Nutritional Management of CKD and Urinary Disease Flashcards

1
Q

What is fibroblast growth factor 23?

A

FGF‐23 is a factor synthesized and secreted by bone cells (fibroblasts)

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2
Q

What is FGF-23’s role in P regulation and how does it interact with Klotho?

A

FGF-23 reduces P in the serum by increasing renal secretion and decreasing intestinal absorption
• FGF-23: The N- terminal peptide binds to tissue receptors, and the C-terminal binds to Klotho.

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3
Q

What is Klotho?

A

Klotho is a transmembrane protein that acts as a coreceptor for FGF-23 in the kidney

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4
Q

What are signs of Klotho deficiency?

A

Animals with Klotho deficiency show signs of FGF‐23 deficiency with high serum phosphate and calcitriol concentration.

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5
Q

What is Klotho’s role in longevity?

A

More klotho-> longer life

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6
Q

What mechanisms are there to help reduce phosphorus in the blood?

A

When phosphorous is high, there are several mechanisms including PTH to help reduce it
• Hyperphosphatemia upregulates a factor called fibroblast-growth factor-23 (FGF-23) from the bone
• This factor reduces activation of vitamin D to calcitriol in the kidney
• Reduces P absorption form the GI tract
• Primary action- joins with a factor called Klotho to increase P excretion in the kidney

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7
Q

When we have kidney disease what is occuring in terms of phosphorus?

A
  • decrease 1,25 vitamin D
  • increase phosphate
  • Decrease in calcium
    This increases PTH levels
    FGF-2 is link between phosphate load and decreased 1,25 vitamin D levels
    This decreased calcium levels cause increased PTH secretion, increased PTH synthesis, and increased cell proliferation
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8
Q

What are the risk factors for CKD?

A

Risk factors for CKD:
• Age (estimated that up to 33% of cats above 13 years have
CKD)
• Body condition
• Hyperlipidemia
• Acute kidney injury
• Vaccination?
• Dietary??

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9
Q

What are the outcomes of CKD?

A

Dehydration (secondary to polyuria)
• Renal Secondary Hyperparathyroidism
• Hyperphosphatemia
• Azotemia/uremia
• Electrolyte & acid/base imbalances
• Hypertension
• Renal hypoxia and/or renal oxidative injury
• Loss of body condition and muscle…

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10
Q

How common is CKD in cats?

A

1/3 of cats above the age of 15 suffer from chronic renal disease

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11
Q

What is the link between obesity and CKD in humans? In dogs?

A

• In people = significant risk factor for development of glomerulosclerosis & failure
• Degree of obesity also correlates with degree of proteinuria in people
In Dogs?
• Associated with mild hypertension in dogs
• Increased HR & increased Na+ resorption from renal tubules
• Glomerular hyperfiltration & renal hypertension, damage to parenchyma

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12
Q

What was the outcome of the study of experimentally induced obesity in dogs

A

Experimentally induced obesity in dogs
• increased mean arterial pressure, increased plasma renin -> altered function & architecture
• Bowman capsule expansion, glomerular cell proliferation, thickening of glomerular & tubular basement membranes, increased mesangial matrix
• Changes in Bowman’s capsule -> pathologic proteinuria?

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13
Q

What are comorbidities that have growing evidence in regards to CKD?

A
  • Evidence accumulates for proteinuria and hyperlipidemia being comorbidities
  • Unknown whether treating one disorders impacts the other
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14
Q

Can food cause CKD?

A
  • May be related to form of phosphorous, and Ca:P ratio
    • A need to establish a safety limit for phosphorous
    • Acidifying diets, limited in potassium, can also lead to CKD
    (Dow et al. 1987)
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15
Q

Is high dietary phosphorus safe in adult animals?

A

While calcium is tightly regulated, phosphorus regulation is not as tight
• Meaning, calcium is usually kept in a tight range in the blood/plasma, whereas phosphorus has a wider range
• Phosphorous in foods can be organic (from fruit, vegetables, grains, meat) or inorganic (phosphoric salts)
• Highly bioavailable phosphorous have been found to damage the kidneys in rats
• In current guidelines, there is no maximum P in cats

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16
Q

Based on all the studies in this lecture what is the overall consensus?

A

Concentrations of P and Ca in many commercially available cat foods are highly variable
• Very low and very high both exist as well as inverted Ca:P ratio (under 1)
- Future limits on P, its forms used and Ca:P should be considered.

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17
Q

What IRIS stage has seen improvement with diet?

A

Benefits for kidney diets have been shown from IRIS CKD 2 and above; therefore, many would not change the diet in stage 1

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18
Q

Is there a correlation between PTH and Creatinine?

A

yes there is.
Much higher PTH at high creatinine levels.

19
Q

What is important about hydration in terms of kidney disease? How can you maintain hydration?

A

Address/prevent dehydration
• Maintain renal perfusion

  • How?
  • Increase water consumption -> water fountains, canned food, etc
  • Subcutaneous fluids -> also contains Na/K (may not be desired) patient tolerance…
  • Feeding tube
  • More physiologic than subcutaneous fluids…
20
Q

What are essential nutritional factors for CKD?

A
  • Maintain hydration & body condition
  • Phosphorus reduction/restriction
  • Protein –reduction?
  • Address electrolyte abnormalities
  • Address acid/base disturbances
  • Sodium content
  • Antioxidants
  • Omega-3 PUFAs (marine sourced)!
21
Q

Should you restrict phosphorus if patient is not hyperphosphatemic?

A

yes. Compensatory mechanism. Negative indications for having high PTH, so though it is not problematic, likely will cause other issues over time.

22
Q

When should we start restricting phosphorus?

A
Stage 2 (early) 
• Stage 1? (no clear evidence, still makes sense to avoid a higher phosphorus 
diet when possible…)
23
Q

What is the goal with reducing phosphorus in stage 3/4 kidney disease? What should we decrease phosphorus to?

A

Phosphorus restriction
• More severe restriction to deal with hyperphosphatemia -> decreased below NRC RA
• Stage 2 (late)
• Stage 3/4

24
Q

What are the diagnostic signs of protein losing nephropathy? How is it treated?

A

Diagnostic signs:
• Elevated UPC
• Rule out non renal causes
• May lead to hypoalbuminemia, loss of ATIII (prevents hypercoagulation, so these patients may be hypercoaguable)

• A negative prognostic indicator; regardless of azotemia
Treatment:
• Dietary protein restriction = decrease renal blood pressure, GFR
• Omega-3 supplementation

25
Q

What is important about protein reduction in patients with CKD?

A

Reduce bioavailable phosphorus…
• Reduce azotemia/uremia
• BUN is only a marker (other uremic toxins too)
• Proteinuria
• Independent of CKD/IRIS stage
• Reduction based on
• UPC/diet history!
• Response…
• Must provide enough digestible protein

26
Q

What is important about protein quality of patients with CKD?

A

Highly digestible
• Protein quality (AA profile)
• Less oxidation of AA -> less uremic toxins
• Less undigested protein reaching the lower GI tract

27
Q

What are the concerns associated with protein reduction?

A

Concerns with palatability or decreased intake
• Decreased E intake -> loss of BCS
• Decreased protein intake below MR -> muscle loss, hypoalbuminemia
• Less aggressive if only reducing phosphorus…
• Generally more aggressive/restrictive with
• Stage 3/4 (azotemia/uremia)
- Proteinuria

28
Q

What is important about potassium in dogs with renal disease?

A

Dogs with renal disease -> Can be
• Normokalemic, hypokalemic, hyperkalemic
• ACE-inhibitors may predispose to K+ retention…
• Canine renal diets
• Typically normal to decreased in K+ content
• Look at product guides for K+ concentration
• Important to choose best option for individual patient
• May need custom home-cooked formulation for severe hyperkalemia or refusal to eat appropriate diet

29
Q

What is important about potassium in cats with renal disease?

A

Cats -> more prone to hypokalemia
- Signs: plantigrade ( neuro signs appear in cats)
• Whole body potassium depletion
• Feline renal diets typically supplemented with K+
• May also need to supplement even more
• Cats can develop hyperkalemia (rare)
• Home-cooked renal diet only good option

30
Q

What is important about sodium in patients with CKD?

A
  • Hypertension contributes to CKD progression
  • Avoid high salt diets
  • May want sodium reduction with hypertension
  • May want lower end if active hypertension
  • Over-reduction activates RAAS… not good either don’t go <0.3 g/1000 kcal…
31
Q

How are B vitamins utilized / indicated in patients with kidney disease?

A
  • Water-soluble
  • Important in energy metabolism!
  • Loss may be increased with polyuria
  • Most don’t have large body stores -> depletion?
  • Most renal diets empirically supplemented
  • Safe!
  • oral over-supplementation difficult
32
Q

What acid base issue can occur with CKD? Why? What is the potential treatments for this condition?

A

Metabolic acidosis can result from CKD
• Increases muscle catabolism

• Disrupts intracellular metabolism
• Bone mineral dissolution?
Treatment :
• Provide alkalinizing agents in diet OR supplement
• Bicarbonate, carbonate, citrate
• Beware potassium…

33
Q

How do antioxidants benefit CKD patients?

A
  • Renal oxidative stress (ROS)
  • Possible contributor to progression
  • May trigger fibrosis or glomerulosclerosis
  • Scarce data on antioxidant use in cats & dogs
  • Vit E, carotenoids, lutein may slow GFR decline in dogs…
34
Q

Is there a benefit to Omega -3 PUFAs in CKD? How can it help?

A
  • Marine sourced (fish oil, krill, algae) bioavailability
  • EPA (eicosapentaenoic acid)
  • DHA (docosahexaenoic acid)
  • Incorporated into cell membranes -> compete with Omega-6
  • Produce less inflammatory eicosanoids
  • May reduce renal interstitial fibrosis, slow GFR decline
  • Improve survival
  • Lower glomerular capillary pressure, decreased inflammation
35
Q

What are diet options for patients with CKD? What resource should not be recommended?

A

Commercial
• Custom formulated home-cooked diet
• Consult veterinary nutritionist
• Do NOT used recipes on-line or in books…

36
Q

What are the pro’s and cons of a kidney friendly commercial therapeutic diet?

A

• Many options
- Look at product guides
• Differences between diets may make some better fit than others
• Different stages, differences in electrolytes, fat content, etc.
• Multiple options for palatability/variety. Be aware that many are high(er) in fat
• May be contraindicated for pancreatitis, hyperlipidemia, etc
- Some multi-function diets now available
• Hydrolyzed/renal diet (adverse food reactions/renal
disease)

37
Q

What do you do if patient refuses appropriate CKD diet?

A
  • Address underlying issues
  • Diet rotation may be appropriate
  • Ensure all diets offered are ok for patient
  • Olfactory changes may affect appetite day to day
  • Assisted feeding (feeding tubes)
  • provide appropriate diet, can still accept treats, etc
  • provided additional water & medications! (improve QOL)
38
Q

What are potential causes of Dysorexia Anorexia relating to CKD?

A
  • Primary disease/ concurrent disease
  • gastritis/ enteritis.
  • Uremic toxins
  • Hormonal changes
  • Anemia
  • Dehydration, electrolyte disorders, metabolic acidosis.
  • Stomatitis/ oral ulcerations, altered smell
  • Unpalatable diet, Food aversion, Medications, Hospitalization.
39
Q

What are the potential causes of an AKI in a patient?

A

Acute kidney failure can be secondary to CKD but can also occur as a result of another primary cause:

  • Toxicity
  • Infectious disease
  • Neoplasia
  • Trauma
  • Heat stroke/ dehydration etc.
40
Q

What are important points to remember/ tips for nutritional management of an AKI?

A
  • The optimal nutritional management of acute kidney injury patients that do not have an underlying CKD is not determined
  • Emphasis should be given to them receiving adequate caloric intake, and if there are electrolyte shift, these should be corrected
  • Long-term management may depend on regeneration of kidney function
  • It may not always be needed or advised to start with a renal diet while hospitalized
  • This may cause food aversion (stress, noise, nausea) for the food
41
Q

What are causes of hypercalcemia, what is the prognosis? When are clinical signs typically seen?

A

Hypercalcemia can be the result of dietary, metabolic, neoplastic, renal, and idiopathic causes in dogs and cats
• In cats, idiopathic hypercalcemia is most common
• The degree of hypercalcemia and its chronicity impacts prognosis
• clinical signs of hypercalcemia are usually most severe when the increase in calcium is rapid
• Most often, clinical signs are noted when usually serum total calcium is higher than 14.0 mg/dL and ionized calcium is greater than 6.5 mg/dL (1.6 mmol/L)
• If serum total calcium increases to 16.0 mg/dL or if ionized calcium increases above 7.5 mg/dL (1.9 mmol/L) -> require hospitalization and immediate care

42
Q

Can diet cause hypercalcemia?

A
  • Some anecdotally recommend feeding a diet with moderately reduced calcium and vitamin D in addition to added insoluble fiber for all-cause hypercalcemia
  • High dietary calcium on its own does not appear to be a cause of hypercalcemia
  • Some cats with CKD may develop hypercalcemia due to excessive phosphorus restriction
43
Q
A