Equine urinary & renal seminar about AKI Flashcards
What is DMSO? And what and how is it used for in horses with urinary issues?
Dimethyl sulfoxide (DMSO) is a chemical compound with strong anti-inflammatory, analgesic (pain-relieving), and penetrative properties. Is also an industrial chemical solvent?
DMSO is sometimes used in horses to help manage urinary tract conditions, particularly those involving inflammation, swelling, or pain.
AKI vs ARF
AKI = acute kidney injury:
* Increase in serum crea by 27 umol/L (0.3 mg/dl) or greater in 48 hrs.
* Increase in serum crea 1.5 times baseline or more over 7 days.
* Oliguria 6 hrs duration in the face of adequate hydration status.
Creatinine can still be normal, but there is an upwards trend.
ARF = acute renal failure:
* Rapid deterioration in renal function over hours to days (48 hours to 7 days), resulting in a failure of the kidney to excrete nitrogenous waste (azotemia) and
maintain fluid, electrolyte and acid-base status.
For this, approximately 75% or more of the nephrons have to be non-functional.
AKI horses usually present with:
DEPRESSION and ANOREXIA
Urination dysfunction
* Oliguria (decreased amount of urine)
small decrease in urination hard to quantify.
* Anuria (no urine)
* Stranguria (painful urination)
Other signs:
* Dehydration
* Tachycardia
* Injected or hyperemic mucus membranes
* Pyrexia
* Mild colic
(May be more severe with ureterolithiasis (calculi in the ureter/ urethra – painful obstruction).)
When you find azotemia, first you need to…
pinpoint is it renal, pre-renal or post-renal?
To figure this out:
* What’s the horse’s hydration status?
* What concentration of urine do kidneys produce?
* Does the horse urinate?
* Can we find a directly treatable cause? (Infection)
What causes AKI broadly speaking? (4)
Decrease in renal perfusion
Renal toxicity
Infections
Immune-mediated cause
Give examples of decreases in renal perfusion that could cause AKI. (6)
Hypovolemia
* Diarrhea
* Septic shock
Dehydration
Acute blood loss
General anaesthesia
Give examples of Renal toxicity that could cause AKI. (9)
NSAIDs (Esp when perfusion already a roblem!)
Aminoglycosides
Tetracyclines
Potentiated sulphonamides (sometimes)
Beta-lactams (sometimes)
Bisphosphonates (sometimes)
Pigment nephropathy
* Acute myositis
* Acute hemolysis
Give examples of infectious causes that could cause AKI. (2)
Ascending infection (from urinary tract)
Leptospirosis
Give an example of an immune-mediated cause of AKI.
Streptococcal infections
Acute kidney injury (AKI) in horses can occur as a complication of Streptococcal infections, particularly Streptococcus equi subsp. equi (which causes strangles) or Streptococcus equi subsp. zooepidemicus (a common opportunistic pathogen).
- immune complex deposition in the kidneys.
- bacterial endotoxins triggers a systemic inflammatory response, leading to renal hypoperfusion and ischemia.
After a one-time toxic renal insult, clinical signs
develop approximately
3 days later.
Typical at-risk of AKI patient:
Colic surgery patient;
colitis patient which has been treated at home
with mostly NSAIDs.
What type of horse is low crea normal in?
Low muscle mass lowers it (cachexic horses and foals)
In addition to renal dysfunction, what can elevated blood urea indicate? (6)
catabolic state
(fever, anorexia, infection, trauma, myositis,
corticosteroid administration)
Describe SDMA in horses.
Serum symmetric dimethylarginine is a byproduct of cellular protein metabolism.
- > 90% eliminated through GFR
- Not absorbed or secreted in tubules
- Not influenced by breed, metabolic status
though slightly higher in foals (20 μg/dl). - Elevation when GFR falls about 40%
Use as a diagnostic tool in horses is not well described because its simply not much more sensitive then crea and is more expensive to run.
VAKI scoring: Veterinary Acute Kidney Injury scoring system (taken from dogs):
Stage 0: increase in sCr <150% from baseline
Stage 1: increase in sCr of 150%-199% or an absolute increase in sCr 0.3 mg/dL (≥26.5μmol/L) from baseline
Stage 2: increase in sCr of 200-299% from baseline
Stage 3: increase in sCr of ≥ 300% from baseline or an absolute sCr 4.0 mg/dL (>354μmol/L)
Transient = can be corrected
Persistent = acute (7-90 days) or chronic kidney disease (azotemia over 90 days) will develop
All horses on aminoglycoside AB…
should have their blood crea monitored.
Look for an upwards trend in serum Cr in a hospitalised sick horse treated with aminoglycosides/ tetracyclines.
We measure Cr every day in all horses on aminoglycosides.
When upwards trend in 24-48 hrs:
* Do urinalysis and look for: proteinuria, glucosuria, cellular or granular casts.
* Discontinue aminoglycoside.
Azotemia with a Urine SG of
>1,035
&
<1,020
> 1,035 prerenal azotemia
<1,020 renal azotemia
How to make a horse pee so you can catch a urine sample (if you’re not looking to palce a catheter).
Rub diluted chlorhexidine soap on their urethra, stimulates them to pee.
What SG is Isosthenuria
SG 1,008-1,012
Adult horses are normally over SG 1.020. Foals (milk diet) are normally hyposthenuric at SG <1,008, generally up to 1.010.
When might you see Proteinuria in horses?
Common in foals for the first 48h (colostrum).
Inflammation/infection can induce proteinuria:
* Renal or lower in urinary tract
* Increased vascular permeability
* Leakage of serum proteins along with leukocytes
* Tubular cells produce more Tamm-Horsfall glycoprotein
When might you see glucosuria in horses?
Normally glucose is reabsorbed in the proximal tubule but if the Tubules are overwhelmed (too much
glucose in plasma) or damaged (renal problem) you get Glucosuria + normoglycemia.
Can also indicate
* Proximal tubule dysfunction
Glucosuria + hyperglycemia can indicate a systemic cause like:
Equine metabolic syndrome
Pituitary Pars Intermedia Dysfunction
corticosteroid therapy
Equine metabolic syndrome
is a disorder in horses characterized by obesity, insulin dysregulation, and an increased risk of laminitis.
It commonly affects easy-keeping breeds such as ponies, Morgans, and Arabians.
Horses with EMS often develop abnormal fat deposits, particularly in the neck (cresty neck) and around the tailhead.
Insulin resistance in EMS leads to inefficient glucose metabolism, predisposing affected horses to painful laminitis.
Management focuses on dietary restrictions, weight control, regular exercise, and sometimes medications like metformin to improve insulin sensitivity.
Essentially horsey type II diabetes. However, unlike humans with Type 2 diabetes, horses with EMS don’t usually develop high blood sugar (hyperglycemia) to the same extent. Instead, their main issue is persistently high insulin levels, which increase the risk of laminitis.
Pituitary Pars Intermedia Dysfunction
also known as equine Cushing’s disease, is a common endocrine disorder in older horses caused by dysfunction of the pituitary gland.
It results in excessive production of ACTH, leading to symptoms such as a long, curly coat that doesn’t shed properly, muscle wasting, lethargy, excessive thirst and urination, abnormal fat distribution, and an increased risk of laminitis.
PPID is diagnosed through blood tests measuring ACTH levels and managed with medications like pergolide (Prascend), along with dietary adjustments and regular veterinary care.
While incurable, early detection and proper management can greatly improve a horse’s quality of life.
Causes of Bilirubinuria. (3)
Increased circulation of conjugated bilirubin.
Hemolytic disease,
hepatic disease,
posthepatic obstruction
Causes of hematuria. (6)
What is it actually measuring?
Reagent strips detect heme so there’s pigment in urine due to either Hemoglobin or myoglobin.
Trauma, hemorrhage,
urolithiasis, inflammation,
neoplasia, myopathy
What type of crystals are normal in adult horses?
And in foals?
Calcium carbonate crystals in adults.
Calcium oxalate crystals in foals.
Since horses consume high-calcium diets (e.g., alfalfa and other forages), their alkaline urine promotes the formation of calcium carbonate crystals, which are a normal finding.
Foals, on the other hand, often have calcium oxalate crystals instead of calcium carbonate. This is likely due to their milk intake, which provides different calcium compounds and influences urine composition.
Describe ultrasound of the left kidney in the horse.
Transabdominal US, 2,5-3MHz probe.
Observe it both Longitudinal and cross sectionally.
Left kidney is found in the 17th ICS, medial to the spleen in the paralumbar area.
Should be <18 cm long.
Assess Size, shape, texture, echogenicity.
Describe ultrasound of the left kidney in the horse.
Right kidney should be found in the 14-16th ICS.
Should be < 15 cm long.
Assess Size, shape, texture, echogenicity.
Describe ultrasound of the horse bladder.
Transrectal, 5 MHz probe
Crystals and mucus are Echogenic.
Look for: Focal wall thickening, wall defects,
masses (cystic calculi).
Foals: transabdominal
Bladder rupture: Increase in hypoechoic peritoneal fluid, Small flaccid bladder.
Fluid deficits should be corrected over
12 hours.
How to tx hyperkalemia in a horse.
Glucose + insulin CRI to Drive K into the cells.
Ca-gluconate slow bolus, Stabilizes myocardium which is unstable in hyperkalemia.
Furosemide CRI to Promote diuresis, excretion of K+ if glu and insulin haven’t done the trick.
signs of fluid overload: (4)
distended jugular pulses,
peripheral oedema,
low PCV,
high blood pressure and central venous pressure
What drugs can you use to Promote renal perfusion and urine output?
dopamine
furosemide
mannitol
You have to continuously monitor urine output, blood pressure and electrolytes if using these for oliguria after AKI.
Describe dopamine for promoting renal perfusion and urine ouput.
Low doses 1-3 µg/kg/min (up to 7).
Works on dopamine receptors in kidneys: vasodilation.
Also: elevates blood pressure: needs to be monitored.
Effect unpredictable.
Try for 4 hours – if no effect, no point to continue.
Describe furosemide for promoting renal perfusion and urine ouput.
After correction of fluid deficits.
CRI better than boluses.
Lowers tubular metabolic rate – may be protective.
Describe mannitol for promoting renal perfusion and urine ouput.
Increases renal tubular oxygen demand.
Increases glomerular blood flow.
Contraindicated in anuric patients.
Increase in intravascular volume may worsen pulmonary edema.
Last ditch option due to possbile side effects.
How can you mitigate the risk of aminoglycosides in horses?
Make sure your patient is hydrated before giving.
Administer a larger dosage, less frequently to give tubular cells time to recover.
Monitor urine sediment daily/ every other day.
Potentially monitor SDMA too.
