The kidneys play an essential role in the maintenance of homeostasis by excreting waste products, such as urea and uric acid, and purposely adjusting the urinary excretion of water and electrolytes (solute) to counter dietary intake and the body’s endogenous production of these from metabolism. The kidneys have a major role in the secretion of hormones. This includes erythropoietin for red blood cell production, renin and angiotensin II affecting renal and systemic haemodynamics, as well as hydroxylated vitamin D affecting calcium, phosphate and bone metabolism. Other functions include peptide hormone catabolism and gluconeogenesis.
A variety of diseases can affect the kidneys leading to a sudden deterioration in renal function (acute kidney injury) or an irreversible deterioration of renal function (chronic kidney disease). Impairment of excretory, regulatory and endocrine functions is seen as kidney function deteriorates and the management of these impairments is the foundation of treatment.
Acute kidney injury (AKI) is characterised by an abrupt and reversible decline in renal function leading to an increase in the blood concentration of urea and creatinine and the inability of the kidneys to regulate fluid and electrolyte balance effectively. An incidence of 0.8 per 100 000 total child population has been reported  with the highest incidence seen in the neonatal period. The incidence in children is increasing with a change in aetiology from primary renal disease to multifactorial causes . In childhood, AKI may be associated with anuria (urine output <1 mL/kg/day), oliguria (urine output <0.5–1.0 mL/kg/hour), a normal urine output or high urine output. The causes of AKI in children are classified as pre-renal, intrinsic renal disease or post-renal  (Table 12.1).
Table 12.1 Causes of acute renal injury in children
|Pre-renal failure||Intrinsic renal failure||Post-renal failure|
|Hypovolaemia (gastroenteritis, haemorrhage)||Diseases of the kidney or vessels (acute glomerulonephritis, acute tubular necrosis, haemolytic uraemic syndrome, vasculitis, hypoplasia)||Obstruction (posterior uretheral valves, calculi, tumours, trauma)|
|Peripheral vasodilation (sepsis, antihypertensive medications)||Myoglobinuria|
|Impaired cardiac output||Intratubular obstruction (uric acid)|
|Bilateral renal vessel occlusion||Iatrogenic factors (removal of solitary kidney)|
|Drugs (ciclosporin, diuretics)||Tumour infiltrate|
|Nephrotoxic drugs (antimicrobials, heavy metals, insecticides, cytotoxic agents)|
Diarrhoea associated haemolytic uraemic syndrome (HUS) remains the commonest cause of intrinsic AKI in childhood. It leads to significant morbidity and mortality during the acute phase . The most common infectious agent causing HUS is enterohaemorrhagic Escherichia coli (EHEC), usually of the serotype 0157:H7 . Foods of bovine origin including beefburgers and unpasteurised milk, as well as contact with farm animals, are major sources for human infection although EHEC has been recovered from many retail foods. HUS is classically characterised by the sudden onset of haemolytic anaemia, thrombocytopenia and the development of AKI after acute gastroenteritis, often with bloody diarrhoea.
Management of AKI
The initial management of AKI focuses on the correction of fluid balance and biochemical abnormalities including hyponatraemia, hyperkalaemia and acidosis which can be life threatening. Further injury to the kidney should be prevented through maintaining adequate blood pressure and avoiding nephrotoxic medication. Transfer to a tertiary nephrology centre is indicated in those children requiring renal replacement therapy (RRT).
Such indications for RRT include
- severe or persistent hyperkalaemia
- fluid overload with hypertension, congestive cardiac failure or pulmonary oedema
- severe uraemia
- metabolic abnormalities including acidosis, hyponatraemia or hypernatraemia, hypocalcaemia
- fluid removal to allow the provision of nutrition
- removal of a dialysable drug or toxin
Choice of renal replacement therapy
The selection of RRT in acutely ill children depends upon the availability of treatment modalities and ventilatory support, the patient’s requirements for fluid and solute removal and haemodynamic stability. The choice is between peritoneal dialysis (PD), continuous renal replacement therapy (CRRT) and intermittent haemodialysis (IHD). Factors determining the choice of RRT include the desired outcome of therapy and clinical condition of the child as indicated in Table 12.2 . PD is the preferred modality in children as it is well tolerated and there are no rapid fluid shifts. IHD is used when there is an urgent need for solute removal. For the critically ill child in the paediatric intensive care unit (PICU), CRRT is the favoured treatment.
Table 12.2 Indications for choice of renal replacement therapy in acute kidney injury
|Indication for dialysis||Clinical condition||Modality indicated|
|PD, isolated ultrafiltration on HD|
|Solute and fluid removal||Stable/unstable||HD, PD, CRRT|
|Tumour lysis syndrome||Stable/unstable||HD followed by CRRT|
|Toxin or drug removal||Stable/unstable||CRRT, IHD for some drugs|
HD, haemodialysis; CRRT, continuous renal replacement therapy; PD, peritoneal dialysis; IHD, intermittent haemodialysis.
Nutritional management of AKI
Children with AKI are highly catabolic. This is usually multifactorial manifesting as anorexia, the catabolic nature of the underlying disorder, increased breakdown and reduced synthesis of muscle protein, increased hepatic gluconeogenesis, nutrient losses in drainage fluids or dialysis and impaired access to food. Input from a paediatric dietitian with experience in renal disease is essential from the onset as the dietary prescription varies with clinical management and the stage of the illness .
Nutritional support aims to provide sufficient energy to avoid catabolism, starvation and ketoacidosis as well as to control metabolic abnormalities. The provision of nutrition is easier once dialysis is initiated since the fluid removed by ultrafiltration allows larger volumes of feed to be given. Nutritional intervention for children with AKI depends on
- clinical management: conservative versus RRT
- biochemical assessment: plasma levels of sodium, potassium, bicarbonate, urea, creatinine, albumin, glucose, calcium, magnesium and phosphate should be regularly monitored and reviewed (Tables 12.3a and 12.3b)
- cause of AKI including the involvement of other organs
- gastrointestinal functioning
- growth parameters: height (if available) and weight plotted on a growth chart ; weight recordings prior to the onset of AKI will help determine a more accurate estimation of dry weight
- dietary history: if the child is eating
Table 12.3 Reference ranges (Central Manchester Foundation Trust)
|(a) Guidelines for normal serum values|
|Sodium (mmol/L)||<1 month||130–145|
|Potassium (mmol/L)||<1 month||3.5–6.0|
|Urea (mmol/L)||1 month||2.0–5.0|
|Albumin (g/L)||<1 month||25–35|
|Calcium (mmol/L)||<2 weeks||1.9–2.8|
|serum total||>2 weeks||2.2–2.7|
|Phosphate (mmol/L)||<1 month||1.4–2.8|
|5 weeks to 1 year||1.2–2.2|
|Glucose (mmol/L)||<1 month||2.5–5.5|
|(b) Guidelines for normal serum creatinine values|
|Age||Serum creatinine (µmol/L)|
|1 month to 1 year||<40|
|16 years to adult male||40–960|
|16 years to adult female||26–86|
Ketones interfere positively. Bilirubin interferes negatively.
Methods of feeding
The child with AKI may initially take oral fluids readily, driven by thirst. However, vomiting is common. Most children fail to achieve nutritional targets through diet alone. As the duration of the acute illness can be prolonged, the passing of a fine bore nasogastric tube is recommended. The tube can be passed at the time of sedation or when anaesthetised for procedures including the insertion of a peritoneal dialysis catheter or arterial line . This allows the provision of early nutritional support because anorexia, vomiting or food refusal can impair management and may increase parental anxiety.
A continuous 24 hour feeding regimen using an enteral feeding pump at a slow rate (10–20 mL/hour) is advantageous in the initial stages of treatment when vomiting is present. As oral intake improves, the transition from continuous to overnight feeding provides the outstanding nutritional prescription until appetite improves sufficiently to allow tube feeding to be discontinued. Those children with persistent diarrhoea may tolerate a hydrolysed protein feed (see Tables 7.6, 7.11) before considering parenteral nutrition.
The parenteral route is only considered when enteral nutrition is not tolerated. Standard hospital parenteral nutrition (PN) regimens are often unsuitable for the child with AKI because of their electrolyte composition and the amount of fluid they provide. An appropriate daily nutritional prescription to meet individual requirements should be agreed by the dietitian, pharmacist and medical staff. When formulating PN, nitrogen and electrolyte modified solutions, together with increased energy from carbohydrate and fat solutions where fluid allowance is limited, need to be considered. On CRRT the loss of nutrients through filtration and dialysis needs to be compensated for in the replacement fluids (see Fluid); levels need to be greater than those found in standard PN regimens. For many children PN is temporary and the enteral route is re-established as soon as gut function returns.
There are few data on the nutritional requirements of critically ill children with AKI and on RRT. Most of the information is derived from adult data.
Little is known about the energy requirements of infants and children with AKI . A minimum of the estimated average requirement (EAR) for energy  for healthy children of the same chronological age provides a guide (Table 12.4). These recommendations can be difficult to achieve during acute treatment; it is important to provide the maximum energy intake tolerated within the prescribed fluid allowance. The early addition of glucose polymers to water (flavoured with squash or cordial if desired) or to drinks of choice is recommended. It is prudent to start at a concentration of 0.5 kcal (2 kJ)/mL, building up to a concentration of 1 kcal (4 kJ)/mL, or 25% carbohydrate (CHO) concentration, depending on individual tolerance. Liquid glucose polymer preparations can also be used, but require dilution with water to be tolerated by children. It is recommended to start with a 1:5 dilution of liquid glucose polymer, building up to a final 1:3 dilution. The neutral preparations can be flavoured with squash or cordial. When fluid is severely restricted, ice cubes and lollies can be prepared with these energy dense solutions and offered at frequent intervals. Energy rich CHO drinks including original bottled Lucozade Energy (17.2% CHO concentration) and Mountain Dew (13% CHO concentration) can be useful alternatives for those children who refuse to drink prescribed energy supplements.
Table 12.4 Nutritional guidelines for the child with acute kidney injury
|(kcal/kg body weight/day)||(g/kg body weight/day)|
|0–2 months||95–120 (400–500 kJ)||1.0–2.1|
|Infants/children/adolescents||EAR for chronological age||1.0|
|0–2 months||95–120 (400–500 kJ)||2.1–2.5†|
|Infants/children/adolescents||EAR for chronological age||1.0–2.5|
|0–2 months||95–120 (400–500 kJ)||1.0–2.1|
|Infants/children/adolescents||EAR for chronological age||1.0–1.8|
|0–2 months||95–120 (400–500 kJ)||2.5–3.0|
|Infants/children/adolescents||EAR for chronological age||2.5|
EAR, estimated average requirement [8, 9]; CRRT, continuous renal replacement therapy.
* These guidelines are rarely achieved in the acute stage when fluid is restricted.
† If dialysis is prolonged, increased protein may be required.
A list of energy supplements that can be considered is given in Table 12.5. These can be successfully added to infant formulas to increase energy density:
- in infants up to 6 months of age, 0.85–1.0 kcal/mL (3.6–4 kJ/mL) is usually tolerated
- in infants from 6 to 12 months of age, 1.0–1.5 kcal/mL (4–6 kJ/mL) should be tolerated
Table 12.5 Nutritional supplements
|Powder, e.g. Polycal, Super Soluble Maxijul, Vitajoule||Add to infant formula, baby juice, cow’s milk, squash, fizzy drinks, tea, milk shake, ice cubes and lollies|
|Liquid, e.g. Polycal||Dilute with water, cordial or fizzy drinks of choice (unless fluid restricted), add to jelly|
|e.g. Calogen, Liquigen||Add to infant formula, cow’s milk, nutritionally complete supplements|
|Combined fat and carbohydrate|
|e.g. Super Soluble Duocal Powder, QuickCal||Add to infant formula, cow’s milk, nutritionally complete supplements|
|e.g. Protifar, Vitapro, Renapro||Add to infant formula, Liquid Duocal, modular feed components|
|Renal specific infant formulas|
|Powder per 100 g: 7.5 g protein, 503 kcal (2104 kJ), 93 mg phosphorus, 3 mmol potassium, 10 mmol sodium||For infants with CKD or conservatively managed AKI|
|20% solution (20 g powder made up to 100 mL with water): 1.5 g protein, 101 kcal (421 kJ), 18.6 mg phosphorus, 0.6 mmol potassium, 2 mmol sodium|
|Powder per 100 g: 7.5 g protein, 494 kcal (2066 kJ), 92 mg phosphorus, 3 mmol potassium, 10.5 mmol sodium|
|20% solution (20 g powder made up to 100 mL with water): 1.5 g protein, 99 kcal (413 kJ), 18 mg phosphorus, 0.6 mmol potassium, 2.1 mmol sodium|
|Nutritionally complete feeds|
|Nutrini per 100 mL: 2.8 g protein, 100 kcal (420 kJ), 50 mg phosphorus, 2.8 mmol potassium, 2.6 mmol sodium||For oral or supplementary tube feeding in children >1 year and weight >8 kg|
|Paediasure per 100 mL: 2.8 g protein, 101 kcal (422 kJ), 53 mg phosphorus, 2.8 mmol potassium, 2.6 mmol sodium||Can be combined with energy supplements|
|Nutrini Energy per 100 mL: 4.1 g protein, 150 kcal (630 kJ), 75 mg phosphorus, 4.2 mmol potassium, 3.9 mmol sodium|
|Paediasure Plus per 100 mL: 4.2 g protein, 151 kcal (632 kJ), 80 mg phosphorus, 3.5 mmol potassium, 2.6 mmol sodium|
|Nepro HP per 100 mL: 8.1 g protein, 180 kcal (722 kJ), 72 mg phosphorus, 2.7 mmol potassium, 3.0 mmol sodium||Consider micronutrient contribution in younger children|
|Low electrolyte supplements (not nutritionally complete)|
|Fortijuce per 100 mL: 4 g protein, 150 kcal (640 kJ), 12 mg phosphorus, 0.2 mmol potassium, 0.4 mmol sodium||Can be diluted with water or fizzy drinks|
|Ensure Plus Juce per 100 mL: 4.8 g protein, 150 kcal (638 kJ), 11 mg phosphorus, 0.4 mmol potassium, 0.5 mmol sodium|
|Renilon 7.5 per 100 mL: 7.5 g protein, 200 kcal (835 kJ), 3 mg phosphorus, 0.6 mmol potassium, 2.6 mmol sodium|
|Vita-Bite per 25 g bar: 0.06 g protein, 137 kcal (571 kJ), <12.5 mg phosphorus, 0.63 mmol potassium, <0.1 mmol sodium|
|Low protein milk substitute|
|Sno-Pro per 100 mL: 0.16 g protein, 89 kcal (371 kJ), <30 mg phosphorus, <1.3 mmol potassium, <3.3 mmol sodium, <20 mg calcium||Use as a substitute for cow’s milk to reduce protein and phosphate intakes|
|Renamil per 100 g: 4.6 g protein, 477 kcal (2003 kJ), 25 mg phosphorus, 0.2 mmol potassium, 2.6 mmol sodium|
CKD, chronic kidney disease; AKI, acute kidney injury.
In children over 12 months of age, or whose weight is >8 kg, a nutritionally complete paediatric feed can be considered and modified as necessary to meet individual requirements (Table 12.5). The energy density can be built up to 1.5–2.0 kcal/mL (6–8 kJ/mL). Fat emulsions can be given as a prescribed medicine during the day.
A few children develop insulin resistance and hyperglycaemia can occur. If managed on PD, this can be exacerbated by the absorption of glucose from the PD fluid together with the intake of high CHO supplements. Insulin infusions need to be considered to control blood glucose levels before the reduction of dietary CHO.
When PN is initiated, a high concentration of dextrose solution up to 25% is indicated, with lipids providing 10%–20% of non-protein energy.
In children with AKI who are being managed conservatively, protein should be limited to the reference nutrient intake (RNI)  level to minimise uraemic symptoms. This needs to be gradually increased as tolerated if RRT is started, with its associated increased solute removal and possible protein losses. The RNI for protein  is not appropriate for the child with AKI on RRT and requirements should be individually determined. The age and weight of the child, the serum biochemistry and RRT modality, when implemented, all need to be considered. Nutritional guidelines are shown in Table 12.4.
Once RRT is established, the following increments can be used as a guide to increase protein intake to the levels given in Table 12.4:
- exclude protein if the serum urea is ≥40 mmol/L
- introduce 0.5 g protein/kg if the serum urea is ≥30 mmol/L and < 40 mmol/L
- give 1 g protein/kg if the serum urea is ≥20 mmol/L and <30 mmol/L
- give the RNI for height age (infants) or chronological age (children) if the serum urea is <20 mmol/L
CRRT allows the nutritional support of highly catabolic states but contributes to nitrogen loss through the filtration of free amino acids and small peptides across haemofilters. Maxvold et al.  demonstrated that at similar blood and dialysate/prefiltered replacement fluid flow rates, there is an equivalent urea clearance with haemofiltration and haemofiltration with dialysis. A negative nitrogen balance occurred in children with AKI on PN containing 1.5 g/kg/day of protein and an energy intake 20%–30% above resting energy expenditure. An 11%–12% loss of dietary amino acids was found on both modalities. A significant daily accumulative glutamine loss may potentiate nitrogen imbalance. A dose adjustment of amino acid formulation may be needed to overcome negative nitrogen balance in children with AKI on CRRT. An adult study by Scheinkestel et al.  showed that a protein intake of 2.5 g/kg/day and meeting energy requirements increased the likelihood of achieving a positive nitrogen balance and improving survival. Nutrition therapy in AKI remains an area of many unanswered questions, especially for those managed on CRRT, and Li et al. illustrate this in their review of adult AKI studies . There are few paediatric studies.
Nutritional supplements, using a nasogastric tube, are frequently used to meet protein requirements in the initial stages of treatment. For infants standard whey based formulas (which are already low in electrolytes and phosphate) are recommended. These can be modified as required. Kindergen and Renastart, renal specific low phosphate, low potassium infant formulas (Table 12.5), can be beneficial for infants not receiving RTT or receiving intermittent haemodialysis when serum biochemistry levels are unstable. Nutritionally complete, energy dense infant formulas (Infatrini, Similac High Energy, SMA High Energy) can be useful if blood biochemistry allows when on RTT. The phosphate content of these feeds is higher than in standard infant whey based formulas so serum phosphate levels should be regularly reviewed. For the older child a number of nutritionally complete supplements are available. These can be used solely or in combinations with their protein, phosphate and potassium contents being assessed prior to use (Table 12.5). If protein hydrolysate formulas are indicated (in particular when the diarrhoeal phase is prolonged in HUS) they should be modified with respect to biochemical parameters as well as to meet individual nutritional requirements. Introduction should be gradual and delivery is usually by the nasogastric route. Once the child’s appetite improves and protein intake is met through eating, energy supplemented drinks can replace nutritionally complete formulas or protein supplements.
The volume of fluid prescribed during conservative treatment is based on insensible fluid requirements of 400 mL/m2 body surface area/day or approximately 20 mL/kg body weight/day, with a 12% increase for each degree Celsius above normal body temperature and a reduction if the child is ventilated. Insensible losses should be added to the previous day’s urine output to give the total daily fluid allowance. On RRT, the fluid prescription is determined by monitoring the volume of fluid removed by ultrafiltration plus insensible losses. Ideally fluid removal on RRT should be flexibly managed to allow the maximum space for increased nutritional fluids. Maximal nutrient intakes using supplements should be provided within the fluid allowance and divided as evenly as possible throughout the day. A written prescription plan should be provided for the ward nurses and families.
Electrolytes and minerals
The intake of electrolytes, especially potassium, is likely to be restricted in conservative management. Serum levels and the use of RRT will dictate requirements thereafter. Any dietary restrictions should be minimised to avoid compromising nutritional intake.
Potassium rich foods including citrus fruits, fruit juices, bananas, potato crisps and chocolate are commonly brought into hospital by relatives. All carers should be advised about choosing foods with a low potassium content when serum potassium levels are elevated so that rich food sources are withdrawn (Table 12.6).
Table 12.6 Potassium rich foods and suggested alternatives
|Potassium rich foods*||Suggested alternatives|
|Banana, apricots, kiwi fruit, grapes, avocado, citrus fruits, e.g. orange, grapefruit; dried fruit, e.g. raisins; tinned fruit in fruit juice; melon, plums, rhubarb, blackcurrants||Apple, pear, satsuma, blueberries, tinned fruit in syrup|
|Hi juice squash, fruit juices including orange, apple, tomato|
Instant coffee and coffee essence
Cocoa, drinking chocolate
|Squash, cordials, Lucozade, lemonade and fizzy drinks, tea|
|Potato crisps and potato containing snacks, nuts, peanut butter, salt substitutes, meat extract, yeast extract||Corn or rice snacks (without added potassium chloride and take account of sodium content), sweetened popcorn, jam, honey, marmalade, syrup|
|Jacket potatoes, chips (oven and frozen), roast potatoes||Rice (boiled or fried), spaghetti, pasta, noodles, bread, chapatti, naan, crackers|
|Mushrooms, spinach, tomatoes, spaghetti in tomato sauce, baked beans, pulses and hummus, tinned and packet soups||Carrots, cauliflower, swede, broccoli, cabbage|
|Chocolate and all foods containing it, toffee, fudge, marzipan, liquorice||Boiled sweets, jellies, mints, marshmallows|
|Chocolate biscuits||Biscuits: plain, sandwich, jam filled, wafer|
|Chocolate cake, fruit cake||Cake: plain sponge filled with cream and/or jam|
Jam tarts, apple pie, doughnuts, plain scones
|Milk, yoghurt, evaporated and condensed milk||Low protein milk substitutes, e.g. Sno-Pro, Renamil|
* Allowance will depend on individual assessment.
Once serum phosphate levels are above the reference ranges, the intake of phosphate rich foods should be moderated. A lower phosphate intake can partly be achieved when protein intake, particularly that of dairy products, is modified (Table 12.7). Cow’s milk is generally restricted or eliminated from the diet during the acute phase because of its high protein, phosphate and potassium content. Avoidance of cow’s milk also reduces the potential cow’s milk protein or lactose intolerance which can follow the diarrhoeal prodrome in patients with HUS. If the milk restriction proves difficult a low protein milk substitute, such as Sno-Pro or Renamil (Table 12.5), can be advised.
Table 12.7 Phosphate rich foods and suggested alternatives
|Phosphate rich foods*||Suggested alternatives|
|Cow’s milk (full cream, semi-skimmed, skimmed)|
Dried milk powder and other milk products
Whey based infant formulas, e.g., Cow & Gate 1, SMA 1, Aptamil 1 for at least 1–2 years
Reduced intake, consider low protein milk substitute (Table 12.5)
|Large portions of meat, poultry and fish|
Processed meats containing phosphate additives
|Reduced portion sizes|
|Yoghurt, fromage frais, mousse, ice cream, milk puddings including custard||Reduce intake|
Custard made with milk substitute
|Evaporated milk, condensed milk, single cream||Double cream†|
|Cheese, e.g. Cheddar, Edam, processed cheese and cheese spread||Limit intake and/or encourage use of cottage cheese or full fat cream cheese|
|Cocoa, chocolate and chocolate containing foods, toffee, fudge||Boiled sweets, mints, dolly mixtures|
|Sardines, pilchards, tuna||White fish|
|Baked beans, pulses||Vegetables|
|Nuts, peanut butter, marzipan||Jam, honey, marmalade, syrup|
|Cola drinks and any others containing phosphoric acid||Squash, cordials, lemonade, Lucozade|
|Convenience and processed foods with phosphorus additives including dicalcium phosphate, disodium phosphate, monosodium phosphate, sodium tripolyphosphate, tetrasodium pyrophosphate||Foods with no phosphorus containing food additives|
* Allowance will depend on individual assessment.
† Caution: vitamin A content (p. 266).
Reduction in sodium intake can aid compliance when fluid intake is restricted by reducing thirst. This can be achieved by the avoidance of salted snacks and a no added salt diet (Table 12.8).
Table 12.8 Sodium rich foods and suggested alternatives
|Sodium rich foods||Suggested alternatives|
|Salted crisps, nuts and savoury snacks||Unsalted crisps, unsalted nuts, rice cakes, unsalted popcorn|
|Tinned and packet soups||Homemade soups|
|Pot savouries||Sweet snacks instead of savoury|
|Tinned foods with added salt||* Reduced salt products, e.g. reduced salt baked beans|
|Bacon, sausages and other processed meats and fish||Fresh meats and fish|
|Cheese and cheese products||Cottage cheese, ricotta and cream cheese|
|Stock cubes, meat and vegetable extracts||Halve the amounts used or use reduced salt varieties;|
|add herbs and spices in their place|
|Pickles, sauces and chutneys|
|Ready-made meals and take-away meals||Homemade meals using fresh ingredients|
* Many processed/manufactured foods contain high amounts of salt and even lower salt varieties can have a high salt content.
The level of the above restrictions depends on each individual child and their clinical condition. They should be frequently monitored to avoid unnecessary restrictions when their appetite is typically poor and their nutrition is easily compromised.
Vitamin supplementation should be considered if dialysis treatment is prolonged. A general paediatric vitamin supplement of water soluble vitamins should be adequate for the majority of children as appetite improves. Iron supplementation may be indicated in some children during the recovery phase, particularly in those who had a poor diet history prior to the onset of AKI.
When on CRRT water soluble vitamins, especially folic acid, thiamin and vitamin C are lost. Requirements when on this treatment are unknown and a minimum of the RNI  should be given. Patients receiving CRRT also lose magnesium and calcium; this often leads to negative balances requiring additional supplementation. Zinc is also abnormally lost but serum levels do not generally fall [13, 14].
As renal function improves and urine output increases, RRT is stopped. Dietary restrictions, where instigated, can gradually be relaxed. Serum electrolytes and dietary intake should be monitored closely as major losses, especially of potassium, during the diuretic phase can occur.
Prior to discharge, advice should be given on returning to a normal diet as renal function continues to improve. The opportunity to educate the child and family about the principles of a well balanced diet can also be taken if poor eating patterns were highlighted during the admission. Where appetite is slow to improve, some children may need to continue energy and vitamin supplements for a short time, with monitoring of their progress in clinic.
Outcome of AKI
The prognosis and outcome for children with AKI depends on the underlying cause. Children with acute tubular necrosis and interstitial nephritis usually recover well. Most children with HUS make a good recovery of renal function but require long term monitoring for proteinuria, hypertension and renal impairment. Factors associated with a poor outcome include multi-organ failure and the need for RRT and these children need secondary or tertiary follow-up .
Chronic kidney disease (CKD) is characterised by an irreversible deterioration of renal function which can progressively decline to end stage renal disease . It defines renal dysfunction as a continuum from mild to severe. The National Institute for Health and Care Excellence (NICE) has adopted the US National Kidney Foundation Kidney Disease Outcome Quality Initiative (NKF KDOQI) classification of CKD into five stages (Table 12.9) . This staging does not apply to children below 2 years of age where ongoing renal maturation is seen. Published UK data in 2009 reveal an incidence of CKD under the age of 16 of 7.4 per million age related population ; the incidence and prevalence for people of South Asian origin is greater than for the white and black population. The causes of CKD in children are different from adults and are shown in Table 12.10 . Initially the poorly formed or damaged kidney adapts by increasing the filtration rate in the remaining nephrons through adaptive hyperfiltration; homeostatic mechanisms are usually maintained within reference ranges at this stage. In the longer term this leads to damage of the remaining nephrons and ultimately to end stage kidney disease.
Table 12.9 Stages of renal failure 
|Stage||Description||GFR (mL/min/1.73 m2)|
|1||Kidney damage with normal or increased GFR||>90|
|2||Kidney damage with mild decrease in GFR||60–89|
|3||Moderate decrease in GFR||30–59|
|4||Severe decrease in GFR||15–29|
|5||Kidney failure||<15 or dialysis|
GFR, glomerular filtration rate.
Table 12.10 Causes of chronic kidney disease in childhood in the UK 
|Renal dysplasia and related conditions||28|
|Primary tubular and interstitial disorders||7|
|Congenital nephrotic syndrome||7|
|Renal vascular disorders||5|
|Malignant and related disorders||2|
Management of CKD
The management of children with CKD is based on a multidisciplinary team (MDT) approach within a specialist tertiary centre where the dietitian is a key team member. The aims of the team are to optimise the quality of life of the child and family whilst treating the complications of the disease and delaying or slowing the progression of renal disease, together with preparing them for RRT. The sequence of events in CKD forms the basis for management of these children irrespective of aetiology and addresses nutrition, growth, fluid and electrolyte balance, acid–base abnormalities, renal bone disease, hypertension, slowing the progression of CKD, anaemia, cardiovascular disease, medication, education and psychosocial support.
A good knowledge of biochemical and haematological parameters is essential to identify variations from normal age specific reference ranges (Tables 12.3a and 12.3b) when formulating dietary management plans. The serum values of particular relevance include urea, creatinine, sodium, potassium, bicarbonate, albumin, calcium, phosphate, alkaline phosphatase, parathyroid hormone (PTH), glucose, cholesterol and triglycerides. Haemoglobin, ferritin and percent hypochromic cells (<10%) can be used to assess iron status in combination with serum iron and total iron binding capacity (TIBC) to calculate the percent transferrin saturation (TSAT = serum iron × 100 divided by TIBC), which should be maintained at >20%.
An assessment of the glomerular filtration rate (GFR) provides an indication of the overall level of renal function. GFR estimation by Cr51 EDTA clearance is used to predict when RRT is likely to be required. GFR should not be measured before 1 year of age as the kidney function may continue to mature during the first year of life and even beyond. GFR can be estimated using the Haycock Schwartz formula: predicted GFR = 40 × ht (cm)/serum creatinine (µmol/L).
The adverse effects of poor nutrition in children are manifested by their influence on the capacity to grow and develop appropriately. There is a complex interrelationship between renal dysfunction and nutrition whereby abnormalities or a decline in renal function frequently lead to changes in nutritional intake or metabolism, as well as poor nutrition complicating CKD. Malnutrition is associated with increased mortality. Early and careful nutritional therapy may improve both growth and mortality in all ages of children with CKD . The aetiology of growth delay and cachexia in children with CKD is multifactorial with inadequate energy intake, uraemic toxicity, anaemia, increased inflammatory response and metabolic and endocrine abnormalities among the foremost causes. The dietitian plays an essential role in optimising the management of these causes and needs to ensure that individualised dietary prescriptions are practical and flexible to aid adherence.
Dietary and anthropometric assessment
There is no simple measure of nutritional status for children with CKD. Nutritional parameters are complicated on account of salt and water imbalances together with the inappropriateness of comparing growth to that of age matched populations. The frequency of nutritional monitoring depends on age, stage of CKD and how well the child is thriving. In order to prevent the development of malnutrition it is recommended that children with stages 3 and 4 CKD are seen 6 monthly and 1–3 monthly respectively . Monthly review is recommended for children <2 years of age with stage 5 CKD and 3–4 monthly in the over 2s. A 24 hour dietary recall in clinic and an annual 3-day food diary analysis are valuable tools when estimating nutritional intakes and individual baseline requirements. Information on prescribed medications, presence or absence of nausea and vomiting, diarrhoea, constipation and energy levels can be helpful in determining the child’s nutritional and medical needs. Dietary intake should be communicated to members of the MDT, where appropriate, to reinforce discussions and recommendations made with the child and family.
Height and weight plotted on growth charts are used to assess nutritional status. At each clinic visit accurate measurements of height or supine length, weight and, for children <2 years of age, head circumference should be obtained and plotted for chronological age on appropriate growth charts. Where the child is within normal percentile ranges for height (>2nd percentile), energy and micronutrient requirements can be based on recommendations for children of the same chronological age [8, 9]. For the child who falls below the normal percentile ranges for height (<2nd percentile), their height age (age at which the child’s height would be on the 50th percentile) should be used for comparison with recommended intakes for energy and micronutrients [8, 9] and adjusted accordingly thereafter. Estimated dry weights need to be used in those children retaining fluid.
Extremes of body mass index (BMI) are associated with increased morbidity and mortality and children with CKD should avoid becoming overweight or obese. However, it is difficult to find a measure of body composition that is relevant for children with CKD. They may not have a normal body composition making a comparison with normal populations inappropriate. CKD may have a disproportionately greater effect on spinal growth and children have been shown to have a low ratio of length of trunk to limb . They also have a relatively high fat mass, low lean mass and increased central adiposity . BMI should not be used as a measure of fatness for children <2 years of age. It can also be misleading in adolescents with CKD due to delayed sexual maturation and linear growth which is further confounded by reduced muscle mass, reduced activity and fluid retention; if BMI is used it is suggested that it is plotted against the child’s height age .
Mid upper arm circumference (MUAC) can be measured 6 monthly and compared to norms for age; MUAC is unlikely to be affected by oedema. Skinfold thickness may be affected by fluid retention. Reduced values for skinfold thickness have been found in children with CKD . These and other measurements for determining body composition, including bioelectrical impedance, are generally used for research purposes only.
Dietary principles in CKD
Nutritional management of children with CKD requires attention to adequacy of energy intake; regulation of protein intake; fluid balance and electrolytes; regulation of calcium and phosphate intakes; adequacy of micronutrient and iron intakes.
Dietary recommendations depend upon age, stage of CKD, management and nutritional assessment. The recommended intakes of energy and protein in conservatively managed children are given in Table 12.11. Children with CKD are typically anorexic and have spontaneous energy intakes below the EAR for age. To achieve the EAR for energy, most children with CKD require energy supplements (Table 12.5). The majority of infants and many young children need to have a feed delivered by a nasogastric or gastrostomy tube to optimise nutrition .
Table 12.11 Nutritional guidelines for the child with chronic kidney disease
|Energy (per kg body weight per day)||Protein (per kg body weight per day)|
|4 years to puberty||Minimum of EAR for chronological age (use height age if <2nd percentile for height)||1.0–1.1|
|Peritoneal dialysis (APD/CAPD)|
|4 years to puberty||Minimum of EAR for chronological age (use height age if <2nd percentile for height)||1.3|
|4 years to puberty||Minimum of EAR for chronological age (use height age if <2nd percentile for height)||1.1|
These guidelines are for the initiation of management and require adjustments based on individual nutritional assessment.
Protein intakes reflect the reference nutrient intake (RNI) in the UK  plus an increment to achieve positive nitrogen balance including any transperitoneal losses .
EAR, estimated average requirement ; APD, automated peritoneal dialysis; CAPD, continuous ambulatory peritoneal dialysis.
The energy requirements for children with CKD are the same as those of normal children. Energy intakes below the EAR contribute to growth failure. The provision of adequate energy is essential to promote appropriate weight gain and growth in all children with CKD and is especially important in stages 3 and 4 to avoid the use of lean muscle mass as an energy source. The EAR for energy for either height age (if the child’s height is <2nd percentile) or chronological age (if the child falls within the normal percentile range) is used as baseline guidelines (Table 12.11) . Raised serum urea levels in combination with increased serum potassium levels can be suggestive of catabolism and the need to increase non-protein energy intake.
High energy, low protein foods
These include sugar, glucose, jam, marmalade, honey, syrup and should be encouraged where possible. The liberal use of polyunsaturated or mono-unsaturated oils in cooking or margarine spread on bread, toast or added to meals and vegetables can contribute significantly to the child’s energy intake. Special low protein dietary products such as bread and biscuits are rarely needed.
Anorexia, nausea and vomiting are features of CKD and can be exacerbated by uraemia. These symptoms, together with an abnormal sense of taste, contribute to a reduced energy intake. Energy supplements are helpful in meeting this deficit. A number of supplements are available and enable a flexible approach (Table 12.5). Combined fat and CHO supplements or glucose polymer alone, if additional fat is not tolerated, can be successfully added to infant formulas, tube feeds and oral nutritional supplements. The concentrations of CHO and fat should be increased gradually to establish tolerance. Assuming normal gut function, the following upper limits for CHO and fat can be worked towards:
- infants <6 months: 12% CHO and 5% fat
- infants >6 months to 1 year: 15% CHO and 6% fat
- toddlers aged 1–2 years: 20% CHO and 7% fat
- older children: 32% CHO and 9% fat
Liquid glucose polymers are useful when diluted with a fizzy drink or diluted squash and the volume used will depend on the fluid allowance. Powdered glucose polymers are useful in children who drink plenty of water or squash. Each day a target amount to use should be negotiated and a personalised record chart can aid compliance.
Children, especially infants and young children, have a high requirement for protein per kilogram body weight because of the demands of growth. A recent systematic review of protein restriction for children with CKD  showed no significant impact on delaying progression of renal failure and there is an association with inferior growth. The correlation between dietary protein intake and proteinuria was also insignificant.
Protein intake should be optimised to allow for the maintenance of nitrogen balance and growth together with the preservation of lean body mass. In CKD, protein must provide at least 100% of the RNI for age to avoid protein becoming a limiting factor in growth . The RNI for height age is advised when the child is <2nd centile for height. Insufficient protein will impact on body composition with a predominance of fat rather than lean tissue being laid down. Children achieve recommended protein intakes more easily than their energy requirements and a protein intake above 3 g protein/kg should be avoided because of the associated phosphorus load and link with cardiovascular morbidity. Where dairy proteins have been limited to restrict phosphate intake, and adequate energy intake has been ensured to promote anabolism, further protein modification is seldom needed. However, when a child’s serum urea remains persistently >20 mmol/L, a gradual protein reduction based on the child’s 3-day dietary record should be initiated to lower the urea level to <20 mmol/L. Protein of a high biological value should comprise 65%–70% of the total dietary protein intake.
Growth retardation is one of the major complications of childhood CKD and correlates with the age of onset. Most children do not reach their genetic height potential despite optimal management. Fall-off in growth velocity or weight can be early indicators of growth failure and potential causes must be explored. The cause of growth failure is multifactorial and includes growth hormone (GH) and insulin-like growth factor 1 (IGF-1), nutritional status, acid–base balance and bone mineralisation . Cytokines are known to suppress the appetite through their action on the central nervous system. Anaemia, chronic infection, corticosteroid therapy and psychosocial factors can also play a part. The paediatric dietitian, as part of the MDT, contributes to optimising the management of these factors where appropriate.
Normal growth in childhood occurs in four phases: prenatal, infantile, childhood and pubertal. Nutrition is important in all growth phases but especially during the infantile stage when growth is at its highest and is less dependent on GH. There is a slowing of growth velocity in the childhood phase when growth is more dependent on the GH/IGF-1 axis . At puberty, which is typically delayed in CKD, there is a rapid increase in growth velocity in response to sex steroids and GH; adequate nutrition is important during this anabolic phase.
The importance of satisfactory nutrition and electrolyte balance in infancy to optimise growth is well recognised  and is the most critical time for nutritional intervention to have an effect on catch-up growth. Supplementary feeding using the enteral route is invariably indicated in this group. There is ongoing debate as to whether older children with renal failure are able to follow their growth percentiles with the provision of adequate nutrition alone. An improvement in height standard deviation score (SDS) has been observed in a small group study  although other studies have not consistently shown an improvement in growth with nutritional supplements . Other factors including the dysregulation of hormones and cytokines are implicated. The most recent KDOQI guidelines suggest that in older children, poor intake may be a result of inadequate growth and not the cause . For children with a height or height velocity for chronological age below –2SDS, growth hormone therapy following the optimisation of nutritional management has been shown to increase height velocity and final adult height . Children with CKD have an inadequate response of GH stimulating IGF-1 production despite normal or raised levels of circulating GH.