CRF & CKD - Green Flashcards

1
Q

What two terms are also commonly used to describe

Chronic Kidney Disease (CKD)/Chronic Renal Disease?

A

Chronic Renal Insufficiency (CRI)

&

Chronic Renal Failure (CRF)

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2
Q

What CS will you see with Chronic Renal Insufficiency?

TQ

A

Isothenuric but not Azotemic

(patient has lost 2/3 of renal fxn)

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3
Q

What CS will you see with Chronic Renal Failure?

A

Isothenuric and Azotemic

(patient has lost 75% of renal mass)

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4
Q

When would a patient be considered to have CRF?

What does this result in?

A

When the kidneys are no longer able to maintain:

  • Excretory fxn
  • Regulartory fxn
  • Endocrine fxn

Resulting in:

  • Retention of nitrogenous waste
  • Derangement of fluids
  • Alterations in electrolytes & acid-base balance
  • Failure of hormone production
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5
Q

Are BUN and Creatinine sensitive indicators for the severity of renal disease?

TQ

A

NO!

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6
Q

Is renal disease more common in dogs or cats?

TQ

A

CATS!

(2x’s as often as dogs)

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7
Q

What is the number one cause of CRF in dogs?

TQ

A

Chronic tubulointerstitial nephritis of unknown cause

(Idiopathic interstitial nephritis)

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8
Q

What are some other causes of CRF in Dogs?

A
  • Chronic Pyelonephritis
  • Chronic Glomerulonephritis
  • Amyloidosis
  • Familial Renal Dz
  • Hypercalcemic Nephropathy
  • Chronic Obstruction
  • Sequele to acute renal disease (Lepto)
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9
Q

What is the number one cause of CRF in Cats?

A

Idiopathic Chronic Tubulointerstitial Nephritis

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10
Q

What are Clinical History findings in CRF?

(Findings are non-specific)

A
  • Polyuria/Polydipsia (common)
  • Vomiting (Dogs)
  • Inappetance/Anorexia
    • due to acidosis, ulcers, etc.
  • Weight loss
    • (chronic cases should have low BCS)
  • Lethargy
  • Small, Irregular, non painful kidneys
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11
Q

What are the PE findings you would see with CKD/CRF?

A
  • Weight loss/ low BCS
  • Poor Haircoat
  • Oral lesions
    • dogs > cats
  • Pale MM
    • from anemia associated w/ chronic renal dz.
  • Dehydration
  • Osteodystrophy
    • young dogs w/ familial renal dz.
  • + Small/irregular non-painful kidneys
  • + Ascites/edema (consider glomerular dz)
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12
Q

How does Renal 2° Hyperparathyroidism cause lesions?

TQ

A

P goes up → Ca2+ does down → Body produces PTH →

Ca2+increases at the expense of bone

(X-ray of skull shows teeth “floating” → Rubber jaw)

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13
Q

What are the laboratory findings you would see in a pt with CRF?

A
  • Non-regenerative anemia / lymphopenia
  • Isosthenuria (67% loss of nephrons)
  • Azotemia (75% loss of nephrons)
  • Hyperphosphatemia (85% loss of nephrons)
  • Decreased serum HCO3-
  • Variable serum Ca2+ (TQ)
  • Mild Hyperglycemia
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14
Q

What type anemia do you see with CRF?

A
  • Non-regenerative (normocytic, normochromic)
    • Variable in magnitude → correlates w/ severity of CRF (creatinine)
    • Serum EPO is low to normal, but inappropriate for the pt’s PCV
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15
Q

What is the trigger point theory of the pathophysiology of CKD/CRF?

A

Once intial critical mass of functioning nephrons are destroyed,

CKD/CRF will progress to End-Stage Renal Dz.

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16
Q

What mechanism contributes most to the progression of CKD?

A

Intraglomerular Hypertension

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17
Q

CKD/CRF is a self perpetuating dz due to Maladaption.

Explain this process.

A
  • Increased glomerular Pressure = Increased glomerular volume
    • due to less functional glomeruli filtering the same amount of blood.
  • Increased protien traffic
    • → mesangial ractions → Glomerulosclerosis → reduced GFR → systemic hypertension → Repeat
    • → increased tubular processing → tubulo-interstitial nephritis → decreased GFR → systemic hypertension → Repeat
  • Snowball effect as more nephrons die
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18
Q

What are the biggest factors in the progression of CRF?

A
  • Intraglomerular HYPERtension (SNGFR)
  • Systemic HYPERtension
  • Renal 2° HYPER-PTH
    • PTH = biggest uremic toxin & is present at toxic levels during CRF
  • Renal mineralization (product of Ca + P)
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19
Q

The International Renal Interest Society (IRIS) has classified canine CKD.

What are the stages and substages based on?

A
  • Stages
    • Creatinine (serum CRE when the animal is relativley stable)
  • Substages
    • Degree of proteinuria & magnitude of systemic HYPERtension
      • Substages do NOT use serum P or PTH
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20
Q

In the IRIS Classification of K9 CKD:

What stages are silent?

What stages are clinically apparent?

A
  • Stage 1 & 2 are silent
  • Stage 3 & 4 are clinically apparent
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21
Q

What are the parameters for the different IRIS Stages of K9 CKD?

A
  • Stage 1 - Non Azotemic CKD, Serum CRE < 1.4
  • Stage 2 - Mild Renal Azotemia, Serum CRE 1.4 - 2.0
  • Stage 3 - Moderate Renal Azotemia, Serum CRE 2.1 -5.0
  • Stage 4 - Severe Renal Azotemia, Serum CRE > 5.0
22
Q

What is the prognosis of lifespan once CKD is clinically apparent (stage 3/4) in dogs?

A

6 m - 1 yr

23
Q

IRIS classification states that most dogs are diagnosed in what stage of CKD?

A

Stage 3 - 46.5%

&

Stage 4 - 34.6%

24
Q

IRIS Classification parameters for the stages of FELINE CKD:

A
  • Stage 1 - Non Azotemic CKD, Serum CRE < 1.6
  • Stage 2 - Mild Renal Azotemia, Serum CRE 1.6 - 2.8
  • Stage 3 - Moderate Renal Azotemia, Serum CRE 2.9 - 5.0
  • Stage 4 - Severe Renal Azotemia, Serum CRE > 5.0
25
Q

What stage are most CATS identified in using the IRIS system?

A

Stage 1 - 33.6%

&

Stage 2 - 37.2%

26
Q

Why are cats in CKD caught at earlier stages than dogs?

A

Because the dz progresses much slower in cats

and is caught on routine geriatiric blood work or when owner brings in for PU/PD

27
Q

In dogs, what are the IRIS substaging catagories of Proteinuria (based on the UPC)?

A
  • Non-Proteinuric UPC = 0 - 0.2
  • Borderline Proteinuric UPC= 0.2 - 0.5
  • Proteinuric UPC = 0.5 - 0.6+
28
Q

What 2 parameters does the IRIS base its substages on?

A
  • Level of Proteinurea
  • Systolic blood pressure
29
Q

Is prognosis better or worse in an animal with CKD and proteinuria?

A

Worse!

(even just a little proteinuria is bad)

30
Q

What type of food should be fed to CRF patients?

A
  • Canned or water soaked kibble
    • High in Energy
    • LOW in phosphorus
    • LOW/Mod Protein
    • High potasium (loose via kidneys)
    • Restricted sodium
31
Q

What is the most important dietary restriction for patients with CRF?

A

Phosphorus!

(When you restrict protein, you are also restricting phosphorus)

32
Q

What are the goals of treating a CRF Uremic patient?

A
  • Make animal feel better
  • Reduce Uremic Lesions
  • Prevent (or slow) further loss of renal function
33
Q

What are the general principles of managing a patient with CRF?

A
  • Search for a reversible cause
    • Pyelonephritis
    • Obstruction (uroliths, neoplasia)
    • HYPERcalcemia
  • Persistantly isosthenuric check for cause of PUPD
    • Image kidneys
    • Check BP
    • Wait to pass judgement on patient prognosis until on fluid therapy for several days (for animals w/ decompesated CRF)
34
Q

Why should you wait until patient has been on fluids for several days to judgeprognosis on CRF patients?

A

Fluids will remove any pre-renal component of azotemia & may reduce serum CRE

35
Q

What should you do initially to medically manage pts w/ CRF?

A
  • Dietary Phosphorus Restriciton
  • Intestinal Phosphate Binders
  • Dietary protein restriction
  • H-2 receptor blockers
36
Q

What should you do secondarily for conservative medical managment of pts with CRF?

A
  • Control of Renal 2° HYPER-PTH
  • ACE inhibition w/ or w/o HYPERtension
  • Control HYPERtension
  • Control metabolic acidosis
  • EPO
37
Q

What are the only good renal diets?

A

The ones the pet will eat!

(got to feed pt! If they won’t eat renal diet, feed them something else)

38
Q

When should you intervene dietarily in a CRF patient?

A
  • Before they are obviously sick
    • may increase interval till uremic crisis
39
Q

Can you give oral valium to a cat?

A

NO!

WIll cause death by acute hepatic failure

40
Q

What can you do to stimulate the appetite of CRF patients?

A
  • H2-receptor blockers (Famotidine®)
  • Metoclopramide
  • Chemical stimulation
    • Cyproheptadine, Valium (cats), Mirtazapine
  • NG- Tube Feeding
  • Decrease BUN (fluids)
  • Alter food warm/broth/fat
41
Q

What do you see in CRF patients with Uremic Gastroenteritis?

A
  • Plasma gastrin concentrations are high (H-2 blockers will reduce)
  • Degree of hypergastrinemia correlates w/ severity of CRF
  • Potential C/S:
    • Anorexia (cats common)
    • Vomiting (more in dog)
    • GI Bleeding
42
Q

Why is P restriction so important in CRF patients?

A
  • Dogs → Slows down the progression of Dz
  • Cats → Decreases mineralization & Fibrosis
43
Q

When should you instruct clients to give phosphate binders to the patient?

(How do they need to give it?)

A

At meal time

44
Q

What are some phosphate binders used in vet med?

A
  • Aluminum Salts (Aluminum Hydroxide)
    • Most common & cheapest w/ good Pi binding
    • Constipation common SE
  • Calcium Carbonate
    • Less P binding than aluminum
    • Must be careful w/ HYPERcalcemic pt’s
  • Calcium Acetate
    • PhosLo = binds 3x’s better than calium carbonate
    • Less risk of HYPERcalcemia
  • Epakitin - chitosan based supplement
    • NO taste aversion
  • Renalzin - not available USA & expensive
  • Sevelamer HCI (Renagel)
    • Expensive, high dose interferes w/ GI absorbtion of folic acid, Vit. D & Vit. K
  • Lanthanum Carbonate (Fosrenol)
    • Not absorbed in the GI, but found in bone & liver (trace) & is nontoxic
45
Q

What are the advantages of hormonal replacement of EPO (human recombinant product) in animals with CRF?

A
  • Resolves Anemia
  • Weight gain
  • Improves:
    • Appetite
    • Haircoat
    • Alertness
    • Activity
46
Q

When do you replace EPO in CRF pt’s?

A

When their PCV is < 20%

47
Q

What are the adverse effects of EPO replacement?

A
  • Antibody formation (high risk 50% 30-160d after start)
  • Vomiting
  • Seizures
  • HYPERtension
  • Uveitits
  • Hypersysitivity reaction (mucocutaneous)
48
Q

When do you use hormonal Calcitriol replacment in CRF patients?

A
  • Only once HYPERphosphatemia is controlled
  • Rapidly lowers serum PTH levels (monitor levels)
  • Watch for hypercalcemia (especially w/ Ca2+ phosphate binders)

FYI: Use extremely low doses & must be made by compounding pharmacy

49
Q

What is important when monitoring BP in a patient with CRF?

A
  • Have a well trained technician
  • Quiet, undisturbed environment
  • Sufficient time for acclimation
  • Correct Cuff size!
  • Several sequential measurements (do 3 & take avg)
50
Q

When shoud you treat Hypertension in CRF patients?

A
  • BP consistently > 160mmHg
  • High BP can lead to fundic lesions:
    • Retinal hemmorrhage
    • Vascular tortuosity
    • Retinal edema
    • Intra-retinal transudate
    • Retinal detachment
51
Q

How do you treat Hypertension in animals with CRF?

A
  • Dietary salt restriction
  • Diuretics
    • Often not used b/c animal is on the verge of dehydration any way
52
Q

What are some CRF findings that are indicative of a poor prognisis?

A
  • Sever intractable anemis
  • Inability to maintain fluid balance
  • Progressive weight loss
  • Advanced osteodystrophy (w/ younger familial animals)
  • Progressive azotemia despite treatment
  • Severe end-stage renal lesions on biopsy