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Clinical Nutrition 3 > Renal Disease 1 > Flashcards

Renal Disease 1 Flashcards

1
Q

Prevalence of CKD in Canada?

A

12.5% of the population

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2
Q

Prevalence of Stage 3-5 in Canada? What % has diabetes and/or hypertension?

A

3.1%

75%

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3
Q

Prevalence of CKD in adults over 65 years?

A

30.8%

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4
Q

Provide 5 risk factors for CKD

A
  • Diabetes
  • Hypertension
  • Autoimmune diseases
  • Systemic infections
  • Urinary tract infections
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5
Q

Provide 4 sociodemographic risk factors for CKD

A
  • Age > 60 years
  • Exposure to certain chemicals and environmental conditions
  • Low incomes/education
  • Ethnicity
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6
Q

Which ethnicities are at a higher risk of CKD?

A
  • African American
  • Hispanic Americans
  • Asians
  • Pacific Islanders
  • American Indians
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7
Q

What is CKD?

A

The irreversible damage of nephrons, where urea can no longer be properly filtered, leading to the build-up of uremic toxins within the blood

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8
Q

What are the symptoms of CKD?

A

-Asymptomatic in earlier phases, but as failure progresses leads to increased fatigue, nausea, vomiting, anorexia, insomnia, uremic syndrome and itching

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9
Q

What is a uremic toxin?

A

An identified substance, which is higher in uremia with associated symptoms which are studies at in vivo levels

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10
Q

What are the confirmed toxins?

A
  • Water
  • Sodium
  • Potassium
  • Hydrogen
  • Inorganic Phosphate
  • Urea
  • Cyanate
  • Oxalic Acid
  • B2-Microglobulin
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11
Q

What are the suspected toxins?

A
  • Leptin
  • AGE’s
  • Uric Acid
  • Creatinine
  • Mg
  • Homocysteine
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12
Q

What are the 3 stages of CKD?

A

1) Decreased renal reserve
2) Chronic renal insufficiency
3) Frank renal failure
4) End stage renal disease

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13
Q

Discuss decreased renal reserve

A

Diminishing renal function but without the accumulation of the end-products of protein metabolism, the patient is asymptomatic

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14
Q

Discuss chronic renal insufficiency

A
  • Further reduction in kidney function, where GFR decreases to 30 ml/min and waste products can begin to accumulate (“tipping point”)
  • Can be mild, moderate or severe
  • Severe will eventually progress o ESRD
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15
Q

Discuss Frank renal failure

A

-Serum creatinine and BUN will rise steadily due to the drop in GFR

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16
Q

Discuss End Stage Renal Disease (ESRD)

A
  • The remaining kidney function cannot adequately regulate the balance of fluids, salts and waste products within the body, and uremia accumulates
  • All body systems will become impaired
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17
Q

What is the % function cut-off for ESRD for those with and without diabetes?

A

With: <15%
Without: <10%

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18
Q

What is needed in ESRD?

A

Dialysis and or transplant to prevent complications and death

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19
Q

What is the main consideration when initiating dialysis?

A

-Symptoms, such as fatigue, poor appetite, fluid overload and electrolyte abnormalities

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20
Q

Discuss creatinine in the Mild, asymptomatic CKD patient

A
  • Creatinine clearance will rapidly drop off as GFR decreases
  • Serum creatinine slowly rises
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21
Q

Discuss creatinine in the Moderate, compensated CKD patient

A
  • Creatinine clearance will continue to steadily decrease from a lower baseline
  • Serum creatinine levels rapidly rise
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22
Q

Discuss creatinine in the severe, decompensated CKD patient

A
  • Creatinine clearance reaches nearly 0

- Serum creatinine continue to rapidly rise, then slightly decrease

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23
Q

CKD complications?

A

Uremic sundrome
Anemia
Fluid imbalances
Electrolyte imbalances

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24
Q

Uremic syndrome?

A

High urea and creatinine

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25
Q

Anemia?

A

Decreased kidney function and less erythropoietin to stimulate RBC production in bone marrow

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26
Q

Fluid imbalances?

A

Na imbalance and edema

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27
Q

Electrolyte imbalances

A

High K+, acidity (H+ retained), PO

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28
Q

CKD tests?

A
  • Creatinine and creatinine clearance rates
  • BUN, electrolytes
  • Iron status measurement
  • 24h protein/sodium
  • PTH
  • Renal biopsy
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29
Q

When may we use 24 hr urine collection?

A

To estimate Na intake in steady state patient s(as urine sodium is usually the most accurate than intake)

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30
Q

How many mg of Na in 1 mmol?

A

23 mg

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31
Q

How to determine how many mg of Na a patient is consuming based on 24 h urine collection?

A

(24 h Na in mmol/day) x (23 mg Na/mmol) = Na mg/day

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32
Q

When should we be cautious in interpreting 24 hour sodium?

A

-If the patient is on diuretics, such as Lasix which are sodium losing

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33
Q

How may CKD be treated?

A
  • Transplant
  • Dialysis
  • Medication
  • Conservative care
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34
Q

What should be reviewed prior to drawing conclusions about symptoms?

A
  • Changes to medications and dosages, such as hyperkalemia within the context of longstanding ACEi use
  • ACEi causes the retention of potassium due to increasing aldosterone
  • The longer they have been on the medications and showing tolerance, less likely the med is the cause of the new symptom
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35
Q

What is a goal of medication?

A

To correct electrolyte imbalance

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36
Q

K supplements?

A
  • Indicated in peritoneal dialysis

- Poor intake, meds, vomiting, diarrhea can cause depletion

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37
Q

PO4 binders?

A
  • may used adjunct to dietary restriction

- Examples are Sevelamer, Lanthanum, Calcium carbonate or citrate

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38
Q

Ca supplements?

A
  • Typically more used as a binder to phosphate than to supplement calcium
  • Due to altered Vitamin D metabolism, decreased Ca absorption, high P04
  • Monitor for hypercalcemia
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39
Q

Antihypertensives?

A
  • ACE inhibitors
  • Diuretics
  • Ca Channel blockers
  • B-blockers
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40
Q

K Depleting meds?

A
  • Thiazides and Loop (Will deplete Na and K+, but retain H20)
  • Excessive fluid can develop, and caution with hyponatremia and edema
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41
Q

Erythropoietin?

A
  • Given often in late stage or on dialysis

- Decreased kidney function means the hormone cannot signal to the bone marrow to make RBCs, may lead to anemia

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42
Q

Iron supplementation?

A
  • At risk of anema
  • Start with oral, and progress to IV
  • Most patients on dialysis are on EPO and Iron supplementation
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43
Q

Discuss dysregulation of Vitamin D and calcium

A
  • Decreased kidney function means decreased calcitriol, and will fail to increase absorption of calcium from GI , and retain calcium from kidneys.
  • Blood calcium will be low, stimulating PTH to demineralize bone –> leading to potential osteodystrophy
  • Recall that vitamin D is activated in the liver, then in the kidneys
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44
Q

Should we supplement with inactive vitamin D?

A

No, as the kidney already has reduced function, less likely to activate as calcitriol

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45
Q

Active vitamin D supplements?

A
  • Calcitriol

- Alfacalcidiol

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46
Q

Primary indications of active vitamin D deficiency?

A

-Secondary hyperparathyroidism (stimulation of PTH to promote bone breakdown and osteoblasts)

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47
Q

Which electrolytes may be altered after we supplement with active vitamin D?

A

-Can increase the absorption of phosphate alongside calcium, caution with hyperphosphatemia

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48
Q

How are antihyperglycemic agents indicated to be administered?

A

Varies, but based on when GFR reached a certain lower threshold, usually <30

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49
Q

Which meds are contraindicated when GFR is less than 30?

A
  • Alpha-glucosidase inhibitors
  • GLP-1 receptor agonists
  • Insulin secretagogues
  • SGLT-2 inhibitors
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50
Q

Which meds can be used at a lower kidney function, <15?

A
  • DPP-4 inhibitors, as long as there is less urine output

- If they are diabetic, there will be a high urine output and the meds will be less effective

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51
Q

What is the mechanism of DPP-4 inhibitors?

A

-Increase incretin levels: GLP-1 and GIP which will inhibit glucagon release, increase insulin secretion, decrease gastric emptying and decrease blood glucose levels

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52
Q

What happens in late stage CKD?

A
  • There is alterations in insulin resistance and retention
  • Blood sugars are hard to control
  • Caution with insulin meds
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53
Q

When is CKD indicated?

A

When there is kidney damage OR GFR <60 ml/min per 1/73m^2 for 3 or more months

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54
Q

What is key when interpreting changes in GFR and lab values?

A
  • Their change over time

- Cannot look at a singular number

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55
Q

Normal?

A

GFR >/= 60 with not kidney damage

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56
Q

Stage 1?

A

-Normal or increased GFR (>/= 90 with kidney damage

57
Q

Stage 2?

A

-Mildly decreased GFR (60-89) with kidney damage

58
Q

Stage 3a?

A

-Mild to moderately decreased GFR (45-59)

59
Q

Stage 3b?

A

-Moderately to severely decreased GFR (30-44 )

60
Q

Stage 4?

A

Severely decreased GFR (15-29)

61
Q

Stage 5?

A

Kidney failure, GFR <15

62
Q

How is kidney damage assessed?

A

-Albuminuria or proteinuria

63
Q

Normal to mildly increased albuminuria? (A1)

A

<30 mg/g

<3 mg/mmol

64
Q

Moderately incresed albuminuria ? (A2)

A

30-300 mg/g

3-30 mg/mmol

65
Q

Severely increased albuminuria? (A3)

A

> 300 mg/g

>30 mg/mmol

66
Q

Very high risk for progression?

A
  • All G4 and G5
  • G3b with A2 and A3
  • G3a with A3
67
Q

No CKD?

A
  • G1 and A1

- G2 and A1

68
Q

When may we have normal GFR but high proteinuria?

A

Sometimes observed in severe diabetic nephropathy

69
Q

If the _____ is not corrected, then the patient is much more likely to progress to later stage CKD

A

proteinuria

70
Q

Why is creatine indicative of kidney function?

A

-Creatinine is produced from the muscles, where our ability to excrete it will be an indication of kidney function

71
Q

When is pre-dialysis indicated?

A
  • eGFR between 13-50 ml/min/1.73m2

- Depends on the individual patient

72
Q

Why may dialysis not be started despite GFR being in range?

A
  • Acceptable laboratory values
  • Lack of physical symptoms
  • Conservative care
73
Q

How can we provide dietary intervention in conservative care?

A
  • Help prevent malnutrition, maintain quality of life, and avoid hypophosphatemia (causes chronic itching), manage potassium to prevent cardiac issues
  • Conservative care is not palliative care
74
Q

What are the 3 key nutritional goals of CKD?

A

1) Delay the progression of CRF
2) Preventing or alleviating the symptoms of uremia and restoring biochemical balance
3) Maintaining/improving QOL and Health where possible

75
Q

How can we delay the progression of CRF?

A

-Provide adequate calories to maintain or achieve ideal body weight

76
Q

What is the paradox with the renal and diabetic diets?

A
  • They contradict each other

- Low potassium in renal, whereas important sources of fibres for diabetics will contain the potassium

77
Q

What are the nutrition goals for pre-dialysis?

A
  • Low or normal protein
  • Restricted phosphorus diet
  • Restricted potassium
  • Restricted sodium
  • Adequate kcals
  • Healthy foods and eating habits
78
Q

What is the overarching theme of nutritional intervention in renal disease?

A

Minimizing renal impairment while preventing malnutrition

79
Q

Protein CKD stages 1-2?

A

0.8-1.4

80
Q

Protein CKD stages 3-4?

A

0.6-0.6

81
Q

Energy CKD?

A

25-35 kcal/kg and adjust for weight loss and weight gain

82
Q

Na CKD?

A

<2400 mg

83
Q

K+ CKD?

A

Usually unrestricted unless serum level is high

84
Q

Phosphorus CKD stages 1-2?

A

-Maintain serum P and PTH WNL

85
Q

Phosphorus CKD stages 3-4?

A

-800-100 mg/day

-

86
Q

Calcium CKD?

A
  • DRI

- Maintain serum levels WNL

87
Q

Fluid in CKD?

A

Usually unrestricted

88
Q

What is the #1 cause of new cases of ESRD

A
  • Diabetes

- Diabetics are most common on dialysis

89
Q

When is CKD indicated in diabetes?

A

-When ACR >/= 2 mg/mmol
AND/OR
-eGFR <60

90
Q

What is ACR?

A

Albuminuria:Creatinine ratio, which is more accurate is assessing kidney damage and proteinuria than the individual values

91
Q

What does a progressive increase in proteinurea cause in diabetes?

A

-Will cause declining renal function, and then followed by ESRD

92
Q

When should we continue to screen annually?

A
  • No transient increase in albuminuria
  • no low GFR
  • No acute injury or non-diabetic kidney disease is suspected
93
Q

When should we screen for CKD in type I diabetics?

A

-Screen annually in post-pubertal individuals with duration of diabetes >/= 5 years

94
Q

When should we screen for CKD in Type 2 diabetes?

A

-At diagnosis and annually after

95
Q

If CKD is suspected, which lab values should be ordered?

A
  • Random urine ACR

- Serum creatinine for eGFR

96
Q

What are potential causes for transient albuminuria?

A
  • Recent major exercise
  • Urinary tract infection
  • Febrile illness
  • Decompensated congestive heart failure
  • Menstruation
  • Acute severe elevation in blood glucose or blood pressure
97
Q

What are the common causes of Diabetic nephropathy, which leads to CKD?

A
  • Hypertension

- Renovascular complications

98
Q

What is one of the hallmark signs of CKD and diabetes?

A

The slow progression and loss of kidney function, those with other renal diagnoses will often have rapid changes, extreme proteinuria and rapidly falling GFR

99
Q

Discuss factors which favour a diagnosis of diabetic nephropathy

A
  • Persistant albuminuria
  • Bland urine sediment
  • Slow progression of disease
  • Reduced eGFR associated with overt proteinuria
  • Known diabetes >5 years, with complication**
100
Q

Discuss factors which favour an alternate renal diagnosis

A
  • Extreme proteinuria (>6 g/day)
  • Persistent hematuria or active urinary sediment
  • Rapidly falling GFR
  • Reduced eGFR with little or no proteinuria
  • Known duration of diabetes <5 years, with no complications
  • family history of non-diabetic kidney disease
101
Q

What has been shown to reduce the development and progression of nephropathy?

A
  • Optimal glycemic control in type I and type II diabetes (Up to 50% risk reduction with intensive therapy)
  • Reduction in proteinuria through ARB/ACEi
  • Optimal BP control
102
Q

How is albuminuria often controlled?

A
  • With ACE or ARB
  • These favour the retention of potassium, which is contraindicated in renal disease
  • However, we know that decreased proteinuria may improve outcomes in the CKD progression of diabetics
103
Q

Why are diabetics with CKD prone to hyperkalemia?

A
  • Likely due to ACE and ARB medications
  • We need to closely monitor potassium and intervene with a low-potassium diet
  • This is especially indicated when creatinine is >30%
104
Q

When should serum K+ and Creatinine need to be checked?

A
  • At baseline
  • Within 1-2 week of initiation or titration
  • During acute illness
105
Q

What should we do when K+ becomes elevated or CR>30% increase?

A
  • Review therapy, especially ACE/ARB

- Then, re-check serum K+ and Cr

106
Q

Intervention in mild to moderate stable hyperkalemia?

A
  • Counsel on low potassium diet
  • Consider adding non-potassium paring diuretics and/or sodium bicarb (if acidosis is indicated)
  • Consider temporarily holding or discontinuing ACEi, ARB, or Direct Renal Inhibitor (DRI)
107
Q

Intervention in severe hyperkalemia?

A
  • Hold or discontinue ACEi, ARB or DRI

- Emergency management strategies

108
Q

Hyperkalemia is often ___

A

factorial

109
Q

What may be sources of potassium which should be assessed during hyperkalemia?

A
  • Medication
  • Diet
  • Medical conditions: decr. renal function, metabolic acidosis, hyperglycemia
  • Fever, trauma, infection and stress
  • Hemolysis
110
Q

When is hyperkalemia more common in diabetic patients?

A

Those with renal tubular acidosis type 4

-Require ACEi or ARB

111
Q

What is the main source of dietary potassium?

A
  • Preservatives in processed foods

- Potassium lactate, chloride and potassium bitartrate

112
Q

How can we manage processed foods with the patient?

A
  • Find “better” processed foods with less additives
  • Consider organic processed foods
  • Cut out cold-cuts, processed meats and teach label reading
113
Q

Other sources of dietary potassium?

A
  • Fruits and vegetables
  • Milk products
  • Nuts, seeds, legumes and lentils
  • Whole grain and high fibre grains
  • Meat and alternatives
114
Q

Which foods are likely already restricted in renal?

A
  • Milk and meats

- Do NOT further restrict to meet potassium requirement, as the protein requirement is more important

115
Q

Bioavailability of phosphorus in food additives?

A

-90-100%

116
Q

Bioavailability for phosphorous in animal protein sources?

A

-40-70%

117
Q

Bioavailability for phosphorus in vegetable protein sources?

A

-40-50%

118
Q

What else impacts the bioavailability of phosphorus?

A
  • Many factors, and a complex process

- The less P you eat, often the more you absorb

119
Q

How should phosphate binders be taken?

A

WITH food, think of as the “salad dressing”

-Will not function once the nutrients are absorbed into the bloodstream, must act in the GI tract

120
Q

What should be verified in milk alterntives?

A
  • That the fortified source of calcium is not bound to phosphate
  • Calcium carbonate vs. calcium phosphate
121
Q

Phosphorous recommendation?

A

800-1200 mg/day, however is quite unrealistic

122
Q

____ is not as dangerous as high potassium

A

Phosphorous

123
Q

There are usually two ____ additives per ______

A
  • Phosphate

- Potassium additive

124
Q

KDIGO recommendations concerning protein?

A

0.8 g/kg of IBW when GFR <30 and no more than 1.3 g/kg for individuals at risk for progression

125
Q

What is the usual range for the relatively “healthy” CKD patient?

A

1.1-1.2 g/kg/day

126
Q

Protein requirement for dialysis patients?

A
  1. 2 g/kg/day

- Someone not on dialysis should probably be below this 1.2 recommendation

127
Q

HBA1C target?

A

7.0%

128
Q

When should treating to an HBA1C target of 7% be contraindicate?

A
  • Patient at risk of hypoglycemia

- Co-morbidities, reduced life expectancy

129
Q

How to we teach protein restriction?

A
  • Through renal exchanges
  • 1 renal exchange = 6-8 g of -protein
  • We consider 50% of protein from HBV sources
130
Q

KDIGO guidelines concerning sodium?

A
  • 1500-2300 mg/day usually more realistic
  • KDIGO specifics <2000 mg/day
  • -> Goals need to be individualized and realistic
131
Q

What may a too-restricted diet cause in renal patients?

A

Malnutrition

132
Q

What factors will complicate the treatment of malnutrition?

A
  • Hyperkalemia
  • Fluid overload
  • HyperP
  • HyperG
  • Dyslipidemia
  • Pat dietary retriction
133
Q

What is novel approach in nephrology?

A

Gluten restriction in IgA nephropathy, where we lose protein from the kidney

134
Q

Discuss tolvapten for polycystic kidney disease -

A
  • PKD patients hava a urine-concentrating defect, and high levels of AVP which play a key role in developing the cysts
  • Tolvapten is an AVP-receptor blocker, where if a diet high in solutes and sodium will result in extreme thirst, and copious amount of urine production
  • It will dilute the urine no matter what
135
Q

How can we intervent nutritionally for those on tolvapten?

A
  • Low sodium and protein diet to alleviate extreme thirst and frequent urination
  • Reduce Na to <2300 mg and protein to 0.8 g/kg, and fluid according to thirst
136
Q

How may we achieve the urine dilution effects of tolvapten through solely dietary intervention?

A
  • By prescribing a low osmolar diet and adjusted water intake
  • Will result in vasopressin reduction
  • The less protein and sodium, the less water needed to achieve the reduced urine osmolality
137
Q

What is the goal urine osmolality for those with PCKD? Why?

A
  • <280 mOsm/kg

- To suppress vasopressin

138
Q

Fluid, sodium and protein intake in PCKD?

A
  • High fluid of 2.6-4.8 L per day
  • Low sodium of 1500-2300 mg
  • Low protein of 0.8 g/kg

Clinical Nutrition 3 (30 decks)

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