Renal: Acute and Chronic Kidney Disease Flashcards

1
Q

Why is it important to detect acute kidney injury ASAP?

A

So you can treat it aggressively = PREVENT irreversible damage and death

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2
Q

What is AKI?

A

Severe and sudden decline in renal function (GFR) = kidneys inability to regulate fluid balance, maintain electrolyte/acid-base balance, and excrete nitrogenous waste

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3
Q

Causes of AKI (6)

A

1) Ischemic = decreased renal blood flow (tubule swelling, obstruction and cell death) = decreased GFR = hypovolemia, decreased CO, renal vasoconstriction, systemic hypotension and vasodilation, thrombosis
2) Toxic = concentrate or metabolize toxin = analgesics/NSAID’s, ACE inhibitors, antibiotics (aminoglycosides), amphotericin B, heavy metals, contrast agents, ethylene glycol, lilies, grapes, raisins, etc.
3) Infection - bacterial pyelonephritis, lepto, tick-borne (Lyme, RMSF, Ehrlichia)
4) Immune-mediated = glomerulonephritis or amyloidosis
5) Neoplasia - lymphoma in cats, adenocarcinoma in dogs
6) Post-renal, obstructive
7) Sepsis = UNCOMMON IN VET MED

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4
Q

Causes of AKI and decreases in GFR (4)

A
  • Tubular obstructions from debris
  • Increased tubular permeability
  • Alterations in renal blood flow
  • Decreased glomerular capillary permeability
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5
Q

Three main phase of AKI

A

1) Initiation
(Extension)
2) Maintenance
3) Recovery

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6
Q

When does the initiation phase of AKI occur? Signs?

A

> Time from renal insult AKI begins
*Tx now can prevent AKI development
*Clinical detection can be difficult = not azotemic, may have decreased urine concentrating ability
+ May see tubular injury on U/A = casts, proteinuria, glucosuria

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7
Q

Duration, signs, and timeline of the maintenance phase of AKI?

A

> Develops after tubular lesions are established
+ Azotemia/uremia, increased/decreased urine output
*Removal of inciting cause = doesn’t restore renal function
- Lasts days to several weeks

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8
Q

Therapy during maintenance phase of AKI?

A

Supportive - maintain hydration and electrolyte balances, keep patient alive until the nephrons can repair and hypertrophy

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9
Q

Duration, signs, and timeline of the recovery phase of AKI?

A

*Renal lesions are repaired, renal function improves
+ Extreme polyuria = GFR increases due to nephron hypertrophy and repair
- May take weeks to months
*Can be complete and result in adequate/normal renal function

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10
Q

What does the reversibility of the AKI depend on? (2)

A
  • Severity and type of injury

- Rapidness and efficacy of removal of the underlying cause

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11
Q

What are we trying to find and focus on with AKI?

A

FIND THE TREATABLE CONDITIONS and treat them!

> Examples:
+ Hypovolemia or hypotension
+ History of NSAID’s or ACE inhibitor use
- Animals with decreased concentrating ability = Addison’s, hypercalcemia, pyometra, drugs (pheno, furosemide, glucocorticoids)

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12
Q

Reason for hospital caused acute kidney injury

A

Anesthesia in high risk patients = decreased renal perfusion and hypotension

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13
Q

Clinical signs of AKI

A
\+ Acute onset of anorexia or vomiting
\+ Painful kidneys
\+ Azotemia = increased BUN, creatinine, phosphorus
\+ Isosthenuria 
\+ Granular or cellular casts
\+ Glucosuria
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14
Q

What do pre/post-renal components, lepto, pyelonephritis, hypercalcemia, ethylene glycol toxicity, lily poisoning, or history of NSAID/ACE-i use have in common?

A

THEY ARE TREATABLE and you may help avoid AKI

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15
Q

Five things you should do with AKI patients

A
  • Take a good history for toxin or drug exposure
    1) Tx aggressively with fluids - r/o pre-renal
    2) Culture urine - pyelonephritis
    3) Tx for lepto
    4) Tx with penicillin/amoxicillin or doxycycline while C&S and lepto are pending
    5) Perform imaging = abdominal U/S or rads
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16
Q

Where and what do we use for fluid rehydration in AKI patients?

A
  • Ideal = jugular catheter
  • Most patients = 0.9% NaCl, LRS, Normosol-R = isotonic
  • Patients w/ acidosis or cardiac abnormalites = hypotonic (0.45% NaCl)
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17
Q

Monitor for signs of overhydration, which include…?

A
\+ Increased RR and HR
\+ Restlessness
\+ Chemosis or runny nose
\+ Increased body weight
\+ Decreased PCV/TP
\+ Increased central venous pressure
\+ Severe cases = peripheral or pulmonary edema, respiratory distress
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18
Q

What other monitoring piece of equipment (other than clinical signs, imaging, infectious dz testing) is helpful in AKI patients?

A

Indwelling urinary catheterization to measure urine output

*Monitor urine output every 2 hrs and electrolyte/acid-base every 4-6 hours

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19
Q

What happens with K+ in AKI patients and what do we do to correct it?

A

> Hyperkalemia due to the decreased production or urine (oliguria or anuria)

  • Should be accomplished by aggressive fluid therapy and diuresis
  • Severe elevations = prevent cardiotoxic effects with Ca++ gluconate, shift K+ into cells with dextrose/insulin/Na+ bicarb
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20
Q

What happens with acid-base balance in AKI patient and what do we do to correct it?

A

> Metabolic acidosis = inability to excrete H+ or uremic acids (worse with anuria or oliguria)

  • Should be accomplished with aggressive fluid therapy and diuresis
  • Severe acidosis = bicarb (BE CAREFUL!)
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21
Q

What happens with Ca++ in AKI patients and what do we do to correct it?

A

> Hypercalemia or hypocalcemia

  • Can be the cause or effect or AKI
  • Tx = supportive = saline diuresis or furosemide (hyper) -OR- add Ca++ (hypo)
22
Q

What happens with P in AKI patients and what do we do to correct it?

A

Hyperphosphatemia - fluid therapy diuresis

23
Q

What do the ins and outs of urine production add to?

A

Ins = outs + 20 mL/kg/day (insensible losses)

24
Q

What is absolute oliguria?

A

< 1 mL/kg/hour

25
Q

How do we treat absolute oliguria?

A
  • Volume expansion = 3-5% of patient’s BW over 4-6 hours (monitor for overhydration)
  • NO change? = furosemide (transient increase in GFR) or mannitol (osmotic diuresis and radical scavenger)
26
Q

Which type of patient do we not use mannitol in?

A

Overhydrated patients = keeps more fluid in circulation

27
Q

What does inadequate production of urine after 12-18 hours of intensive therapy or uncorrectable overhydration indicate?

A

POOR PROGNOSIS without dialysis

28
Q

What type of fluid do we use, in most patients, for maintenance fluids?

A

Half-strength saline - 0.45% NaCl, Normosol-M, or Plasmalyte-M

29
Q

What do we use to calculate maintenance fluids?

A

> 40-60 mL/kg/day

*Replace any ongoing losses = vomiting and diarrhea

30
Q

What should you suspect with signs of chronic kidney failure in young animals?

A

Congenital - dysplasia/aplasia, familial glomerulonephropathy, congenital amyloidosis, Fanconi syndrome, polycystic kidney disease

31
Q

Difference between polycystic disease in dogs and cats

A
  • Cats = can live a long live, mean = 7 years

- Dogs = puppies become ill after only a few months

32
Q

Causes of secondary or acquired CKD?

A
  • Secondary to glomerular disease = proteinuria causing tubular injury
  • Secondary to AKI = necrosis and decreased # of nephrons
  • Degenerative changes = decreased number of nephrons

> Remaining nephrons hypertrophy = increase GFR and cause glomerular hypertension = protein loss = tubular damage

33
Q

Clinical signs of CKD

A

*Vary depend on the severity of disease
+ Weight loss, muscle wasting
+ PU/PD or dehydration due to isosthenuria with 2/3 (66%) loss
+ Lethargy, inappetence, anorexia, vomiting, oral ulceration due to azotemia with 3/4 (75%) loss

34
Q

What is IRIS staging based off of?

A

Serum creatinine levels

35
Q

What is IRIS substaging based off of? (2)

A

1) UPC = persistent proteinuria

2) Blood pressure = evidence of hypertension

36
Q

How do we treat the proteinuria encountered with CKD? (2)

A
  • Tx if azotemic and > 0.5 in dog, > 0.4 in cat
    1) Renal diet = low protein
    2) ACE inhibitor = benazepril (less is metabolized by kidney)
37
Q

How do we treat the isosthenuria and dehydration with CKD? (4)

A

1) Always ensure access to water
2) Feed canned food, ideally renal diet
3) Offer low to no Na+ chicken broth
4) SQ fluids
+/- Esophageal feeding tube

38
Q

How do we treat the electrolyte abnormalities (K+, P, Na+) with CKD? (3)

A

1) Feed renal diet (low in Na+, supplements K+, low in P)
2) Supplement K+
3) Maintain hydration to diurese P
+/- Phosphorus binders

39
Q

How do we treat the metabolic acidosis that occurs with CKD? (2)

A

1) Maintain hydration
2) Renal diet (buffered)
- If TCO2 < 18 = oral Na+ bicarb or K+ citrate

40
Q

How do we treat the azotemia that occurs with CKD? (2)

A

1) Maintain hydration

2) Feed a renal diet (low protein)

41
Q

How do we treat the hypertension that accompanies CKD? In cats and dogs?

A
  • Treat if systolic > 160 mm Hg
  • Cats = amlodipine
  • Dogs = ACE-inhibitor, +/- amlodipine
42
Q

How do we treat the anemia that accompanies CKD?

A

*Reserved for patients with significant anemia (PCV < 20%)
- Darbepoietin = synthetic erythropoietin
+/- Supplemental iron

43
Q

How do we treat the secondary renal hyperparathyroidism that accompanies CKD?

A

Supply calcitriol (active vitamin D)

44
Q

What makes renal diets so great?

A
  • Low in Na+
  • Low in P
  • Low in protein
  • Supplements K+
45
Q

What is a common sequelae to the dehydration that accompanies CKD?

A

Constipation

46
Q

Why is hyperphosphatemia a problem with CKD?

A

Increases the secretion of PTH = uremic toxin –> associated with the progression of kidney disease

47
Q

What effects do ACE-inhibitors and amlodipine have?

A
  • ACE inhibitor = dilate efferent arteriole, inhibit RAAS activation
  • Amplodipine = dilates afferent arteriole
48
Q

What type of patient do we not give calcitriol to?

A

Hyperphosphatemic or hypercalcemic animals = causes increased resorption from the GI tract

49
Q

Why does ulceration occur with CKD and what do we use to treat it?

A
  • Caused by decreased gastrin clearance by the kidneys

- Tx = H2 blockers (famotidine) or proton pump blockers (omeprazole)

50
Q

Things you need to rule out when CKD patients decompensate (3)

A

1) Pre-renal causes = dehydration
2) Renal causes = infection (pyelonephritis), general disease progression
3) Post-renal = ureteroliths

  • Tx with fluids and Unasyn while you’re waiting
51
Q

Why are CKD cats prone to cystitis?

A

No longer able to concentrate their urine