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
The magnitude of azotemia does NOT tell you....
* AIRF vs. CRF **_OR_** * Source (pre-renal, renal or post-renal)
26
When will **hyper**kalemia typically occur?
With severely impaired renal excretory fxn & oliguria
27
What does the presence of severe **hyper**echogenicity on U/S suggest in patients with AIRF?
Possibility of ethylene glycol intoxication
28
**What anatomic structure can you U/S to potentially help differientiate AIRF from CRF in dogs?**
**Parathyroid gland** **AIRF⇒normal sized parathyroid glands (2 to 4 mm)** **CFR ⇒ enlarged parathyroid glands (4 to 8 mm)**
29
Why is a renal biopsy good for DXing AIRF? (4)
* Confirm renal azotemia * Differentiates AIRF from CRF * Gives a prognosis * Differentiates nephritis (Lepto) from nephrosis
30
Which causes of AIRF have a *poor to grave* prognosis?
* Aminoglycosides⇒ poor to grave * **Easter lily ⇒ poor to grave** * Ethylene glycol ⇒ grave
31
Which causes of AIRF have a *fair* prognosis?
* Bacterial pyelonephritis ⇒ fair * Lepto ⇒ fair to good w/ appropriate treatment
32
Key points about **Hemodialysis**?
* 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
**What happens if we don't perform dialysis on AIRF patients with high level azotemia?**
**_\> 80% will die or be euthanized due to:_** Hyperkalemia Metabolic acidosis Severe azotemia Overhydration & pulmonary edema
34
Treatment goals for AIRF! | (NB: no "quick fix")
* **Avoid *hypo*tension** * **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
What is the lethal dose of Ethylene glycol in the dog & cat?
Dog ⇒ 4.4 mL/Kg Cat ⇒ 1.5 mL/Kg
36
Is Propylene Glycol dangerous for pets?
May cause illness but is usually NOT fatal
37
How does ethylene glycol kill our patients?
Ethylene glycol + Alcohol dehydrogenase = **Glycolate (Glycolic acid)** [it is the metabolite that does all the damage]
38
What is the downside of the Colorimetric test for Ethylene glycol?
**Ethylene glycol** is rapidly absorbed from the GIT of dogs & ## Footnote **is undetectable in plasma 48 hrs post ingestion**
39
How do you TX Ethylene glycol toxicity?
* 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
Why is 4-methyl pyrazole (Fomepizole) preferred to ethanol?
4-methyl pyrazole does not have CNS suppression