Chronic Renal Disease Flashcards

1
Q

What hormones are produced by the kidney and what do they do?

A

EPO: produces RBC
Renin: controls BP
Calcitriol: active Vitamin D which increases calcium absorption

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2
Q

What hormones act on the kidney?

A

Aldosterone: Na/K pump
ADH: vasopressin or anti diuretic hormone: increases water absorption
PTH: parathyroid hormone; maintains your calcium and phosphorous

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3
Q

Where does the problem lie in ARF?

A

problem is in proximal tubule

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4
Q

Where does the problem lie in CRF?

A

problem is in the whole nephron

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5
Q

If SDMA is >45 what stage of IRIS are we in?

A

Stage IV

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6
Q

What is chronic kidney dz?

A

Loss of fxn’al renal tissue d/t a prolonged process (generally > 2 months)
Usually progressive and irreversible
CKD often smolders for many months or yrs before it becomes clinically apparent (>stage 2)

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7
Q

Why is CKD important?

A

Affects animals of all ages
Incurable dz :(
Prolonged survival is common (especially in cats)

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8
Q

T/F CKD leads to nephron disease and loss

A

True

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9
Q

If the animal is no longer able to concentrate their urine, how many of their nephrons have failed?

A

66% (renal insufficiency)

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10
Q

If the animal is azotemic, how many of their nephrons have failed?

A

75%

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11
Q

What are the 5 major failures of CKD and what does their failure result in?

A
  1. failure of excretion of nitrogenous wastes = uremia
  2. failure of {urine} = PU/PD
  3. failure to synthesize calcitriol (Vit D3) = hypocalcemia and renal secondary hyperparathyroidism
  4. failure to synthesize erythropoetin = anemia
  5. failure to catabolize peptide hormones (e.g. gastrin) = uremic gastritis

These things can initiate systemic hypertension
Can result in defective hemostasis

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12
Q

What is the classical presenting signs?

A

PU/PD: NOCTURIA! most common presenting sign= peeing their bed at night

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13
Q

What are other clinical signs?

A

Anorexia, diarrhea, hypersalivation, weight loss . . . think about it, this has been going on for a while. It’s chronic so they’re gonna have depression, pale mucous membranes, small kidneys, hypertensive retinopathies, loose teeth/deformed jaw, poor body condition

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14
Q

What will our urinalysis show us for dog and cat?

A

Unable to concentrate urine/ inappropriately concentrates urine.

Dog SG: 1008- 1022
Cat SG: 1008-1030

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15
Q

What will CKD definitely have on diagnostic findings?

A

Often will have azotemia and will DEFINITELY have an inappropriately concentrated urine

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16
Q

What will our Biochem results show us?

A
  1. Hyperphosphatemia
  2. Hypo/hyperkalemia
  3. Hypo/hypercalcemia
  4. Metabolic acidosis
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17
Q

Why do we see hyperphosphatemia with CKD?

A

kidneys are primary route of phosphate excretion

reduced renal fxn –> phosphate retention

Stage I and II CKD: compensatory mechanisms keep P in line
Stage III and IV: compensatory mechanisms fail: phosphate increases

18
Q

What effects will we see with hyperphosphatemia?

A

Unlikely to directly cause CS
Drives renal secondary hyperparathyroidism
Causes progression of dz
Leads to reduced survival :(

19
Q

Why do we see hypokalemia and what does it result in?

A

It’s d/t reduced intake and increased renal potassium loss

Results in:

  1. neuromuscular weakness
  2. anorexia –> wt loss
  3. impaired protein synthesis –> wt loss
  4. decreased renal fxn (reversible!)
  5. promotes PU/PD
20
Q

Where are our calcium levels at in CKD?

A

Total calcium unchanged or slightly decreased

HyperCa can lead to secondary renal failure or cause renal failure

21
Q

Why does metabolic acidosis happen?

A

Reduced excretion of H+ ions by kidney

Tends to be mild in CRF

22
Q

Why do we see non regenerative anemia?

A
Erythropoietin deficiency 
Decreased life span of RBC
Effect of PTH on bone marrow and RBCS
Anemic of chronic dz
GI hemorrhage 

Results in lethargy and inappetance

23
Q

What else should we look for on our urinalysis?

A

Evidence of concurrent UTI

24
Q

T/F Proteinuria may cause CRF and vice versa

A

True

25
Q

What is the danger of the proteinuria in CKD?

A

potential cause of renal injury

proteinuria increases risk of developing end stage CKD

risk factor for mortality

therapies to reduce magnitude of proteinuria are often renoprotective

use ace inhibitors (benazepril) or ARB (telmisartan)

26
Q

What is the significance of BP ?

A

Kidney dz leads to abnormal BP
Hypertension can cause kidney dz
Leads to ocular, cerebral, and CV damage
Can occur at ANY stage of CKD . . . not just advanced stages

27
Q

When a diagnosis of CKD is suspected, what 3 things are important to look at?

A
  1. creatinine
  2. proteinuria
  3. BP
28
Q

Briefly explain the 4 stages of IRIS for CKD

A

Stage 1: ID primary dz and start specific therapy to eliminate dz if possible
Stage 2 and 3: renoprotective therapy to try and slow progression
Late Stage 3 and 4: symptomatic therapy

29
Q

What are our aims for tx?

A

Tx underlying cause if possible: UTI, hypertension, hyperCa, proteinuria etc

Improve clinical signs and QOL: dehydration, appetite etc

Slow progression: Tx hyperP, hypertension, proteinuria

30
Q

T/F Pyelonephritis is common (UTI).

A

True! Especially in cats. Antibiotics for 4-6 weeks. Repeat culture at least once 1 week post tx

31
Q

How do we tx dehydration?

A

Short term: IV fluids (includes KCl); subcu fluids

Long term: Oral fluids (wet food and such); subcu fluids; feeding tube placement

32
Q

What is the major thing we are trying to control with a renal diet?

A

Trying to get that phosphorous under control. Food that is high energy, high quality reduced protein, Na restricted, potassium supplemented, increased B vitamins, increased fiber, omega 3 supplements.

We also give intestinal phosphate binders and mix with meal to manage phosphorous.

33
Q

What stages of IRIS does diet really help with?

A

Likely beneficial in stage II CKD and definitely beneficial in stages III and IV

Helps reduce risk of uremic crisis - in dogs and cats!

34
Q

What should we NOT tx the non regenerative anemia with even if the animal has PCV

A

anabolic steroids!!! we can have bad side effects: increase protein turnover –> increase urea or increase water retention –> reduce renal perfusion

35
Q

Regarding long term tx, what is the first choice drug for treating hypertension in dogs?

A

Ace inhibitors!

What about in cats?! Amlodipine

36
Q

How do ACE inhibitors work?

A

Inhibit conversion of AGI to AG II
Reduce glomerular capillary pressure & glomerular size
REDUCE PROTEINURIA!
Reduce Na and water retention
Limit pro fibrotic effects AG II on the kidneys
Slow progression of renal dz in cats
Improve appetite in proteinuric cats

37
Q

What are Angiotension Receptor Blockers (ARBs)?

A

Newly licensed drug for cats
Telmisartan
Licensed for reduction of proteinuria associated w CKD in cats

38
Q

How do we tx proteinuria?

A

ACE inhibitors or ARBs

39
Q

Is acute decompensation of CRF aka “acute on chronic dz” reversible?

A

Yes, and can return to stable plateau

40
Q

What is the prognosis for CKD in dogs and cats?

A

Dogs: typically months to a year or two
Cats: Stage II: MST 3 yrs and max 8.5 yrs
Stage IV: MST: 35 days :(

41
Q

What are the 6 major key points to remember about CRF?!

A
  1. CRF is a chronic, progressive dz
  2. early diagnosis of CKD may prolong survival
  3. azotemia and inappropriately concentrated urine are hallmarks of CRF
  4. importance of diet in management of CKD
  5. animal can survive years w CRF
  6. cats do better than dogs