murphy A, et al. Body composition and nutritional intake in children with chronic kidney disease. Pediatr Nephrol 2006;21:1730-8.  Back to cited text no. 22
Sgambat K, Roem J, Mitsnefes M, Portale AA, Furth S, Warady B, et al. Waist-to-height ratio, body mass index, and cardiovascular risk profile in children with chronic kidney disease. Pediatr Nephrol 2018;33:1577-83.  Back to cited text no. 23
Sgambat K, Clauss S, Moudgil A. Comparison of BMI, waist circumference, and waist-to-height ratio for identification of subclinical cardiovascular risk in pediatric kidney transplant recipients. Pediatr Transplant 2018;22:e13300.  Back to cited text no. 24
Ravindranath J, Pillai PP, Parameswaran S, Kamalanathan SK, Pal GK. Body fat analysis in predialysis chronic kidney disease: Multifrequency bioimpedance assay and anthropometry compared with dual-energy X-ray absorptiometry. J Ren Nutr 2016;26:315-9.  Back to cited text no. 25
Zemel BS, Leonard MB, Kelly A, Lappe JM, Gilsanz V, Oberfield S, et al. Height adjustment in assessing dual energy x-ray absorptiometry measurements of bone mass and density in children. J Clin Endocrinol Metab 2010;95:1265-73.  Back to cited text no. 26
Foster BJ, Leonard MB. Measuring nutritional status in children with chronic kidney disease. Am J Clin Nutr 2004;80:801-14.  Back to cited text no. 27
Correa M, Laing DG, Hutchinson I, Jinks AL, Armstrong JE, Kainer G, et al. Reduced taste function and taste papillae density in children with chronic kidney disease. Pediatr Nephrol 2015;30:2003-10.  Back to cited text no. 28
Manley KJ. Taste genetics and gastrointestinal symptoms experienced in chronic kidney disease. Eur J Clin Nutr 2015;69:781-5.  Back to cited text no. 29
Chou HC, Chien CL, Huang HL, Lu KS. Effects of zinc deficiency on the vallate papillae and taste buds in rats. J Formos Med Assoc 2001;100:326-35.  Back to cited text no. 30
Cheung WW, Paik KH, Mak RH. Inflammation and cachexia in chronic kidney disease. Pediatr Nephrol 2010;25:711-24.  Back to cited text no. 31
Iorember FM. Malnutrition in chronic kidney disease. Front Pediatr 2018;6:161.  Back to cited text no. 32
Cruz-Mora J, Martínez-Hernández NE, Martín del Campo-López F, Viramontes-Hörner D, Vizmanos-Lamotte B, Muñoz-Valle JF, et al. Effects of a symbiotic on gut microbiota in Mexican patients with end-stage renal disease. J Ren Nutr 2014;24:330-5.  Back to cited text no. 33
Pisano A, D'Arrigo G, Coppolino G, Bolignano D. Biotic supplements for renal patients: A systematic review and meta-analysis. Nutrients 2018;10. pii: E1224.  Back to cited text no. 34
Tao S, Tao S, Cheng Y, Liu J, Ma L, Fu P, et al. Effects of probiotic supplements on the progression of chronic kidney disease: A meta-analysis. Nephrology (Carlton) 2018. doi: 10.1111/nep.13549. [Epub ahead of print].  Back to cited text no. 35
Boirie Y, Broyer M, Gagnadoux MF, Niaudet P, Bresson JL. Alterations of protein metabolism by metabolic acidosis in children with chronic renal failure. Kidney Int 2000;58:236-41.  Back to cited text no. 36
Parekh RS, Flynn JT, Smoyer WE, Milne JL, Kershaw DB, Bunchman TE, et al. Improved growth in young children with severe chronic renal insufficiency who use specified nutritional therapy. J Am Soc Nephrol 2001;12:2418-26.  Back to cited text no. 37
Quan A, Baum M. Protein losses in children on continuous cycler peritoneal dialysis. Pediatr Nephrol 1996;10:728-31.  Back to cited text no. 38
Lim VS, Kopple JD. Protein metabolism in patients with chronic renal failure: Role of uremia and dialysis. Kidney Int 2000;58:1-10.  Back to cited text no. 39
Asghar W, Nazir W, Khalid N. A question mark on emerging zinc-related nutritional deficiencies in Pakistani population. Asia Pac J Public Health 2018;30:500-2.  Back to cited text no. 40
Joyce T, Court Brown F, Wallace D, Reid CJ, Sinha MD. Trace element and vitamin concentrations in paediatric dialysis patients. Pediatr Nephrol 2018;33:159-65.  Back to cited text no. 41
Esmaeili M, Rakhshanizadeh F. Serum trace elements in children with end-stage renal disease. J Ren Nutr 2019;29:48-54.  Back to cited text no. 42
Nagraj SK, Naresh S, Srinivas K, Renjith George P, Shrestha A, Levenson D, et al. Interventions for the management of taste disturbances. Cochrane Database Syst Rev 2014;11:CD010470.  Back to cited text no. 43
Filler G, Felder S. Trace elements in dialysis. Pediatr Nephrol 2014;29:1329-35.  Back to cited text no. 44
Akchurin OM, Schneider MF, Mulqueen L, Brooks ER, Langman CB, Greenbaum LA, et al. Medication adherence and growth in children with CKD. Clin J Am Soc Nephrol 2014;9:1519-25.  Back to cited text no. 45
Blydt-Hansen TD, Pierce CB, Cai Y, Samsonov D, Massengill S, Moxey-Mims M, et al. Medication treatment complexity and adherence in children with CKD. Clin J Am Soc Nephrol 2014;9:247.  Back to cited text no. 46
Hui WF, Betoko A, Savant JD, Abraham AG, Greenbaum LA, Warady B, et al. Assessment of dietary intake of children with chronic kidney disease. Pediatr Nephrol 2017;32:485-94.  Back to cited text no. 47
Taylor JM, Oladitan L, Degnan A, Henderson S, Dai H, Warady BA, et al. Psychosocial factors that create barriers to managing serum phosphorus levels in pediatric dialysis patients: A retrospective analysis. J Ren Nutr 2016;26:270-5.  Back to cited text no. 48
Palmer SC, Hanson CS, Craig JC, Strippoli GF, Ruospo M, Campbell K, et al. Dietary and fluid restrictions in CKD: A thematic synthesis of patient views from qualitative studies. Am J Kidney Dis 2015;65:559-73.  Back to cited text no. 49
Berlin KS, Hains AA, Kamody RC, Kichler JC, Davies WH. Differentiating peer and friend social information-processing effects on stress and glycemic control among youth with type 1 diabetes. J Pediatr Psychol 2015;40:492-9.  Back to cited text no. 50
Datye KA, Moore DJ, Russell WE, Jaser SS. A review of adolescent adherence in type 1 diabetes and the untapped potential of diabetes providers to improve outcomes. Curr Diab Rep 2015;15:51.  Back to cited text no. 51
Maikranz JM, Steele RG, Dreyer ML, Stratman AC, Bovaird JA. The relationship of hope and illness-related uncertainty to emotional adjustment and adherence among pediatric renal and liver transplant recipients. J Pediatr Psychol 2007;32:571-81.  Back to cited text no. 52
Shaw RJ, Palmer L, Blasey C, Sarwal M. A typology of non-adherence in pediatric renal transplant recipients. Pediatr Transplant 2003;7:489-93.  Back to cited text no. 53
Kogon AJ, Matheson MB, Flynn JT, Gerson AC, Warady BA, Furth SL, et al. Depressive symptoms in children with chronic kidney disease. J Pediatr 2016;168:164-700.  Back to cited text no. 54
Ameh OI, Cilliers L, Okpechi IG. A practical approach to the nutritional management of chronic kidney disease patients in Cape Town, South Africa. BMC Nephrol 2016;17:68.  Back to cited text no. 55
Milazi M, Bonner A, Douglas C. Effectiveness of educational or behavioral interventions on adherence to phosphate control in adults receiving hemodialysis: A systematic review. JBI Database System Rev Implement Rep 2017;15:971-1010.  Back to cited text no. 56
Powell PW, Hilliard ME, Anderson BJ. Motivational interviewing to promote adherence behaviors in pediatric type 1 diabetes. Curr Diab Rep 2014;14:531.  Back to cited text no. 57
Coleman-Jensen A, Rabbitt MP, Gregory CA, Singh A. Household Food Security in the United States in 2017. United States Department of Agriculture Economic Research Service. Economic Research Report No. (ERR-256); 2017. p. 44.  Back to cited text no. 58
Dharmaraju N, Mauleshbhai SS, Arulappan N, Thomas B, Marconi DS, Paul SS, et al. Household food security in an urban slum: Determinants and trends. J Family Med Prim Care 2018;7:819-22.  Back to cited text no. 59
[PUBMED]  [Full text]  
Misselhorn A, Hendriks SL. A systematic review of sub-national food insecurity research in South Africa: Missed opportunities for policy insights. PLoS One 2017;12:e0182399.  Back to cited text no. 60
Omuemu VO, Otasowie EM, Onyiriuka U. Prevalence of food insecurity in Egor local government area of Edo state, Nigeria. Ann Afr Med 2012;11:139-45.  Back to cited text no. 61
  [Full text]  
Ihabi AN, Rohana AJ, Wan Manan WM, Wan Suriati WN, Zalilah MS, Rusli AM, et al. Nutritional outcomes related to household food insecurity among mothers in rural Malaysia. J Health Popul Nutr 2013;31:480-9.  Back to cited text no. 62
Banerjee T, Crews DC, Wesson DE, Dharmarajan S, Saran R, Ríos Burrows N, et al. Food insecurity, CKD, and subsequent ESRD in US adults. Am J Kidney Dis 2017;70:38-47.  Back to cited text no. 63
Starr MC, Fisher K, Thompson K, Thurber-Smith K, Hingorani S. A pilot investigation of food insecurity among children seen in an outpatient pediatric nephrology clinic. Prev Med Rep 2018;10:113-6.  Back to cited text no. 64
Jomaa L, Naja F, Cheaib R, Hwalla N. Household food insecurity is associated with a higher burden of obesity and risk of dietary inadequacies among mothers in Beirut, Lebanon. BMC Public Health 2017;17:567.  Back to cited text no. 65
Clegg DJ, Hill Gallant KM. Plant-based diets in CKD. Clin J Am Soc Nephrol 2019;14:141-3.  Back to cited text no. 66
Juarez-Congelosi M, Orellana P, Goldstein SL. Normalized protein catabolic rate versus serum albumin as a nutrition status marker in pediatric patients receiving hemodialysis. J Ren Nutr 2007;17:269-74.  Back to cited text no. 67
Verseput C, Piccoli GB. Eating like a rainbow: The development of a visual aid for nutritional treatment of CKD patients. A South African project. Nutrients 2017;9. pii: E435.  Back to cited text no. 68
Schreiber B. Levocarnitine and dialysis: A review. Nutr Clin Pract 2005;20:218-43.  Back to cited text no. 69
Fritz IB, Arrigoni-Martelli E. Sites of action of carnitine and its derivatives on the cardiovascular system: Interactions with membranes. Trends Pharmacol Sci 1993;14:355-60.  Back to cited text no. 70
Shuren J, Hippler S, Long K. (2002, July 22). Decision Memo for Levocarnitine for End Stage Renal Disease. Centers for Medicare and Medicaid Services. Retrieved from: www.cms.gov. [Last accessed on 2019 Apr 02].  Back to cited text no. 71
Roszkowska-Blaim M, Skrzypczyk P. Residual renal function in children treated with chronic peritoneal dialysis. ScientificWorldJournal 2013;2013:154537.  Back to cited text no. 72
Rees L, Azocar M, Borzych D, Watson AR, Büscher A, Edefonti A, et al. Growth in very young children undergoing chronic peritoneal dialysis. J Am Soc Nephrol 2011;22:2303-12.  Back to cited text no. 73
Kistler BM, Fitschen PJ, Ikizler TA, Wilund KR. Rethinking the restriction on nutrition during hemodialysis treatment. J Ren Nutr 2015;25:81-7.  Back to cited text no. 74
Kalantar-Zadeh K, Ikizler TA. Let them eat during dialysis: An overlooked opportunity to improve outcomes in maintenance hemodialysis patients. J Ren Nutr 2013;23:157-63.  Back to cited text no. 75
South AM, Fainman B, Sutherland SM, Wong CJ. Children tolerate intradialytic oral nutrition. J Ren Care 2018;44:38-43.  Back to cited text no. 76
Mekahli D, Shaw V, Ledermann SE, Rees L. Long-term outcome of infants with severe chronic kidney disease. Clin J Am Soc Nephrol 2010;5:10-7.  Back to cited text no. 77
Ledermann SE, Scanes ME, Fernando ON, Duffy PG, Madden SJ, Trompeter RS. Long-term outcome of peritoneal dialysis in infants. J Pediatr 2000;136:24-9.  Back to cited text no. 78
Ledermann SE, Shaw V, Trompeter RS. Long-term enteral nutrition in infants and young children with chronic renal failure. Pediatr Nephrol 1999;13:870-5.  Back to cited text no. 79
Ramage IJ, Geary DF, Harvey E, Secker DJ, Balfe JA, Balfe JW. Efficacy of gastrostomy feeding in infants and older children receiving chronic peritoneal dialysis. Perit Dial Int 1999;19:231-6.  Back to cited text no. 80
Raval MV, Phillips JD. Optimal enteral feeding in children with gastric dysfunction: Surgical jejunostomy vs. image-guided gastrojejunal tube placement. J Pediatr Surg 2006;41:1679-82.  Back to cited text no. 81
Marsen TA, Beer J, Mann H; German IDPN-Trial group. Intradialytic parenteral nutrition in maintenance hemodialysis patients suffering from protein-energy wasting. Results of a multicenter, open, prospective, randomized trial. Clin Nutr 2017;36:107-17.  Back to cited text no. 82
Haskin O, Sutherland SM, Wong CJ. The effect of intradialytic intralipid therapy in pediatric hemodialysis patients. J Ren Nutr 2017;27:132-7.  Back to cited text no. 83
Goldstein SL, Baronette S, Gambrell TV, Currier H, Brewer ED. NPCR assessment and IDPN treatment of malnutrition in pediatric hemodialysis patients. Pediatr Nephrol 2002;17:531-4.  Back to cited text no. 84
Orellana P, Juarez-Congelosi M, Goldstein SL. Intradialytic parenteral nutrition treatment and biochemical marker assessment for malnutrition in adolescent maintenance hemodialysis patients. J Ren Nutr 2005;15:312-7.  Back to cited text no. 85
Juarez MD. Intradialytic parenteral nutrition in pediatrics. Front Pediatr 2018;6:267.  Back to cited text no. 86
Heiwe S, Jacobson SH. Exercise training for adults with chronic kidney disease. Cochrane Database Syst Rev 2011;10:CD003236.  Back to cited text no. 87
LeBrasseur NK, Walsh K, Arany Z. Metabolic benefits of resistance training and fast glycolytic skeletal muscle. Am J Physiol Endocrinol Metab 2011;300:E3-10.  Back to cited text no. 88
Penny JD, Salerno FR, Brar R, Garcia E, Rossum K, McIntyre CW, et al. Intradialytic exercise preconditioning: An exploratory study on the effect on myocardial stunning. Nephrol Dial Transplant 2018. doi: 10.1093/ndt/gfy376.  Back to cited text no. 89
Sgambat K, Clauss S, Moudgil A. Cardiovascular effects of metabolic syndrome after transplantation: Convergence of obesity and transplant-related factors. Clin Kidney J 2018;11:136-46.  Back to cited text no. 90
Litwin M, Niemirska A. Metabolic syndrome in children with chronic kidney disease and after renal transplantation. Pediatr Nephrol 2014;29:203-16.  Back to cited text no. 91
Garro R, Warshaw B, Felner E. New-onset diabetes after kidney transplant in children. Pediatr Nephrol 2015;30:405-16.  Back to cited text no. 92
Wilson AC, Mitsnefes MM. Cardiovascular disease in CKD in children: Update on risk factors, risk assessment, and management. Am J Kidney Dis 2009;54:345-60.  Back to cited text no. 93
Ladhani M, Lade S, Alexander SI, Baur LA, Clayton PA, McDonald S, et al. Obesity in pediatric kidney transplant recipients and the risks of acute rejection, graft loss and death. Pediatr Nephrol 2017;32:1443-50.  Back to cited text no. 94
Terrace JD, Oniscu GC. Paediatric obesity and renal transplantation: Current challenges and solutions. Pediatr Nephrol 2016;31:555-62.  Back to cited text no. 95
Sgambat K, Cheng YI, Charnaya O, Moudgil A. The prevalence and outcome of children with failure to thrive after pediatric kidney transplantation. Pediatr Transplant 2019;23:e13321.  Back to cited text no. 96
Delano MJ, Moldawer LL. The origins of cachexia in acute and chronic inflammatory diseases. Nutr Clin Pract 2006;21:68-81.  Back to cited text no. 97
Ettenger R, Chin H, Kesler K, Bridges N, Grimm P, Reed EF, et al. Relationship among viremia/Viral infection, alloimmunity, and nutritional parameters in the first year after pediatric kidney transplantation. Am J Transplant 2017;17:1549-62.  Back to cited text no. 98
Expert Panel on Integrated Guidelines for Cardiovascular Health and Risk Reduction in Children and Adolescents, National Heart, Lung, and Blood Institute. Expert panel on integrated guidelines for cardiovascular health and risk reduction in children and adolescents: Summary report. Pediatrics 2011;128 Suppl 5:S213-56.  Back to cited text no. 99
Sacks FM, Appel LJ, Moore TJ, Obarzanek E, Vollmer WM, Svetkey LP, et al. Adietary approach to prevent hypertension: A review of the dietary approaches to stop hypertension (DASH) study. Clin Cardiol 1999;22:III6-10.  Back to cited text no. 100
Osté MCJ, Gomes-Neto AW, Corpeleijn E, Gans ROB, de Borst MH, van den Berg E, et al. Dietary approach to stop hypertension (DASH) diet and risk of renal function decline and all-cause mortality in renal transplant recipients. Am J Transplant 2018;18:2523-33.  Back to cited text no. 101
Yemini R, Nesher E, Winkler J, Carmeli I, Azran C, Ben David M, et al. Bariatric surgery in solid organ transplant patients: Long-term follow-up results of outcome, safety, and effect on immunosuppression. Am J Transplant 2018;18:2772-80.  Back to cited text no. 102
Thompson K, Flynn J, Okamura D, Zhou L. Pretreatment of formula or expressed breast milk with sodium polystyrene sulfonate (Kayexalate(®)) as a treatment for hyperkalemia in infants with acute or chronic renal insufficiency. J Ren Nutr 2013;23:333-9.  Back to cited text no. 103
Nelms CL. Optimizing enteral nutrition for growth in pediatric chronic kidney disease (CKD). Front Pediatr 2018;6:214.  Back to cited text no. 104
US Government Printing Office. USDA Dietary Guidelines for Americans. 7th ed. Washington, DC: US Government Printing Office; 2010.  Back to cited text no. 105
Manickavasagar B, McArdle AJ, Yadav P, Shaw V, Dixon M, Blomhoff R, et al. Hypervitaminosis A is prevalent in children with CKD and contributes to hypercalcemia. Pediatr Nephrol 2015;30:317-25.  Back to cited text no. 106


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  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]


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