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Internal Medicine/ Ettinger > Chronic Kidney Disease > Flashcards

Chronic Kidney Disease Flashcards

1
Q

What does it mean if there is an elevation in creatinine?

A

it means at least 75% of the renal function have been injured/ lost

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2
Q

What type of CKD is associated with dogs? cats?

A

Dogs: tubulointerstitial nephritis
Cats: tubulointerstitial nephritis

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3
Q

What are the 6 factors that should be considered to establish a diagnosis of CKD in pets?

A
  1. nature of the primary disease
  2. severity/ duration of clinical signs, uremia?
  3. probability of improving renal function
  4. severity of intrinsic renal function impairment
  5. rate of progression
  6. age
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4
Q

Who survives longer with CKD - cats or dogs?

A

cats

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5
Q

What’s the prognosis of cats with CKD?

A

varies with stage
- baseline PO4 and IRIS staging
- hypertension is not primary determinant of survival bust does affect severity of proteinuria
- amlodipine can also decrease proteinuria

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6
Q

What’s the prognosis for dogs with CKD?

A

MST from diagnosis = 8m (226 days)
- IRIS stage and BUN = prognostic
- proteinuria = risk factor for developing uremia and death
- arterial hypertension = risk factor for death
- higher body condition score lived longer
- CKD less progressive in familiar or congenital cases that are not associated with proteinuria
- a slower progression also noted for young dogs with acquired CKD (ex. toxins)

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7
Q

Define uremic syndrome.

A

The clinical syndrome associated with loss of kidney function

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8
Q

What are some clinical signs associated with uremia?

A
  • PU/PD
  • GI derangement: anorexia, nausea/ vomiting, diarrhea/ melena
  • weight loss, muscle loss
  • lethargy, depression
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9
Q

What are the 3 major mechanisms involved in the pathogenesis of uremia?

A
  1. disturbed excretion of electrolytes and water
  2. reduced excretion of organic solutes (ex. uremic toxins)
  3. impaired renal hormone production
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10
Q

What are some signs associated with disturbed excretion of electrolytes and water?

A

As GFR decreases, the remaining functional nephrons will have to work harder to maintain the balance. Some electrolytes have better compensatory mechanisms than other (ex. Na vs PO4). Clinical signs include:
- edema
- hypertension
- hyponatremia
- hyperkalemia
- metabolic acidosis
- hyper-PO4

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11
Q

What’s a major difference in excretion of electrolytes vs organic solutes in the kidneys?

A

excretion of organic solutes is generally not actively regulated - so as it begins to rise with a decline in GFR, it will progressive increase as renal functions declines

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12
Q

What are some abnormalities associated with uremic toxins?

A
  • inhibition of ATPase
  • inhibition of platelet function
  • leukocyte dysfunction
  • loss of RBC membrane lipid asymmetry
  • insulin resistance
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13
Q

Does lowering the urea concentration = lowering the uremic toxin level?

A

thought it’s a good reflection, it isn’t conclusive evidence for reducing uremic toxin

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14
Q

What happens to cytokines and growth factors in uremia?

A

there is an accumulation due to decreased catabolism by the kidneys
- some peptide hormones (ex. PTH, insulin, glucagon) increased in CKD patients due to lack to catabolism and increased glandular secretion

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15
Q

What are some essential hormones produced by the kidneys?

A
  • erythropoietin
  • calcitriol
  • prostaglandins
  • kinins, renin
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16
Q

What’s the sequalae of decrease calcitriol?

A
  • renal secondary hyperparathyroidism
  • renal osteodystrophy
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17
Q

What are some GI consequences of

A
  • nausea, vomiting, loss of appetite (can be waxing/ waning)
  • stomatitis
  • GI ulcers
  • diarrhea, colitis
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18
Q

Define uremic gastropathy.

A
  • edema
  • mucosal and submucosal blood vessel mineralization
  • glandular atrophy
  • more common in cats than dogs
  • increased gastrin and reduced renal clearance may lead to GI ulceration
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19
Q

How common is uremic gastropathy?

A
  • gastric mineralization is increased with increased CKD III and IV in cats
  • increased Ca-PO4 product = increase severity
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20
Q

How frequent is dysphagia in CKD?

A

dysphagia/ oral discomfort in 8% of uremic cats and 38% of end stage CKD
- halitosis
- stomatitis
- periodontal disease

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21
Q

How common in uremic enterocolitis?

A
  • less common and less dramatic than uremic gastritis
  • likely due to the irritation effect of increased ammonia product in the colon associated with high urea
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22
Q

What’s the pathophysiology for dilute urine in CKD patients?

A
  • loss of functional nephron = the remaining nephrons will have an increased solute load
  • impaired genesis of a hypertonic gradient in the renal medulla (ex. impaired countercurrent multiplier system)
  • impaired responsiveness to ADH
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23
Q

What’s the major mechanism thought to contribute to hypertension in CKD patients?

A
  1. fluid retention
  2. activation of renin-angiotensin-aldosterone system
  3. sympathetic stimulation
  • retention of salt in cats may be a major driver in hypertension and ACEi don’t always work
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24
Q

Is the hypertension in CKD patients primary or secondary?

A

dogs/cats = hypertension commonly secondary
- primary hypertension = uncommon

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25
Q

What’s the IRIS staging system?

A
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26
Q

What’s the role of hypoxia-inducible factor in CKD?

A

HIF-2 is a transcription factor that regulars EPO production
- also regulates intestinal iron uptake

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27
Q

What are the 6 main reasons for anemia in CKD patients?

A
  1. insufficient renal EPO production –> relative decrease of EPO
  2. shorted RBC lifespan
  3. nutritional abnormalities (iron, B12, folate)
  4. EPO inhibitors in uremic plasma
  5. blood loss
  6. myelofibrosis
28
Q

How does renal secondary hyperparathyroidism occur in CKD patients?

A
  • reduced GFR = increased PO4 retention –> direct stimulation of PTH
  • PTH can lead to increased fibroblast-growth-factor 23 (FGF23)
  • FGF23 mitigate PO4 retention but also decrease calcitriol activity by inhibiting renal 1-alpha-hydroxylase activity
  • decline in calcitriol stimulates PTH secretion
  • PTH –> stimulates 1-alpha-hydroxylase activity –> increases calcitriol level
  • calcitriol then inhibits PTH (negative feedback)
  • to normalize calcitriol, there is an increased PTH secretion
  • ultimately, there aren’t enough functional nephrons to produce enough calcitriol –> decreases PTH inhibition
  • but deficiency in calcitriol lead to skeletal resistance to PTH (helps with stimulation of osteoclast bone resorption), and elevates the set-point for calcitriol induced PTH suppression
  • uremic toxins also inhibits suppression of PTH induced by calcitriol
  • low GI calcium absorption also happens due to impaired calcitriol
  • persistent hyperparathyroidism even with normal or elevated Ca2+
29
Q

How common is renal osteodystrophy?

A

uncommon
- maybe seen in young, growing animal
- mostly bones of the skull
- may also see parathyroid hyperplasia

30
Q

How does CKD contribute of metabolic acidosis?

A
  • though there is increased H+ excretion per nephron, the decreased # of functional nephrons cannot keep up to the H+ excretion
  • there is usually no lack of reabsorption of bicarbonate in dogs/ cats (may be selective tubular disorder)
31
Q

What’s the sequelae of chronic metabolic acidosis?

A
  • anorexia, nausea, malnutrition
  • lead to negative Ca balance, hypokalemia, renal dysfunction, and taurine depletion
  • promote protein catabolism
  • also blocks the adaptive response to protect degradation of skeletal muscles
32
Q

How is BUN elevation promoted in CKD patients?

A
  • decreased protein synthesis from uremia
  • accelerated proteolysis due to metabolic acidosis
  • the combination increases BUN
33
Q

How urea is synthesized?

A

nitrogen derived from amino acid catabolism
- BUN is typically related to dietary protein content

34
Q

How does hyperphosphatemia develop for CKD?

A
  • at first, there is compensatory decrease in reabsorption of PO4 (FGF23 and PTH)
  • as disease progresses, the adaptive mechanism reaches limits –> increase in PO4
35
Q

What’s the consequence of hyperphophatemia?

A

it contributes to CKD progression

36
Q

How reliable is tCa level for cats with CKD?

A

total calcium can be elevated but only a small proportion will have increased ionized calcium
- could be due to calcium bound to other organic or inorganic anions (ex. citrate, PO4, sulfate).

37
Q

How common is hypokalemia?

A

uncommon in dogs, more seen in cats
- sodium restricted diet promotes kaliuresis
- hypokalemia worsens the CKD

38
Q

What’s another endocrine disorder that can be responsible for CKD in cats?

A

hyperaldosteronism

39
Q

What’s the relationship between GFR and creatinine?

A

Every time the GFR decreases by 1/2, the creatinine level 2x

40
Q

Why not just make the range for creatinine narrower?

A

then creatinine becomes less specific to GFR

41
Q

What factors other than GFR can influence BUN level?

A

Increase BUN can be seen with:
- decreased renal perfusion
- upper GI bleed
- increased protein catabolism/ intake
- corticosteroids use

Decrease in BUN can be seen with:
- liver dysfunction

serum BUN = glomerular filtration + tubular reabsorption

42
Q

What’s the relationship between uremia, azotemia, and kidney disease?

A
  • kidney disease can occur without azotemia or uremia
  • azotemia doesn’t mean kidney disease
  • uremia is always associated with azotemia but not the reverse
  • uremia can occur without kidney disease
43
Q

Does renal azotemia respond to fluid therapy?

A

no, the animal will never be able to regain concentration ability

44
Q

How is SDMA synthesized?

A

from protein degradationW

45
Q

Why is SDMA a good marker for GFR?

A

over 90% is filtered without reabsorption
itself has little physiologic activity

46
Q

Which treatment for CKD has the greatest benefit and scientific evidence?

A

Renal diets!

47
Q

What are some qualities of renal diets?

A
  • low Na, PO4
  • high quality protein
  • acid/ base neutral
  • added B vitamins
  • calorie dense
  • added soluble fiber
  • added fatty acids, and omega 3
  • K supplement for cats
48
Q

What is actually more physiologically appropriate to give for fluid therapy at home?

A

Water via feeding tube

(Na containing fluid can make things worse)

49
Q

What are some common complications of GI uremia?

A

Dogs: uremic gastritis, ulcers
- thought to be due to increased gastrin level

Cats: gastric mineralization and fibrosis

Both can have decreased appetite, nausea, and vomiting

50
Q

How are the GI signs due to uremia managed?

A

Dogs: can use H2 blockers, proton pump inhibitors, sucralfate for the gastric ulcers

Both: anti-nausea: maropitant, ondensatron

Both: appetite stimulant- mirtazapine, cyproheptadine
- esophageal feeding tube

51
Q

How is metabolic acidosis managed in CKD patients?

A

Usually through diet
- if very acidosis (pH <7.10) can consider oral K-citrate supplements

52
Q

How common is hypokalemia in CKD patients?

A

Dogs- uncommon
Cats- common in IRIS stage II-III, not IV

53
Q

What are 4 possible reasons for hypokalemia in cats?

A
  1. Decreased dietary intake
  2. Diuresis from PU
  3. Activation of RAAS due to dehydration
    4 restricted salt intake
54
Q

What are some implications of hypokalemia in cats?

A
  1. Further promotes renal damage by reducing renal blood flow and GFR (angiotensin vasoconstriction)
  2. Promote PU
  3. Muscle weakness (polymyopathy, cervical ventral flexion)
55
Q

How is hypokalemia treated?

A

Best with oral supplementations - ex. K-citrate, can also help to alkaline / reduce risk of acidosis
- SC if can’t tolerate oral or in emergency

56
Q

How common is hyperkalemia in CKD patients?

A

Uncommon, can be noted with feeding tube, use of ACEi or ARB
- diet modification

57
Q

What are some complications associated with hypertension?

A
  • worsens the kidney disease
  • end organ injury: retinopathy, cerebral hemorrhage/ stroke, ventricular hypertrophy
  • proteinuira
58
Q

What’s are some indications for hypertension treatment?

A

If persistent systolic pressure >180mm Hg
- >200mg Hg = emergency, need to start treatment immediately
- presence of end organ injury

59
Q

What are the goals for hypertensive therapy?

A
  • slow and gradually reduction toward ~160mm Hg
  • ACEi, amlodipine good for both dogs and cats
  • don’t do ACEi and ARB at the same time —> risk of hyoerkalemia
  • monitor every 3m, titrate to effect
60
Q

What’s the cause of anemia in CKD patient?

A
  • lack of EPO production
  • decreased nutrient intake (iron, folate, protein, etc) can also contribute
  • there may be GI bleeding, and altered RBC lifespan
  • thrombocytosis and hypochromasia –> GI bleeding/ iron deficiency
61
Q

What’s the treatment for CKD induced anemia?

A

Erythropoietin stimulating agent
- ex. darbepoietin
- should see improvement in PCV 2-8 weeks
- repeated dosage may lead to neutralizing anti-EPO antibody formation

62
Q

What’s the likelihood of developing neutralizing antibodies to EPO?

A

25-30% of cats, up to 50% of dogs
- these antibodies will cross-react with all exogenous and endogenous EPO –> essentially the pet has pure red cell aplasia –> will need to be on blood trasnfusion
- darbepoetin may be less immunogenetic due to longer half-life/ less dosing

63
Q

What are some side effects of EPO?

A
  • antibody formation
  • allergic reaction
  • hypertension
  • seizure
64
Q

What’s the benefit of calcitriol therapy?

A

Calcitriol = most active metabolite of Vitamin D. Supplementation in dogs with CKD III and IV slows disease progression/ mortality

  • involved in Ca and PO4 uptake from GI tract, suppresses PTH production and secretion, suppresses parathyroid gland growth, and activates cellular receptors
  • PO4 retention and hyperphosphatemia, and increased FGF-23 reduce calcitriol
65
Q

When should renal diets be recommended?

A
  • renal diet: dogs CKD stage III-IV, cats CKD stage II-IV
  • all dogs with proteinuria
66
Q

What are management goals for CKD?

A
  • renal diet (if needed)
  • treatment for limiting proteinuria and hypertension
67
Q
A

Internal Medicine/ Ettinger (93 decks)

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