Chronic Kidney Disease Nutrition Guide 2022



• Acute kidney injury (AKI): sudden, rapid deterioration of kidney function caused by injury or illness; often reversible. 

• Chronic kidney disease (CKD): abnormality of the structure or function of kidneys, lasting >3 months; often progressive. Has been classified into stages 1–5 (Table 29.1) 

• Established renal failure (ERF); a description of those who have reached stage 5 CKD and require renal replacement therapy (dialysis). 

CKD is categorised into stages according to glomerular filtration rate (GFR).

Contributing causes

Chronic kidney disease 
  • Diabetic nephropathy
  • Hypertension
  • Infection, e.g. chronic pyelonephritis or sepsis 2o to severe urinary tract infection
  • Polycystic kidney disease
  • Tumour, e.g. multiple myeloma, amyloidosis
  • Familial, e.g. Alport’s syndrome
  • Unknown reasons

Stages of chronic kidney disease

Stage 1: Normal kidney function, but urinalysis, structural abnormalities or genetic traits indicate kidney disease 
GFR = >90 (ml/min/1.73 m2)

Stage 2:  Mildly low kidney function 
GFR = 60 - 89 (ml/min/1.73 m2)

Stage 3a: Moderately low kidney function
GFR = 45 - 59 (ml/min/1.73 m2)
Stage 3b: Moderately low kidney function
GFR = 30 - 44 (ml/min/1.73 m2) 

Stage 4:  Severely low kidney function 
GFR = 15 - 29 (ml/min/1.73 m2)

Stage 5: Very severe, or end stage kidney failure (also known as ERF) 
GFR = <15 (ml/min/1.73 m2)

Malnutrition in renal disease

  • 20–60% of all patients with CKD (stages 3–5) are malnourished. 
  • Poor nutritional status prior to initiation of dialysis is associated with poorer outcomes on dialysis. 
  • Despite its limitations as an indicator of nutritional status, low serum albumin levels are independently associated with i risk of death in haemodialysis (HD), peritoneal dialysis (PD), and transplant patients. 
  • Malnutrition in CKD is multi-factorial. Insufficient oral intake due to poor appetite is often problematic. 
  • Other contributory factors include chronic inflammation, co-morbid conditions, metabolic acidosis and accumulation of uraemic toxins resulting in increased muscle catabolism and appetite suppression. 
  • Delayed start to dialysis and overzealous attempts to control protein intake in the pre-dialysis period can compromise nutritional status. 
  • Malnutrition is a particular problem in HD patients who have i requirements, but often miss meals if dialysis coincides with meal times.

Nutrition support

Renal patients who are malnourished or unable to achieve an adequate intake from food should be advised to supplement their oral intake with high energy and/or high protein foods (food fortification) or proprietary products or provided with enteral or parenteral nutrition support.
  • Care must be taken to ensure that supplements are compatible with other dietary restrictions.
  • Fluids from supplements contribute to the daily fluid allowance. Where necessary, nutrient-dense supplements should be selected.
  • If enteral feeding is required, attention must be given to the total fluid intake. Patients may need daily HD or more hypertonic PD exchanges.
  • Gastrostomy feeding is increasingly being used in both HD and PD patients at home. In PD patients, a short period of peritoneal rest while the gastrostomy tube placement site heals is often instigated.
  • Specifically formulated renal enteral feeds are available to provide fluid, electrolyte-restricted, nutrient-dense feeds (Table 29.3).
  • Parenteral nutrition may be preferred in patients with impaired GI function:
    • energy requirements are best provided using a combination of both glucose and fat so as not to exceed the glucose oxidation rate 4–5g glucose/kg/day (including glucose derived from dialysate during continuous renal replacement therapy (CRRT); 
    • excessive glucose is associated with i risk of metabolic disturbances leading to i CO2 production and lipogenesis; 
    • provision of fat should not exceed 1 g/kg/day in AKI; 
    • routine use of low electrolyte parenteral nutrition regimens in patients with AKI receiving dialysis (especially CRRT) may cause electrolyte depletion, and necessitate administration of additional potassium, phosphate, or magnesium, or the use of standard parenteral formulae; 
    • close monitoring of serum biochemistry is paramount, especially at the onset of feeding.

Nutritional products widely used in renal disease 

Energy supplements 
  • Glucose polymers: Caloreen (Nestlé), Polycal (Nutricia Clinical), Vitajoule (Vitaflo) 
  • Fat: Calogen (Nutricia Clinical), Liquigen (SHS)
  • Combined: Duocal (SHS), Duobar (SHS), Pro-Cal (Vitaflo) 
Protein powders: Casilan 90 (Heinz), Renapro (KoRa) 

Oral Supplements: Ensure Plus (Abbott), Fortijuce (Nutricia Clinical), Fresubin 2 kcal Drink (Fresenius Kabi), Resource Dessert Energy (Nestlé) etc.

Nutritional considerations in chronic kidney disease

Mineral bone disease 

As the GFR falls <60 ml/min, the kidney’s ability to adequately regulate calcium and phosphate homeostasis is also reduced. This can result in sec- ondary hyperparathyroidism, metabolic bone disease and i calcification of the vasculature, known collectively as mineral bone disease (MBD). A chain of interrelated biochemical abnormalities occur in MBD. 

Management of mineral bone disease 

Management intensifies with higher stages of CKD.

• Phosphate intake can be restricted to as little as 800–1000 mg/day. 
Emphasis should be placed on reducing phosphate from foods with low nutrient density e.g. fizzy drinks, processed cheese and pre-mixed dried baking products (e.g. cake mix). Many high phosphate foods are also good protein sources, so care should be taken not to compromise the nutritional status of the patient with excessive restriction. 

• Phosphate binders can be used when it is not possible to control the phosphate with diet alone. These are available as various compounds, but all bind with phosphate in the GI tract to prevent systemic absorption with variable efficacy and GI side effects. 

• Vitamin D deficiency is highly prevalent in the general population as well as in CKD. Controversy exists over the best type of vitamin D to prescribe. Either 25 vitamin D, 1,25 vitamin D (active form) or a precursor to 1,25 vitamin D can be used in CKD and will differ between centres.

Cardiovascular risk 

Cardiovascular disease (CVD) accounts for as many as 50% of deaths in CKD. An individual with kidney disease is more likely to die of CVD than reach the stage of requiring dialysis. Traditional CVD risk factors account for only some this i risk. CVD risk can be reduced with a combination of changes in diet, lifestyle, and physical activity. 

Traditional modifiable CVD risk factors in CKD
  • Hypertension: in addition to medical management, a no-added-salt diet (80–100mmol/day) is beneficial Hyperlipidaemia: renal patients present with high cholesterol and high triglycerides. Therapeutic diet and lifestyle changes could have benefits over and above pharmaceutical control of lipids.
  • Weight management.
  • Lifestyle choices: particularly smoking and low physical activity levels. 
  • Diabetes.
CKD specific modifiable CVD risk factors
  • Deranged mineral metabolism (as described above) is associated with calcification of the heart and blood vessels. 
  • Anaemia can contribute to left ventricular hypertrophy
  • Volume overload; inflammation and malnutrition.

Common in CKD, due to iron deficiency and/or a relative lack of erythropoietin, which develops when GFR falls <60ml/min, and should be investigated if Hb <13g/dl (4 and post-menopausal 5) and <12g/dl (pre-menopausal 5). Intravenous or oral iron can be given as first line treatment (Table 29.9) ferritin levels should not exceed 800 ng/ml. Epoetin, synthetic erythropoietin which stimulates erythropoiesis, can be used to maintain Hb levels between 10.5–12.5 g/dl.


Diabetes is the cause of renal failure in approximately 40% of CKD patients. The nutritional priorities in the diabetic with kidney disease are:
• Optimal glycaemic control (HbA1c <7.0% or <53 mmol/mol).
• Optimal management of blood pressure and proteinuria. 
• Emphasis on management of modifiable CVD risks. 
• Weight management.

Weight management

Where possible, obese patients (BMI>30 kg/m2) should be encouraged to lower their body weight through diet and exercise. Weight loss goals should be realistic and tailored to the individual patient. 

Reasons for weight management in CKD
  • Increased risk of CVD, diabetes, hypertension and some cancers. 
  • Extra weight may interfere with a patient’s ability to mobilize and lead an independent life. 
  • Longer Hemodialysis sessions may be required to dialyse a heavier person. 
  • Being obese may d the chance of receiving a kidney transplant.


Patients at all stages of CKD should be encouraged to take regular exercise. It can be a challenge to recommend safe and appropriate ways to exercise if the patient is elderly or infirm although there are multiple resources available and physiotherapy consultation can support. Nutrition in chronic kidney disease stages 3 and 4

An individual can stay at these stages of kidney disease for any time from a couple of months to decades. 

Ideally, they will be reviewed as an out-patient by their nephrologist or general practitioner thus providing ample opportunity for nutritional assessment and intervention along the continuum of their chronic disease management. 

A new patient requires full dietary assessment and subsequent nutritional advice should be tailored to the specific needs of the individual with a view to minimizing the risk of potential disease progression and related risk factors (e.g. CVD).

Nutritional requirements 

Energy requirements are normal, i.e. 30–40 kcal/kg ideal body weight (IBW)/day. 

Protein maximum intake 1 g/kg IBW/day (a mild degree of restriction), especially in patients consuming excessive protein or for the short- term management of uraemic patients awaiting the start of dialysis. Reducing protein intake below 0.75 g/kg IBW/day is not recommended, because although this is thought to reduce uraemic symptoms and lower rate of decline in renal function, benefits are marginal when compared with higher risk of malnutrition. Protein intake may d spontaneously as the GFR reduce below <25 mL/min. It is more likely that patients nearing ERF will require nutrition support to achieve an adequate intake, rather than restrictions. Timely initiation of dialysis will d extent of malnutrition. 

Phosphate: early restriction may help prevent renal bone disease, secondary hyperparathyroidism, and may slow progression to ERF. Phosphate containing foods are shown in Table 29.6. 

Potassium: restriction is required if consecutive K+ levels run >5.5mmol/L as is often the case with the use of ACE (angiotensin converting enzyme) inhibitors or ARBs (angiotensin receptor blockers) which reduce renal potassium excretion. Other non-dietary sources of hyperkalaemia are shown below. 

Fluid: restrictions are usually only required in CKD if there is a marked d urine output (<1000 ml/day), severe oedema, or a history of coronary heart failure. Fluid restriction may occasionally be necessary in poorly controlled diabetes. 

Sodium intake: a mild restriction of 80–100 mmol is recommended.

Chronic kidney disease in the elderly

Nephron mass and 6 GFR deteriorates with normal aging. Many elderly individuals in whom CKD is diagnosed may never require dialysis. This should be taken into account before advising on overzealous dietary restrictions, particularly in the very elderly.

Phosphate containing foods 

Drinks: Some fizzy drinks including most cola, beer, hot chocolate, milk shakes, milk and other milky drinks. 

Dairy products: Processed cheese, red cheddar, custard, and yogurt. 

Meat: All meat and fish contain some phosphate but are necessary to meet protein requirements. Avoid high fat, high sodium processed and canned meats. Avoid liver and other organ meats. 

Fish: Oily fish and shellfish are significantly higher in phosphate than white fish. 

Others: Dried beans and peas. Bran products particularly all-bran and bran buds. Pumpkin seeds and sunflower seeds. Nuts and peanut butter. Whole grain products. 

Phosphate additives: Phosphate containing additives in various formats have 100% bioavailability. These are added to a variety of commonly used foods including processed meat and cheese, freeze dried foods, bakery products and beverages. Phosphate is not reported in the nutritional information, but should be listed in the ingredients list. E101, E106, E339-343, E450-452, E540-545, E1410, E1412, E1414, and E1442 all contain phosphates.

Non-dietary causes of hyperkalaemia 

Metabolic factors: Hyperparathyroidism, acidosis, insulin insufficiency. 

Drugs: K+ containing drugs, e.g. penicillin, senna. Drugs affecting K+ excretion, e.g. ACE inhibitors, ARBs, B-blockers, non-steroidal anti-inflammatory drugs (NSAIDs). K+ sparing diuretics, e.g. amiloride, spironolactone. 

Cellular trauma: Haemolysed blood sample, post-blood transfusion, infection, gastrointestinal haemorrhage, crush injury, gangrene. 

Constipation: Reduced gut excretion. 

Dialysis: Inadequate dialysis. 

Reference: Oxford Handbook of Nutrition and Dietetics - Joan Webster-Gandy, Angela Madden, Michelle Holdsworth



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