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KD (RD) Flashcards

1
Q

1 in 10 people in the UK have ?

A

1 in 10 people in the UK have CKD

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2
Q

What is the typical age range of people with CKD?

A

Typical age range of peoeple with CKD:
65-74

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3
Q

Where does 65% of AKI start?

A

65% of AKI starts in the community

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4
Q

1 in 5 emergency hospital admissions have ?

A

1 in 5 emergency hospital admissions have AKI

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5
Q

What do Specialist Kidney dietitians typically do?

A

Specialist Kidney dietitians usually treat:
* Patients that require renal replacement therapy (RRT): e.g. dialysis
* Patients with AKI that need RRT

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6
Q

What do general dietitians usually do?

A

General dietitians usually:
* Treat patients with CKD
* Treat patients with AKI
* Prevention, health promotion, public health, policy, industry

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7
Q

Diet aims for DIALYSIS, PREDIALYSIS & AKI

A

Diet aims for DIALYSIS, PREDIALYSIS & AKI:
* Control fluid overload
* Control high blood potassium
* Control high blood phosphate

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8
Q

What are the 2 electrolytes that are the target of dietary modification in DIALYSIS, PREDIALYSIS & AKI?

A

electrolytes that are the target of dietary modification in DIALYSIS, PREDIALYSIS & AK:
* Potassium (K)
* Phosphate (PO4)

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9
Q

Nutritional advice for Early CKD, Prevention of CKD, Prevention of AKI

A

Nutritional Advice for Early CKD, Prevention of CKD, Prevention of AKI:
* Healthy eating
* Low processed foods
* Low salt
* High F&V
* High intake of nuts&seeds
* High intake of fish
* Pulses to replace meat
* High quality, non processed meats
* Dietary patterns: MED DIET, NORDIC DIET, DASH DIET.
* AKI: Protect fluid intake

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10
Q

Contributing causes of CKD

A

Contributing causes of CKD:
* Diabetic nephropathy
* HTN
* Infection
* Nephrotic syndrome: large amounts of protein leak into the urine, causing fluid retention and swelling.
* Polycystic kidney disease
* Tumour
* Genetics
* Idiopathic

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11
Q

Contributing causes of AKI

A

Contributing causes of AKI:
* Hypovolaemia
* Heart failure
* Sepsis
* MOF
* Acute glomerulonrephritis: inflammation of the tiny filters in the kidneys (glomeruli)
* Toxic reaction (poison, drugs)
* Urinary output obstruction

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12
Q

Main functions of the kidneys

A

Main functions of the kidneys:
* Blood filtration
* Waste removal
* Blood pressure regulation
* Electrolyte balance
* Fluid balance
* Acid-base balance
* RBC production
* Vit D activation
* Excretion of drugs & toxins

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13
Q

What do the kidneys do? (Lecture slide)

A

What the kidneys do (Lecture slide):
* Pass all of our blood through 40x/day
* Make 180L of glomerular filtrate per day
* Reabsorb 99% of filtrate in the tubules
* Have 145 miles of filtering tubes
* Take 20-25% of the cardiac output
* Use 25% of energy

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14
Q

Name the things that can damage the kidneys over time

A

Things that can damage the kidneys over time:
* Poisons e.g. ethylene glycol crystals
* Products of metabolism e.g. acid load
* Excess nutrients e.g. phosphate, vitamin c (oxalate can cause kidney stones)
* NSAIDS: cause inflammation in tubules> fail to maintain blood flow to nephron by inhibition of prostaglandin production

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15
Q

Prevention of kidney disease nutrition

A

Prevention of kidney disease nutrition
* DASH DIET
* MED DIET
* NEW NORDIC STYLE DIET
* Low processed foods
* Low salt
* Rich in F&V
* Rich in seeds & nuts
* Rich in fish
* Pulses to replace some meat

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16
Q

Hansrivijit et al. 2020 “Mediterranean diet and the risk of chronic kidney disease: A systematic review and meta-analysis”

A

Hansrivijit et al. 2020 “Mediterranean diet and the risk of chronic kidney disease: A systematic review and meta-analysis”
* 9 prospective observational studies (2010-2019) with 18519 participants
* Using the MeDiterranean diet Score scoring system, The MED diet was found to reduce CKD risk by 10%
* MED diet: reduces creatinine levels (serum)
* MED diet: stabilizes eGFR
* High consumption of: F&V, olive oil, moderate wine lowers inflammation & oxidative stress
* High fibre: inversely correlates with mortality and inflammatory markers in CKD subpopulation
* A prospective RCT and PREVEND study showed: consumption of 2 to 3 glasses of white wine per day was associated with decreased CRP, IL-6 levels, proteinuria and increased eGFR.

Pros:
* Used validated scoring system: MDS
* Included studies of all languages
* All community subjects

Limitations:
* Small number of observational studies: 4 were suitable for meta-analysis
* Excluded other scoring systems for mediterranean diet adherence
* No UK studies included: how applicable to UK population?

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17
Q

Quintela et al. (2021) “Dietary patterns and chronic kidney disease outcomes: A systematic review”

A
  • 24 studies
  • Multiple regions in the world: mostly USA
  • Cohort & cross-sectional studies
  • Newcastle-Ottawa used to judge quality of studies
  • Prudent, MED & DASH diet: associated with higher eGFR, lower levels of albuminuria & inflammatory markers and reduced CVD risk
  • Low protein, salt restriction, and reduced alcohol, glycaemic control are important for protection against CKD.
  • High saturated fat, protein, salt and acids: promote glomerular hyperfiltration, HTN & metabolic acidosis
  • High saturated fat reduces glomeruli, GFR, and increases CVD risk
  • Unsaturated fat, fibre, antioxidants: reduce inflammation & oxidative stress
  • Plant based reduce glomerular hyperfiltration
  • High protein: cause kidney damage via increased glomerlular pressure: hyperfiltration & renal dysfunction
  • Fibre: promotes gut bacteria, reduces uremic toxins
    More research needed for effective dietary strategies for CKD prevention
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18
Q

Name the disrupted kidney functions that can be treated with diet

A

The disrupted kidney functions that can be treated with diet:
* Blood pressure: no added salt restriction/ fluid restriction
* Fluid balance: fluid restriction/ salt restriction
* Electrolytes: potassium control
* Bone metabolism: phosphate control
* Toxins: nutritional support/ lower protein diets?
* Acid/base balance: plant based diets

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19
Q

We are born with ? times more kidney function than we actually need

A

We are born with 3 times more kidney function than we actually need

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20
Q

What does kidney function decline with?

A

Kidney function declines with age

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21
Q

Creatinine is a marker of ? ?

A

Creatinine is a marker of kidney function. High creatinine is an indicator of kidney issues.

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22
Q

When does creatinine rise?

A

Creatinine rises when there is only 1 THIRD of capacity left

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23
Q

There could be loss of 2 THIRDS of kidney function and creatinine would be ?

A

There could be loss of 2 THIRDS of kidney function and creatinine would be normal

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24
Q

How is blood pressure treated by diet?

A
  • Blood pressure: no added salt restriction/ fluid restriction
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25
Q

How is fluid balance treated by diet?

A
  • Fluid balance: fluid restriction/ salt restriction
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26
Q

How are electrolytes managed by diet?

A
  • Electrolytes: potassium control
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27
Q

How is bone metabolism managed by diet?

A

l
* Bone metabolism: phosphate control

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28
Q

How are toxins managed by diet?

A
  • Toxins: nutritional support/ lower protein diets?
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29
Q

How is the acid/base balance managed by diet?

A
  • Acid/base balance: plant based diets
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30
Q

What is an Acute Kidney Injury?

A

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

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31
Q

What are the characteristics of an AKI?

A

Characteristics of an AKI:
* Sudden disruption to kidney function
* Function declines over </=2days
* Acute condition
* Recovery is possible but it could lead to CKD
* It is not a disease. It is a disruption to kidney function usually caused by something else.

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32
Q

What are the characteristics of CKD?

A

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.

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33
Q

What % of people admitted to ICU have an AKI?

A

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

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34
Q

How do you classify AKIs dietetically?

A

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

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35
Q

What are the 3 cause classifications of AKI?

A

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)

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36
Q

What is diuresis?

A

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

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37
Q

What is key for the prevention of AKI?

A

Adequate fluid intake is key for AKI prevention

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38
Q

Excess vitamin C can cause ? ?

A

Excess vitamin C can cause kidney stones

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39
Q

Which macronutrient isn’t affected by AKI?

A

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

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40
Q

What does dietetic treatment of AKI depend on?

A

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

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41
Q

When is an AKI often present?

A

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

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42
Q

What percentage of hospitalised patient with AKI present with a degree of malnutrition?

A

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

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43
Q

Validated Screening tools for AKI

A

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

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44
Q

Which screening tools may be used for AKI although not specific to AKI?

A

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.

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45
Q

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

A

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

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46
Q

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

A

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

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47
Q

What did Jackson et al., 2018 find when comparing the MUST and Renal iNUT screening tools?

A

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)

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48
Q

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

A

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

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49
Q

AKI Non-Catabolic without RRT Requirements

A

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.

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50
Q

AKI Non-Catabolic ON RRT Requirements

A

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.

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51
Q

AKI Catabolic without RRT Requirements

A

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.

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52
Q

AKI Catabolic on HD Requirements

A

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.

53
Q

AKI Catabolic on CRRT Requirements

A

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.

54
Q

AKI Protein Requirements
* Non-Catabolic without RRT
* Non-Catabolic ON RRT
* Catabolic without RRT
* Catabolic on HD Requirements
* Catabolic on CRRT Requirements

A

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

55
Q

Are most people with AKI malnourished?

A

Yes, most people with AKIs are malnourished.

56
Q

Dietetic Classification of AKI

A

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?

57
Q

AKI Classification by cause & nutritional relevance

A

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.

58
Q

Which type of AKI cause is likely to alter nutritional requirements?

A

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

59
Q

Patients with pre-existing chronic kidney disease (CKD) may present with ?

A

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

60
Q

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

A

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.

61
Q

What state do patients with intra-renal AKI typically present in?

A

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

62
Q

What are the nutritional requirement guidelines for AKI based on?

A

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

63
Q

Advised treatment for non-catabolic AKI (Think Kidneys)

A

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.

64
Q

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

A

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

65
Q

Patient with AKI & MOF measured energy requirements

A

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

66
Q

AKI on ICU estimation of energy requirements

A

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.

67
Q

ICU AKI energy estimation & BMI >26

A

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

68
Q

Limitations of predictive formulas

A
  • 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).
69
Q

AKI & estimation of energy requirements

A
  • 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.
70
Q

AKI on ICU estimation of protein requirements

A
  • 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
71
Q

AKI & electrolyte management

A

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.

72
Q

What are gastrointestinal cationexchange resins?

A

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.

73
Q

AKI & fluid requirements

A

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

74
Q

AKI & micronutrient requirements

A

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

75
Q

AKI KDIGO 20-30kcal/kg/day comments

A

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.

76
Q

Medical treatment of AKI

A
  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
77
Q

AKI – Dietitians Role

A

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?

78
Q

AKI Nutritional Considerations

A

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

79
Q

AKI Dietetic Interventions

A

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

80
Q

AKI course of illness

A

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

81
Q

CKD statistics

A

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

82
Q

What is eGFR?

A

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

83
Q
A
83
Q

Proteinuria is an ? risk factor for CardioVascularDisease

A

Proteinuria is an independent risk factor for CardioVascularDisease

83
Q

eGFR & African descent

A

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

84
Q

CKD staging

A

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

85
Q

CKD & proteinuria

A

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

86
Q

CKD Stages 1-3 Nutritional Requirements/ Interventions

A

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)

87
Q

What are some of the consequences of kidney disease?

A

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

88
Q

What are possible causes of Hyperkalaemia?

A

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

89
Q

When might Hyperphosphataemia occur? What is it associated with?

A

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

90
Q

How is Hyperphosphataemia usually treated with diet?

A

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

91
Q

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

A

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

92
Q

Which nutritional components may be targeted in CKD?

A

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

93
Q

Diet for CKD 1-2

A

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

94
Q

Diet for CKD 3

A

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

95
Q

Diet for CKD 4-5

A

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

96
Q

Low Potassium Diet

A

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

97
Q

How is CKD categorized?

A

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

98
Q

How is AKI categorized?

A

AKI is categorized according to serum creatinine and urinary output.

99
Q

Why is phosphorous absorption reduced in plants?

A

Plants have reduced phosphorous absorption because of phytates

100
Q

An individual with CKD is more likely to die of ? than reach the stage of requiring ?

A

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

101
Q

Why is anaemia common in CKD?

A

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

102
Q

Reasons for weight management in CKD

A

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

103
Q

The nutritional recommendations provided by the Renal Association are aimed at what?

A

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

104
Q

Which novel equation may be beneficial for the estimation of energy requirements in CKD patients?
Why?

A

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.

105
Q

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 what?

A

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

106
Q

CKD & CVD risk

A

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

107
Q

Is targetting traditional risk factors of CVD in CKD patients effective?

A

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

108
Q

Risk factors for CVD in CKD

A

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

109
Q

What does low potassium do?
What should be advised?

A

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

110
Q

Dietary patterns to protect the kidneys and prevent CVD complications

A

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.

111
Q

Resources for CKD patients

A

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

112
Q

Why did the European Foods Standards Authority review the safety of phosphate additives in 2019?

A

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

113
Q

EFSA Phosphate Report

A

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.

  1. 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.
  2. 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.
  3. 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.
114
Q

Which types of foods are phosphate additives commonly used for?

A

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

115
Q

High phosphorous intake can contribute to?

A

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

116
Q

Limitation of phosphorous being listed in ingredients list but not in the nutritional information

A

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

117
Q

Main sources of phosphorous/ phosphate in diet

A

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

118
Q

In the general population: Higher end of normal range serum phosphates are associated with :

A

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)

119
Q

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

A

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

120
Q

What happens when the kidney gets rid of excess phosphate for us?

A
  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
121
Q

What happens if there is High Serum Phosphate in CKD ?

A

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 &

122
Q

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

A

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

123
Q

The limitations of pooling analyses

A

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.

124
Q

Amount of phosphate absorbed from different foods

A

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

125
Q

Low Phosphate Diet for later CKD when serum phosphate rises

A
  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

126
Q

Why is a low acid diet/alkalising diet recommended in CKD?

A

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

127
Q

What are acid sources and what are neutralising alkaline sources?

A

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

CCD (16 decks)

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