Acute Intrinsic Renal Failure - Green Flashcards

1
Q

T/F: In order to have Acute, Intrinsic Renal Failure (AIRF), oliguria or anuria must be present.

A

False

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2
Q

What is the first thing detectable during the development of AIRF?

A

Sub-maximal urine concentration

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3
Q

What findings in the urine sediment are most typical of severe AIRF during the early stages?

A

Renal tubular epithelial casts

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4
Q

Which drugs are NOT a true nephrotoxin?

(causes 2° renal damage)

A

NSAIDs

Only cause problems in volume depleted animals

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5
Q

Is dialysis a good choice for treating severe AIRF?

A

YES

will make a difference, especially if started early

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6
Q

What is the prognosis for azotemic patients suffering AIRF due to Ethylene glycol toxicity?

A

Poor!

Nearly all patients that present w/ azotemia will die or be euthanized

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7
Q

What is the prognosis for azotemic patients suffering AIRF due to Leptospirosis?

A

Good

Most will survive

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8
Q

Which drug will help rapidly improve renal fxn in AIRF patients w/ Leptospirosis?

A

Amlodipine

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9
Q

What are the 3 most common causes of AIRF?

A
  1. Nephritiis due to Lepto
  2. Nephrosis due to a Nephrotoxin
  3. Ischemic Nephrosis
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10
Q

Is systemic arterial hypotension required for Ischemic Nephrosis AIRF?

A

NO!!

Just cause BP is normal doesn’t necessarily mean the kidneys are happy

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11
Q

List some Nephrotoxins that can cause AIRF.

A
  • Ethylene glycol
  • Aminoglycosides
  • Cisplatin
  • Cholecalciferol-containing rodenticides
  • Calcipotriene
  • Humoral hypercalcemia of malignancy
  • Arsenic
  • Lead
  • Easter lily ⇒ CATS
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12
Q

Pathophysiology of AIRF?

A
  • Afferent arteriolar constriction
    • vaso-motor nephropathy
    • hypotension
  • Obstruction
    • Intra/Extra-luminal
  • Tubular Backleak across damaged tubules
  • Decreased permeability
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13
Q

What is the mechanism of injury for Nephrotoxic AIRF?

A

Direct cell injury rather than ischemia

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14
Q

What 2 things, occuring simultaneously, dramitcally increase the risk of renal injury in AIRF p’s?

A

Exposure to nephrotoxins ​& Renal ischemia

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15
Q

Describe the Latent (Induction) Phase of AIRF.

A
  • Often not detected
  • Minimal to absent C/S
  • Early ID & removal of inciting cause can result in return to normal renal fxn
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16
Q

Key points about the Maintenance Phase of AIRF.

A
  • Changes in urine output
    • Oliguria, normal or polyuria
  • Signifies a critical amt of lethal tubular cell injury
  • Patient experiences a 1-3 wk course before normal restoration of renal fxn can occur
  • Removal of the inciting cause wil NOT result in an immediate return of normal renal fxn.
  • Characterized by a severe decrease in renal blood flow & GFR
  • Mod. to severe metabolic acidosis
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17
Q

Key points about the Recovery Phase of AIRF.

A
  • Return of normal BUN & Creatinine is possible
  • Partial improvement = chronic renal failure
18
Q

How can you DX AIRF?

A
  • HX
    • absence of longstanding PU/PD, potential for renal ischemia or nephrotoxin exposure, oliguria, polyuria
  • PE
    • Normal body condition
    • Normal sized kidneys
  • UA
  • CBC/Chem
    • PCV @ onset
  • Renal biopsy
  • Lab samples before TX are helpful
19
Q

List possible PE findings in a patient with AIRF.

A
  • signs of uremia are usually more severe than in those w/ pre-renal azotemia (may be similar to CRF patients)
  • Uremic breath
  • Oral ulcers/tongue necrosis
  • Hypothermia (nephrosis) OR hyperthermia (nephritis)
  • Absence of pallor to mucous membranes
  • Postural changes due to renal pain
  • Normal to enlarged kidneys
20
Q

What can occur once you place dehydrated AIRF patients on fluids?

A

Overhydration → edema

21
Q

Is anemia a common finding in AIRF patients?

A

NOT early on

(more common with CRF)

22
Q

Can USG help you differentiate btwn AIRF & CRF?

A

NO

Both have low USG

23
Q

An increased number of what type of crystal supports the DX of ethylene glycol toxicity?

A

Oxalate crystals

24
Q

What will the urine sediment often look like in patients with AIRF?

A

Increased WBC, RBC & tubular epithelial cells

25
Q

The magnitude of azotemia does NOT tell you….

A
  • AIRF vs. CRF OR
  • Source (pre-renal, renal or post-renal)
26
Q

When will hyperkalemia typically occur?

A

With severely impaired renal excretory fxn & oliguria

27
Q

What does the presence of severe hyperechogenicity on U/S suggest in patients with AIRF?

A

Possibility of ethylene glycol intoxication

28
Q

What anatomic structure can you U/S to potentially help differientiate AIRF from CRF in dogs?

A

Parathyroid gland

AIRF⇒normal sized parathyroid glands (2 to 4 mm)

CFR ⇒ enlarged parathyroid glands (4 to 8 mm)

29
Q

Why is a renal biopsy good for DXing AIRF?

(4)

A
  • Confirm renal azotemia
  • Differentiates AIRF from CRF
  • Gives a prognosis
  • Differentiates nephritis (Lepto) from nephrosis
30
Q

Which causes of AIRF have a poor to grave prognosis?

A
  • Aminoglycosides⇒ poor to grave
  • Easter lily ⇒ poor to grave
  • Ethylene glycol ⇒ grave
31
Q

Which causes of AIRF have a fair prognosis?

A
  • Bacterial pyelonephritis ⇒ fair
  • Lepto ⇒ fair to good w/ appropriate treatment
32
Q

Key points about Hemodialysis?

A
  • P’s w/ severe baseline azotemia are NOT successfully managed w/o dialysis
  • Early hemodialysis= increased survial rate
  • Dialysis may be needed for several months if patient has severe AIRF
33
Q

What happens if we don’t perform dialysis on AIRF patients with high level azotemia?

A

> 80% will die or be euthanized due to:

Hyperkalemia

Metabolic acidosis

Severe azotemia

Overhydration & pulmonary edema

34
Q

Treatment goals for AIRF!

(NB: no “quick fix”)

A
  • Avoid hypotension
  • Meticulous attention to fluid therapy
    • Oliguria: < 1 mL/Kg/hr
    • Over each 4 hr period⇒ give (20 mL/kg) + measured urine output of preceding 4 hrs
  • TX Hyperkalemia
    • Regular Insulin & glucose or Ca2+ gluconate
  • Diruetics
    • Furosemide, Dopamine or Mannitol
  • PREVENTION!!!!!!!
35
Q

What is the lethal dose of Ethylene glycol in the dog & cat?

A

Dog ⇒ 4.4 mL/Kg

Cat ⇒ 1.5 mL/Kg

36
Q

Is Propylene Glycol dangerous for pets?

A

May cause illness but is usually NOT fatal

37
Q

How does ethylene glycol kill our patients?

A

Ethylene glycol + Alcohol dehydrogenase = Glycolate (Glycolic acid)

[it is the metabolite that does all the damage]

38
Q

What is the downside of the Colorimetric test for Ethylene glycol?

A

Ethylene glycol is rapidly absorbed from the GIT of dogs &

is undetectable in plasma 48 hrs post ingestion

39
Q

How do you TX Ethylene glycol toxicity?

A
  • TIMING IS CRITICAL ⇒ don’t wait for definitive test results
  • Give them Ethanol or 4-methyl pyrazole to bind up alcohol dehydrogenase & prevent the formation of glycolate
    • Ethanol ⇒ w/in 2-4 hrs of ingestion
    • 4-methyl pryrazole ⇒ w/in 8 hrs of ingestion
  • Furosemide is usually futile⇒ they’ve already absorbed it
40
Q

Why is 4-methyl pyrazole (Fomepizole) preferred to ethanol?

A

4-methyl pyrazole does not have CNS suppression