KD (RD) Flashcards

Question

How is fluid balance treated by diet?

Answer 1

* Fluid balance: fluid restriction/ salt restriction

Answer 2

* Electrolytes: potassium control

Answer 3

l * Bone metabolism: phosphate control

Answer 4

* Toxins: nutritional support/ lower protein diets?

Answer 5

* Acid/base balance: plant based diets

Answer 6

An Acute Kidney Injury (AKI) is sudden disruption to kidney function resulting in a failure to maintain fluid, electrolyte and acid-base homeostasis.

Answer 7

Characteristics of an AKI: * Sudden disruption to kidney function * Function declines over

Answer 8

Characteristics of CKD * Gradual loss of kidney function * Function declines over months or years * Chronic/long term condition * Damage is not reversible, it is permanent. * There is a defined disease process.

Answer 9

~50% of patients admitted to the ICU have an AKI

Answer 10

To classify AKIs dietetically: * Consider if the patient is in a catabolic or non catabolic state * Consider whether the patient is receiving renal replacement therapy or not

Answer 11

The 3 cause classifications of AKI: * **Pre-Renal** (most AKIs ~65%): "before the kidneys". * Due to low blood volume/ hypotension 1. Dehydration, People who need help to hydrate, Burns/Diarrhoea, Sepsis, Blood loss, Diuretics. 2. Can be reversed * **Post-Renal:**: * Due to obstruction/blockage of urine output 1. kidney stones/enlarged prostate 2. Can be reversed * **Intra-Renal/ Intrinsic** : * Due to cell damage 1. Acute Tubular Injury (Prolonged pre-renal AKI)/Acute Tubulointerstitial Nephritis (Infection/Allergies) /Acute Glomerulonephritis (Bacterial)/Vasculitis (Auto immune)

Answer 12

Diuresis: An increase in the amount of urine made by the kidney and passed from the body.

Answer 13

Adequate fluid intake is key for AKI prevention

Answer 14

Excess vitamin C can cause kidney stones

Answer 15

Energy isn't affected by AKI. The standard formula for the concurrent illness should be used of ABW. ICU: 70% for first 3 days

Answer 16

Dietetic treatment of AKI depends on: * the degree of AKI * underlying clinical condition * metabolic state * inflammatory status * treatment employed

Answer 17

AKI is often present when there is sepsis and multi organ failure. Therefore common in CRITICAL CARE.

Answer 18

Between 24 and 60% of all hospitalised patients with AKI present with a degree of malnutrition.

Answer 19

Validated Screening tools for AKI * There are no validated screening tools specifically for AKI.

Answer 20

Other screening tools that can be used for AKI: * Renal Nutrition Screening Tool (RNST) (for CKD) * Renal Inpatient Nutrition Screening Tool (Renal iNUT) (for CKD) * The screening tools for CKD are more sensitive than other generic screening tools. * MUST: Could be used but may mask weight changes caused by fluid changes.

Answer 21

Advantages & Disadvantages of the Renal Nutrition Screening Tool (RNST) (for CKD) **Advantages** * Validated * Specific to CKD patients * Includes appropriate markers: PEW, electrolyte imbalances, dietary restrictions * Cost effective **Disadvantages** * Reliance on self-reported data, may not be appropriate for use in CC. * Not validated for use in AKI * Its validated for use in non-dialysis CKD stage 3-5 adults

Answer 22

Advantages & Disadvantages of the Renal Inpatient Nutrition Screening Tool (Renal iNUT) (for CKD)

Answer 23

In patients admitted to a renal unit Jackson et al. 2018 found: * iNUT was more sensitive than MUST in identifying increased malnutrition risk (92.1% vs 44.4%) (more than twice as more sensitive) * iNUT was more sensitive than MUST in identifying dietetic referral (69.8% vs 15.9%) need (more than 4 times as sensitive)

Answer 24

Typically, patients with pre-renal or post-renal injuries present in a non-catabolic state

Answer 25

AKI Non-Catabolic without RRT Requirements * **Pro: 0.8-1.0g/kg/day** * Energy: Not affected by AKI itself. Use standard formula for concurrent illness. ITU: 70% for first 3 days. * Fluid: Individually assessed. Usually by med team. Use low volume feeds to allow daily adjustment. * Electrolytes: Monitor & adjust. Watch diuresis.

Answer 26

AKI Non-Catabolic ON RRT Requirements * **Pro: 1.1-1.5g/kg/day** * Energy: Not affected by AKI itself. Use standard formula for concurrent illness. ITU: 70% for first 3 days. * Fluid: Individually assessed. Usually by med team. Use low volume feeds to allow daily adjustment. * Electrolytes: Monitor & adjust. Watch diuresis.

Answer 27

AKI Catabolic without RRT Requirements * **Pro: 1.3g/kg/day** * Energy: Not affected by AKI itself. Use standard formula for concurrent illness. ITU: 70% for first 3 days. * Fluid: Individually assessed. Usually by med team. Use low volume feeds to allow daily adjustment. * Electrolytes: Monitor & adjust. Watch diuresis.

Answer 28

AKI Catabolic on HD Requirements * **Pro: 1.2-1.5g/kg/day** * Energy: Not affected by AKI itself. Use standard formula for concurrent illness. ITU: 70% for first 3 days. * Fluid: Individually assessed. Usually by med team. Use low volume feeds to allow daily adjustment. * Electrolytes: Monitor & adjust. Watch diuresis.

Answer 29

AKI Catabolic on CRRT Requirements * **Pro: Up to 1.7g/kg/day** * Energy: Not affected by AKI itself. Use standard formula for concurrent illness. ITU: 70% for first 3 days. * Fluid: Individually assessed. Usually by med team. Use low volume feeds to allow daily adjustment. * Electrolytes: Monitor & adjust. Watch diuresis.

Answer 30

AKI Protein Requirements * Non-Catabolic without RRT: 0.8-1.0g/kg/day * Non-Catabolic ON RRT: 1.1-1.5g/kg/day * Catabolic without RRT: 1.3g/kg/day * Catabolic on HD Requirements: 1.2-1.5g/kg/day * Catabolic on CRRT Requirements: Up to 1.7g/kg/day

Answer 31

Yes, most people with AKIs are malnourished.

Answer 32

Dietetic Classification of AKI 1. Is the patient Catabolic or Non-catabolic **Catabolic** e.g. sepsis, trauma, MOF **Non-catabolic** e.g. dehydration, medication, obstruction Assessment of catabolism: inflammatory markers, underlying condition, clinical status, clinical observation 2. Is the patient on RRT or not?

Answer 33

AKI Classification by cause & nutritional relevance * Pre renal: There is typically no change in the nutritional requirements of patients with a pre-renal AKI. * Post-renal: There is typically no change in the nutritional requirements of patients with a post-renal AKI. * Intra-renal: This is a more severe form of injury and is likely to alter nutritional requirements.

Answer 34

Intra-renal AKI is most likely to alter nutritional requirements because it is a serious form of injury.

Answer 35

Patients with pre-existing chronic kidney disease (CKD) may present with **AKI.**

Answer 36

Acute illness in addition to underlying CKD is more **likely** to impact on and alter nutritional needs. These patients have an **increased** risk of worsening of their nutritional status when admitted with AKI and should be monitored closely.

Answer 37

Typically, patients with an intra-renal injury present in a catabolic state

Answer 38

The nutritional requirement guidelines for AKI based on low grade evidence & expert opinion.

Answer 39

Advised treatment for non-catabolic AKI (Think Kidneys) * Oral diet alone, or the addition of nutritionally-dense supplementary sip feeds (ONS) will frequently be sufficient to meet the patients’ needs * Oral diet/ ONS not enough: artificial nutrition support should be established.

Answer 40

There are **no** randomised controlled trials on nutrition and AKI, which remains an under researched area

Answer 41

In individuals with AKI and multiorgan failure, measured energy requirements are only 20%-30% above the estimated basal metabolic rate values

Answer 42

AKI on ICU estimation of energy requirements * use critical care specific equations that aim to avoid risks of over and underfeeding (Fiaccadori et al 2021). * weight based equations: 20-25kcal/kg/day (Singer et al, 2019) * PENN state equation (Frankenfield et al 2009). * BMI >26: estimation of energy requirements should be based on IBW * Acutely unwell patients with AKI on ICU: Days 1-3: hypocaloric feeding up to 70% of energy expenditure * Acutely unwell patients with AKI on ICU: Day 4: energy can be increased up to 80-100% of measured REE.

Answer 43

Energy intake should be based on Ideal Body Weight for those with a BMI over 26 kg/m2 (Singer et al, 2019).

Answer 44

* Indirect calorimetry is the gold standard for estimation of energy requirements * Predictive formulas may frequently lead to incorrect energy need estimation and close monitoring to avoid underfeeding and overfeeding is needed (Sabatino et al, 2017).

Answer 45

* AKI has no effect on the patient’s energy requirements. * AKI & MOF: measured energy requirements are only 20%-30% above the estimated basal metabolic rate values (KDIGO 2012). * KDIGO guidelines for AKI (2012): 20–30 kcal/kg/day in patients with any stage of AKI. * ICU settings indirect calorimetry is considered the gold standard to estimate energy requirements. * AKI & ICU: weight based equations (20-25kcal/kg/day) (Singer et al, 2019) or the PENN state equation (ICU) (Frankenfield et al 2009). * predictive formulas may frequently lead to incorrect energy need estimation and close monitoring to avoid underfeeding and overfeeding is needed (Sabatino et al, 2017). * ICU& BMI >26: estimation of energy requirements should be based on IBW * Acutely unwell patients with AKI on ICU: Days 1-3: hypocaloric feeding up to 70% of energy expenditure * Acutely unwell patients with AKI on ICU: Day 4: energy can be increased up to 80-100% of measured REE.

Answer 46

* Protein requirements are influenced by the patient’s clinical condition, severity of AKI, metabolic state and RRT * Protein estimation should be individual to the patient's condition and treatment goals * Not receiving RRT & not catabolic : protein turnover is not increased. 0.8–1.0 g/kg/day * Not receiving RRT & catabolic (no ventilator): 1.0-1.3g/kg/day * Receiving RRT & catabolic (on ventilator): Start with 1.0- 1.2g/kg/day. Aim to achieve 80% of estimated protein requirements * Receiving RRT 1.5-1.7g/kg/day (depending on RRT treatment). 2.EFFORT trial: patients who were mechanically ventilated, critically unwell, with AKI and high SOFA score at baseline, not on RRT and receiving high protein dose (prescribed 2.0g/kg; on average received 1.6g/kg) were associated with higher harm than those having less protein 1.2 or less. * ICU & BMI >26: estimation of energy requirements should be based on IBW

Answer 47

AKI & electrolyte management * significant electrolyte changes may present: elevated potassium and phosphate levels. * Electrolyte intake should be individualised according to the patient’s biochemistry, clinical condition and dietary provision. Frequent monitoring of blood biochemistry is essential. * High potassium or high phosphate blood levels; Low potassium and low phosphate diets can be implemented * Not all patients with AKI and hyperkalaemia require dietary potassium restriction. * Cause of hyperkalaemia should be considered before implementation of dietary restriction. * Recent increased use of gastrointestinal cationexchange resins to support in the emergency management of acute life-threatening hyperkalaemia. * Dietary restriction of phosphate may limit an individual’s food choice. Allowing more liberal phosphate consumption to help promote food intake is a better approach. * Short-term: maintainance of good nutritional intake is of greater priority than achieving phosphate control. * If kidney function recovers & potassium and phosphate blood levels are normal: restrictions can be relaxed. Polyuric phase:low electrolyte levels: oral or intravenous supplementation may be required. * ICU patients: Persistent hypophosphatemia may present, correlated with increased mortality. * Hypophosphatemia may be an effect of the RRT (particularly in CRRT, treatment is likely to be pharmacological.) * Patients with hypophosphatemia: nutritional intake should be assessed to ensure that a deficiency in protein intake is not present.

Answer 48

Gastrointestinal cationexchange resins: * medications that are used to remove an excess of a particular positively charged ion that has accumulated in the body. * colonic necrosis and other fatal gastrointestinal adverse events can be side effects.

Answer 49

AKI & fluid requirements * Medical team should advise on fluid provision * Clinical condition, stage of AKI and current treatment important for establishing fluid requirements.. * Equations to estimate fluid requirements may be not useful * MDT approach is needed to establish the optimal fluid intake for the patient as well as the volume within which nutrition support can be given if required. * Daily weights, strict fluid balance and medical assessment are key tools * Oliguric/ fluid overloaded patients: fluid restriction * Thirst & fluid restriction: sodium restriction to help control * Polyuric: increased fluid intake to cover the large urine volumes and insensible losses

Answer 50

AKI & micronutrient requirements * Requirements for micronutrients are not well defined. * Caution should be taken when interpreting serum micronutrient levels * AKI & acute phase response: blood levels altered * Vitamins A, D, E, C, minerals selenium and zinc are lower in AKI. May be related to inflammatory processes, RRT or medication, not true deficiencies. * CRRT: Micronutrient losse may be significant. * High vitamin C (>250mg/day) are potentially toxic due to the risk of secondary oxalosis in kidney failure, although ensuring adequate ascorbic acid status may confer some benefit (Honore et al, 2020). * AKI & parenteral nutrition: Vitamin A toxicity has been reported. ? monitor Vitamin A levels * AKI & parenteral nutrition: ? selective supplementation to combat losses from RRT/CRRT? * CRRT & selenium: daily losses of 0.97μmol, ? supplementation *not known if micronutrient supplementation to compensate for RRT losses improves outcomes

Answer 51

AKI KDIGO 20-30kcal/kg/day * Advise that 20-30kcal/kg/day is sufficient for all AKI patients regardless of severity ** Evidence** Unclear how they got 20-30 when evidence suggests 25-30. Evidence is weak, based on small studies. One study didn't have a control group. 1. RCT 10 critically ill patients with AKI receiving PN. 30kcal/kg/day vs 40kcal/kg/day. * 40kcal/kg/day: no increased positive effect on N balance/ 40 kcal: associated with hyperglycaemia, hypertriglyceridaemia, positive fluid balance. * Limitations: Small study of 10 patients, all patients critically ill, all patients receiving PN. 2. Retrospective study, 40 patients, with AKI receiving Continuous Veno-Venous Hemofiltration. 3. * Less negative/ weakly positive N balance associated with 25 kcal/kg/day. 4. Limitations: Small study of 40 patients, all receiving CVVH.

Answer 52

1. Treat or remove cause, for example: * Rehydration * Stone removal * Stop NSAIDS 2. Supportive - Manage complications, for example: * Stop potassium sparing diuretics, * start Insulin and dextrose * Manage fluid overload * Correct acidosis * Start temporary Renal Replacement Therapy

Answer 53

AKI – Dietitians Role * Supportive – ensure adequate nutrition in N+V * Manage complications * Communicate assessment to nephrologists * Interventions: Not usually able to eat enough: Fluid restriction Low k diet Low phosphate diet ? adequate nutrition within the fluid restriction? ?control serum potassium with diet?

Answer 54

AKI Nutritional Considerations 1. Catabolic or Not-Catabolic? 2. RRT or No-RRT? 3. Fluid retention? 4. Uraemic toxins? 5. Malnutrition is common in AKI and indepedent predictor of mortality (42% patients with AKI are malnourished) 6. Energy: not affected by AKI (suggested 20-30kcal/kg KDIGO) 7. Protein: affected by AKI severity, metabolic state & clinical cndition. * x RRT & catabolic: 1.0-1.3g/kg * x RRT & not catabolic: 0.8-1.0g/kg 8. Fluid: equations may not be useful. MDT needed. ?daily weights, fluid balance, medical ax. Polyuric? increase fluid intake 9. Electrolyte changes: Increased potassium & Increased phosphate: ? low K or PO4 diet 10. Micronutrients: interpret with caution. A, D, E, C, selenium and zinc usually lower in AKI

Answer 55

AKI Dietetic Interventions * High potassium or phosphate: Low potassium or low phosphate diet * Fluid balance: fluid restriction, sodium restriction to help control * Polyuric: Increase fluid intake

Answer 56

AKI course of illness * Hours : e.g if only rehydration is needed and it is given quickly * Months:e.g if cause is rhabdomyolosis or antifreeze

Answer 57

CKD statistics * 1 in 10 people have CKD in the UK * 1 in 5 men and 1 in 4 women aged 65-74yrs has CKD * 1000 children in the UK have CKD * People of black and Asian origins are 5x more likely to develop kidney disease than Caucasian ethnicity * 1.4 million/yr CVD deaths worldwide are due to CKD * CKD has increased risk of CVD –even if it doesn’t progress to dialysis

Answer 58

eGFR: * estimated glomerular filtration rate * measure of kidney function * an attempt to standardise serum creatinine measurements

Answer 59

Proteinuria is an **independent** risk factor for CardioVascularDisease

Answer 60

eGFR & African descent * x1.159 for eGFR adjustment is not accurate or valid * based on unjustifiable assumptions about the relationship between Black ethnicity and muscle mass. * could lead to people of African descent not getting the care they need soon enough * African descent at greater risk of CKD

Answer 61

CKD staging * Stage 1: eGFR: =/> 9 kidneys still working well or mild damage. may or may not have any symptoms. * Stage 2: eGFR: 60-89 Mild damage to kidneys * Stage 3a: eGFR: 45-59 mild to moderate damage, kidneys still work well * Stage 3b: eGFR: 30-44 mild to moderate damage, kidneys don't work as well as they should * Stage 4: 15-29 Severe kidney damage, close to not working at all * Stage 5: <15 Severe kidney damage, not working at all or close to not working at all

Answer 62

CKD & proteinuria * Protein can be let into the urine by a damaged and ‘leaky’ glomerulus * Protein in the urine carries a risk of long-term damage to kidney tubules * Proteinuria is an independent risk factor for CVD * So, we can add on the degree of risk from proteinuria, classified by: ACR = Albumin : Creatinine Ratio in Urine A1 is microalbuminuria, A2 and A3 are below nephrotic syndrome range

Answer 63

CKD Stages 1-3 Nutritional Requirements/ Interventions * Use Usual eg PENG - Healthy Eating, nutritional support - * weight reduction * lipid modification as needed - * Fresh foods, plant based - * Restrict sodium to 100mmol/day (Renal Association 2019)

Answer 64

Consequences of kidney disease: * Impaired excretion of waste products: taste changes, nausea, vomiting * Electrolyte imbalance (Na+, K+, Mg++, PO4, Ca++) * Fluid overload * Metabolic acidosis * Secondary hyperparathyroidism * Metabolic dysfunction * Insulin resistance leading to glucose intolerance * Impaired lipid clearance * Reduction of erythropoietin production which leads to anaemia

Answer 65

Possible causes of hyperkalaemia (not exhaustive): * Medication that raises K in blood: angiotensin converting enzyme inhibitors, angiotensin receptor blockers, potassium sparing diuretics, some immunosuppresants * Dietary related (kidney function is severely affected usually) * Metabolic acidosis * Diabetic ketoacidosis/poor diabetes control (very poor controlled blood glucose) * Haemolysed samples * Blood transfusion * Some solid tumour & tumour lysis * Rhabdomyolysis, crush injuries, burns * Hypoaldosteronism * Iatrogenic (oral/IV potassium replacement) * Extreme exercise * Infection/sepsis * Rapid catabolism

Answer 66

Hyperphosphataemia may occur in CKD 4-5 and is associated with mineral bone disease, soft tissue calcification & increased mortality rates in patients on dialysis.

Answer 67

Hyperphosphataemia is usually treated with limiting dietary phosphorous without compromising protein intake. And phosphate binders if appropriate.

Answer 68

A low potassium diet should only be employed in CKD 4-5 when **HYPERKALAEMIA** arises (PENG)

Answer 69

Nutritional components that may be targeted in CKD: * Potassium * Phosphate * Alkalising diet * Salt * Fluid * Protein

Answer 70

Diet for CKD 1-2 * Good fluid intake * <5g salt/day Consider: * Alkalising diet * Avoid phosphate additives * Not excessive protein Depending on patient’s situation and priorities Explaining above mechanisms may help understand how healthy eating applies in CKD

Answer 71

Diet for CKD 3 * End of CKD 3: Increased K: consider other factors, if diet: LOWER potassium diet * Good fluid intake * <5g salt/day **Consider:** * Alkalising diet * Avoid phosphate additives * Not excessive protein * Depending on patient’s situation and priorities * Explaining above mechanisms may help understand how healthy eating applies in CKD

Answer 72

Diet for CKD 4-5 * Increased PO4: LOWER phosphate diet * Fluid retention: FLUID RESTRICTION * Increased K: consider other factors, if diet: LOWER potassium diet * Good fluid intake * <5g salt/day **Consider:** * Alkalising diet * Avoid phosphate additives * Not excessive protein * Depending on patient’s situation and priorities * Explaining above mechanisms may help understand how healthy eating applies in CKD

Answer 73

Low Potassium Diet * Continue to ↑ home cooked plant based * Optimise non-diet causes: Diabetes control, Constipation, Acidosis.Trend of blood results ?wait. Dialysis – adequacy, start, attend! Medications * Avoid potassium additives * Cooking- Boil rather than steam, bake fry * Choose lower k fruit + veg * Limit meat portions * Limit fruit +veg * Limit milk * Soaking some foods may reduce potassium content

Answer 74

CKD is categorized according to glomerular filtration rate and albumin creatinine ratio.

Answer 75

AKI is categorized according to serum creatinine and urinary output.

Answer 76

Plants have reduced phosphorous absorption because of phytates

Answer 77

An individual with CKD is more likely to die of **Cardiovascular Disease** than reach the stage of requiring **DIALYSIS**

Answer 78

Anaemia is common in CKD because of iron deficiency or a relative lack of etythropoietin.

Answer 79

Reasons for weight management in CKD * Wt loss may reduce proteinuria, blood pressure and insulin resistance * BMI >35kg/m2 with co-morbidities is likely to reduce the chance of kidney transplant * Excess wt increases risk of CVD, diabetes, HTN & some cancers * Excess wt may impair mobility and independence

Answer 80

The nutritional recommendations provided by the Renal Association are aimed at reducing the prevalence of undernutrition in CKD

Answer 81

The eREE-CKD equation may be beneficial for estimation of energy requirements in CKD but it needs further development with people who are unstable in CKD: eREE-CKD (kcal) = (1 if male; 0 if female) × 106.0 − [1 if diabetes mellitus (DM); 0 if non-DM] × 51.6 − 4.7 × age (y) + 13.1 × weight (kg) + 645.5 (R2 = 0.779). Both bias and precision of the eREE-CKD were significantly better than the Harris–Benedict, WHO, and Schofield equations (P < 0.001) and similar to the Mifflin equation Accuracy of the eREE-CKD was significantly better than the Harris–Benedict, WHO, Mifflin, and Schofield equations (P < 0.001). Bias, precision, and accuracy of the eREE-CKD equation were consistent when applied to subgroups categorized according to high-sensitivity C-reactive protein concentrations and CKD stages, respectively.

Answer 82

Hu et al. found that greater adherance to a healthy dietary pattern in CKD: general healthy eating (AHEI-2010), DASH, MED diet was associated with: * lower adjusted risk of CKD progression * Mediterranean diet associated with highest reduction of risk

Answer 83

CKD & increased CVD risk Those with CKD: * are more likely to die of CVD than reach need for dialysis * 4-20% more likely to have a sudden cardiac death than people in general population * 50% of people on dialysis die of a cardiac event

Answer 84

Apparently targetting traditional risk factors of CVD in CKD patients is ineffective

Answer 85

**Risk factors for CVD in CKD** 1. Protein breakdown products * Small amounts of amine compounds that the kidney usually removes increase CVD risk * Protein in the urine * Increases CVD risk and CKD progression 2. Early internal compensation * Phosphate * Acid load There is evidence that the internal compensations increase CVD risk and CKD progression There is evidence that these processes are irreversible

Answer 86

Low potassium stimulates sodium absorption in the distal nephron and ↑ BP, so encourage more fruit + veg

Answer 87

Dietary patterns to protect the kidneys and prevent CVD complications * Mediterranean diet * DASH diet * New Nordic Styl * Eatwell Guide Characteristics: Low fat, low salt, low in processed foods, rich in f&v, rich in fibre, rich in nuts &seeds, pulses to replace some meat.

Answer 88

Resources for CKD patients * BDA Kidney Dietitian Specialist group * Kidney kitchen * Recipes * Ethnicity specific recipes * Wt loss magazine * Cooking on a budget magazine

Answer 89

The European Foods Standards Authority reviewed the safety of phosphate additives in 2019 because: * People consume more phosphate additives than they previously did * Emerging evidence of risk

Answer 90

EFSA Phosphate Report Tolerable Daily Intake (TDI): 40 mg/kg body weight per day for phosphates, expressed as phosphorus. Includes all sources of dietary phosphorus, including both naturally occurring and added phosphates. 2. Dietary Exposure: EFSA found that some population groups, particularly infants, toddlers, children, and adolescents, may exceed the TDI from their diet. This is particularly concerning for individuals who consume a lot of processed foods containing phosphate additives. 3. Health Concerns: Excessive phosphate intake has been associated with potential health risks, particularly for people with impaired kidney function, as they may have difficulty excreting excess phosphorus. High phosphorus levels in the blood can contribute to cardiovascular issues and bone health problems. 4. Recommendation: EFSA suggested stricter regulations and better labeling to help consumers understand and manage their phosphate intake, particularly from food additives. * EFSA’s findings highlight the importance of balancing phosphate intake from natural and processed sources to avoid exceeding safe levels.

Answer 91

Phosphate additives are commonly used in processed foods to improve texture, flavor, and shelf life.

Answer 92

High phosphorous intake can contribute to CVD issues and bone health problems

Answer 93

Limitation of phosphorous being listed in ingredients list but not in the nutritional information * Doesn't give indication of how much phosphorous there is * Typically added as an additive * How can consumers know what they are having

Answer 94

Main sources of phosphorous/ phosphate in diet: * Processed foods * Foods with phosphate additives * Supplements

Answer 95

In the general population: Higher end of normal range serum phosphates are associated with : * Coronary calcification in young men * Increased mortality in those with CVD * CV events (predictor) * Surrogate marker of aging (from animal studies)

Answer 96

UK adults can eat up to 2.7g phosphorus per day which is about **5** times our requirement in phosphorus

Answer 97

1. Large amounts of phosphate concentrate in the kidney tubules * Large amounts overtime can crystalise calcium phosphate in the kidney 2. Internal compensation * Processes start in response to hormonal control of phosphate and calcium balance involving bones and blood levels

Answer 98

If there is High Serum Phosphate in CKD: 1. Parathyroid glands become overactive 2. Calcium and phosphate are mobilised from bone to blood 3. Causing: Renal bone disease &

Answer 99

Evidence shows that bones and heart suffer in higher phosphate intakes even with **healthy** kidneys

Answer 100

The limitations of pooling analyses: * From studies we know phosphate additives can double phosphate in ham * Packets of different brands of ham are used to illustrate that the UK composition of food data will pool all the samples and analyse together. This gives misleading values, which are not useful to us in classifying whether a food or diet is high or low in phosphate.. * Value given in HMSO Composition of Foods will be somewhere in between * Applies to the range of foods - processed meats, plant milks, dried packet foods, cheeses and spreads, biscuits.

Answer 101

Amount of phosphate absorbed from different foods: * Organic (naturally occurring): 20-50% (Plants: 20-40%, Animals: 50% * Inorganic: (Food additives )90-100% This is why it is important to make a swap to Organic sources

Answer 102

1. Avoid non nutrient sources of phosphates first 2. Encourage fresh rather than processed - if not likely to interfere with nutrition 3. Teach phosphate additives labelling -if not likely to interfere with nutrition 4. Use mainly meat and white fish rather than cheese, eggs milk, and bony fish (lower phosphate to protein ratio). And choose pulses and nuts (fibre inhibits absorption) But: 5. Conflict with protein- need to work out alternative protein sources they can manage 6. Conflict with nutritional support – blood results? is low phosphate diet needed now? 7. Care not to ↑ phosphate additives – eg swapping cheese sandwiches for ham could be worse 8. Match binders to food First 3 items on the list are avoiding inorganic phosphate ie additives first. This should be advised in earlier CKD, but recheck here that they have this information first when serum phosphate rises. Then if serum phosphate remains raised choose lower phosphate to protein ratio sources to protect protein intake, and also make sure they have optimum binder prescription to lowerabsorption

Answer 103

Low acid/alkalising diet recommended in CKD because: * Acid is inflammatory, associated with: * Accelerated CKD progression * Muscle wasting * Hypertension * Bone disease * Aging * Increased mortality

Answer 104

Acid sources: * All proteins- methionine and cysteine more so * Phosphate in diet is acidic * Salt increases acid load

KD (RD) Flashcards

(129 cards)