Week 3- Large Animal Renal Disease Flashcards
(42 cards)
What is Acute Kidney Injury defined as?
Sustained decrease in GFR leading
to azotaemia and fluid and acid-base disturbances.
What does Renal Injury usually accompany?
Sudden drop in RBF, GFR and OU
What is Acute Kidney Injury characterised by?
- Rapid & sustained increase in blood urea and creatinine concentrations.
- Disturbances to fluid, electrolyte & acid-base homeostasis
What are the main clinical signs of Acute Kidney Injury?
- Anorexia
- Abdominal Discomfort
- Dehydration
- Depression/ Dullness
- Pigmenturia
What should you think of when you see severe conjunctival oedema in horses?
Acute Kidney Injury
How would you do a Urinary fractional electrolyte excretion?
- Collect simultaneous serum and urine samples.
- Separate serum from the cellular fraction promptly.
- Comparison of electrolyte clearance compared to creatinine.
- Elevated values are indicative of renal tubular failure.
- Affected by fluid therapy.
How would you do a Urinary GGT:creatinine ratio?
- Secretion of GGT into urine is specific to the proximal tubular cells.
- Indicative of glomerular damage
What nephrotoxins might cause acute renal tubular necrosis?
- Antibiotics
- Aminoglycosides
- Tetracyclines
- NSAIDs
- Pigments (myoglobin/haemoglobin)
- Bisphosphonates
- Vitamin D toxicosis
- Heavy metals * Lead, mercury, arsenic
- Plants * Oak/acorns, red maple, onions…
What does vasomotor nephropathy go on to cause?
**Acute Tubular Necrosis **
* Severe enteritis/colitis
* Haemorrhagic shock
* Septic Shock
What two Aminoglycosides/ Nephrotoxins are commonly used in Equine Practice?
- Gentamicin in adults
- Amikacin in foals (& local perfusions & intra
-articular injections in adults)
How do aminoglycosides cause nephrotoxicity?
- Filtered into the renal filtrate, then absorbed by the
epithelial cells of the proximal tubules - Cumulative toxicity occurs once the cells are
saturated with the drug (3
-5 days after
administration) - Disrupts cell metabolism
→ tubular cell swelling
→
cell death
→ sloughing into lumen - Acute tubular necrosis
When is aminoglycoside nephrotoxicity more likely?
- Incorrect dosing (↑ frequency)
- Hypovolaemia
- Co-administration with other nephrotoxic drugs or furosemide
- Bisphosphonates, NSAIDs, polymyxin B
- Concurrent pigmenturia
What aminoglycosides can a normal kidney tolerate?
» Normal kidney can tolerate single high doses of Aminoglycosides and can clear the
drug from the tubular cells
» Impaired organelle function → proximal tubular epithelial cell damage
How would you diagnose nephrotoxicity/ aminoglycosides?
Diagnosis is based on development of clinical signs
of AKI during (or in the few days after) treatment with
aminoglycosides
* Prognosis is generally very good if recognised early
What is Amikacin considered to be?
is considered less toxic than gentamicin,
but costs usually restricts its use to foals or local
infusion/joint administration
When does NSAID toxicty occur?
Toxicity usually only occurs when NSAIDs given at very high doses
* Usually with direct IV administration
* Or when frequent therapeutic doses are given to
dehydrated/hypovolaemic patients
* Often concurrent GI ulceration
What is common with daily oral administration of phenylbutazone?
Clinical renal toxicity is not common with daily administration of oral
phenylbutazone at normal doses
* Although chronic interstitial nephritis has been reported
* Worth periodic assessment of patients on long-term NSAIDs
What is the effect of renal prostaglandins on the kidneys?
Renal prostaglandins (PGs) are important mediators of renal vascular control during
periods of renal hypoperfusion (dehydration/hypovolaemia).
* PGs are potent vasodilators of the afferent renal arteriole
* Inhibition of PG synthesis can lead to prolonged renal arteriole vasoconstriction;
→ Renal medullary crest necrosis
What is the treatment for NSAID nephrotoxicty
Stop NSAIDs
* Fluid therapy
* Monitor renal parameters!
What two bisphosphonates are considered to be nephrotoxins?
*Tiludronate
*Clodronate
What is myoglobin toxicity?
more toxic than haemoglobin (but renal disease
also reported in marked haemolytic anaemia)
What happens when pigment accumulates in proximal tubules?
Tubular obstruction
→ Necrosis to epithelial cells
→& further increasing accumulation of debris
How would you diagnose pigment nephropathy?
Diagnosis based on documenting the presence of rhabdomyolysis in the face of marked
azotaemia/clinical signs of AKI
* Clinical history
* CK & AST
» Gross pigmenturia will not always be noted
* Presence of red/brown urine is indicative of pigmenturia (or haematuria), but is not always
present at the time of the horse developing signs of renal disease
» Care with NSAIDs in myopathy cases
* Fluid bolus/ongoing fluid therapy alongside NSAIDs if needed
* Monitoring bloodwork and USG
How would you treat pigment nephropathy?
- Restore hydration status
- Increase GFR
- Twice maintenance crystalloids +/- diuretics
- Monitor urine output and signs of fluid retention (bwt, PCV/TP, oedema)
- Alternative analgesics
