Acute Intrinsic Renal Failure - Green Flashcards
T/F: In order to have Acute, Intrinsic Renal Failure (AIRF), oliguria or anuria must be present.
False
What is the first thing detectable during the development of AIRF?
Sub-maximal urine concentration
What findings in the urine sediment are most typical of severe AIRF during the early stages?
Renal tubular epithelial casts
Which drugs are NOT a true nephrotoxin?
(causes 2° renal damage)
NSAIDs
Only cause problems in volume depleted animals
Is dialysis a good choice for treating severe AIRF?
YES
will make a difference, especially if started early
What is the prognosis for azotemic patients suffering AIRF due to Ethylene glycol toxicity?
Poor!
Nearly all patients that present w/ azotemia will die or be euthanized
What is the prognosis for azotemic patients suffering AIRF due to Leptospirosis?
Good
Most will survive
Which drug will help rapidly improve renal fxn in AIRF patients w/ Leptospirosis?
Amlodipine
What are the 3 most common causes of AIRF?
- Nephritiis due to Lepto
- Nephrosis due to a Nephrotoxin
- Ischemic Nephrosis
Is systemic arterial hypotension required for Ischemic Nephrosis AIRF?
NO!!
Just cause BP is normal doesn’t necessarily mean the kidneys are happy
List some Nephrotoxins that can cause AIRF.
- Ethylene glycol
- Aminoglycosides
- Cisplatin
- Cholecalciferol-containing rodenticides
- Calcipotriene
- Humoral hypercalcemia of malignancy
- Arsenic
- Lead
- Easter lily ⇒ CATS
Pathophysiology of AIRF?
-
Afferent arteriolar constriction
- vaso-motor nephropathy
- hypotension
-
Obstruction
- Intra/Extra-luminal
- Tubular Backleak across damaged tubules
- Decreased permeability
What is the mechanism of injury for Nephrotoxic AIRF?
Direct cell injury rather than ischemia
What 2 things, occuring simultaneously, dramitcally increase the risk of renal injury in AIRF p’s?
Exposure to nephrotoxins & Renal ischemia
Describe the Latent (Induction) Phase of AIRF.
- Often not detected
- Minimal to absent C/S
- Early ID & removal of inciting cause can result in return to normal renal fxn
Key points about the Maintenance Phase of AIRF.
- 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
Key points about the Recovery Phase of AIRF.
- Return of normal BUN & Creatinine is possible
- Partial improvement = chronic renal failure
How can you DX AIRF?
-
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
List possible PE findings in a patient with AIRF.
- 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
What can occur once you place dehydrated AIRF patients on fluids?
Overhydration → edema
Is anemia a common finding in AIRF patients?
NOT early on
(more common with CRF)
Can USG help you differentiate btwn AIRF & CRF?
NO
Both have low USG
An increased number of what type of crystal supports the DX of ethylene glycol toxicity?
Oxalate crystals
What will the urine sediment often look like in patients with AIRF?
Increased WBC, RBC & tubular epithelial cells
The magnitude of azotemia does NOT tell you….
- AIRF vs. CRF OR
- Source (pre-renal, renal or post-renal)
When will hyperkalemia typically occur?
With severely impaired renal excretory fxn & oliguria
What does the presence of severe hyperechogenicity on U/S suggest in patients with AIRF?
Possibility of ethylene glycol intoxication
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)
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
Which causes of AIRF have a poor to grave prognosis?
- Aminoglycosides⇒ poor to grave
- Easter lily ⇒ poor to grave
- Ethylene glycol ⇒ grave
Which causes of AIRF have a fair prognosis?
- Bacterial pyelonephritis ⇒ fair
- Lepto ⇒ fair to good w/ appropriate treatment
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
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
Treatment goals for AIRF!
(NB: no “quick fix”)
- 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!!!!!!!
What is the lethal dose of Ethylene glycol in the dog & cat?
Dog ⇒ 4.4 mL/Kg
Cat ⇒ 1.5 mL/Kg
Is Propylene Glycol dangerous for pets?
May cause illness but is usually NOT fatal
How does ethylene glycol kill our patients?
Ethylene glycol + Alcohol dehydrogenase = Glycolate (Glycolic acid)
[it is the metabolite that does all the damage]
What is the downside of the Colorimetric test for Ethylene glycol?
Ethylene glycol is rapidly absorbed from the GIT of dogs &
is undetectable in plasma 48 hrs post ingestion
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
Why is 4-methyl pyrazole (Fomepizole) preferred to ethanol?
4-methyl pyrazole does not have CNS suppression