6 Equine Renal and Urinary NOTES

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Questions and Answers

A horse presents with a history of polyuria and polydipsia. Laboratory analysis reveals azotemia and a urine specific gravity of 1.025 after rehydration. Which classification of azotemia is MOST consistent with these findings, and what is the underlying pathophysiological mechanism?

  • Post-renal azotemia; obstruction of urine outflow leading to back pressure on the kidneys.
  • Pre-renal azotemia; decreased glomerular filtration rate due to dehydration.
  • Renal azotemia; impaired tubular concentrating ability despite dehydration.
  • Pre-renal azotemia; appropriate renal response to dehydration, but underlying renal disease is present. (correct)

Equine urine is often alkaline, which can affect urinalysis results. Which of the following statements accurately describes the impact of alkaline urine on protein detection in equine urinalysis?

  • Alkaline pH causes a false negative result for protein on urine dipsticks, underestimating true proteinuria.
  • Alkaline pH can lead to a false positive result for protein on urine dipsticks, even in the absence of true proteinuria. (correct)
  • Alkaline pH has no significant impact on the accuracy of protein detection using sulfosalicylic acid turbidimetry.
  • Alkaline pH directly degrades urinary proteins, leading to falsely low protein concentrations regardless of the detection method.

Non-steroidal anti-inflammatory drugs (NSAIDs) are a recognized cause of acute kidney injury in horses. What is the PRIMARY mechanism by which NSAIDs contribute to renal damage in these animals?

  • Vasoconstriction of the afferent arteriole leading to decreased glomerular filtration pressure.
  • Blockade of prostaglandin-mediated vasodilation of the afferent arteriole, particularly in hypovolemic states. (correct)
  • Direct nephrotoxicity through the formation of reactive oxygen species in renal tubular cells.
  • Induction of tubulointerstitial nephritis due to an immune-mediated hypersensitivity reaction to NSAID metabolites.

In managing a horse with acute kidney injury and oliguria, which of the following diuretic strategies is MOST likely to be beneficial in promoting urine production and addressing fluid overload, considering the potential limitations and side effects of each?

<p>Carefully titrating intravenous fluid therapy to optimize hydration while monitoring urine output, and considering furosemide only if fluid overload persists despite adequate perfusion. (A)</p> Signup and view all the answers

Differentiating between upper and lower urinary tract disease in horses based solely on clinical signs can be challenging. Which of the following clinical signs is MOST suggestive of LOWER urinary tract disease rather than primary renal disease?

<p>Pollakiuria and stranguria. (C)</p> Signup and view all the answers

Monitoring serum creatinine is crucial in managing equine renal disease. A horse initially presents with a serum creatinine of 2.0 mg/dL. After several days, the creatinine level increases to 4.0 mg/dL. According to the provided text, what is the MOST accurate interpretation of this change in creatinine regarding renal function?

<p>Renal function has decreased by 50%. (B)</p> Signup and view all the answers

Hypercalcemia is a notable clinicopathological finding in equine chronic renal failure, differing from small animal renal disease. Which of the following statements BEST explains the underlying mechanism contributing to hypercalcemia in horses with chronic renal failure?

<p>Decreased renal excretion of calcium due to reduced glomerular filtration rate. (B)</p> Signup and view all the answers

Considering the dietary management of chronic renal failure in horses, which of the following feeding strategies is MOST crucial for minimizing disease progression and related complications, based on the principles outlined in the text?

<p>Restricting dietary calcium intake and feeding grass hay or pasture to minimize calcium load on the kidneys. (C)</p> Signup and view all the answers

Glomerulonephritis in horses can manifest in two primary forms based on pathophysiology. Which of the following options accurately distinguishes between these two forms in terms of the immune mechanism involved?

<p>Type III Hypersensitivity (immune complex-mediated) and Anti-Basement Membrane Antibody-mediated. (A)</p> Signup and view all the answers

A horse is diagnosed with urinary incontinence characterized by a patulous urethra and a flaccid bladder on rectal palpation. Which type of urinary incontinence is MOST consistent with these findings, and what is a potential underlying neurological cause mentioned in the provided text?

<p>Lower motor neuron ('paralytic') incontinence; associated with polyneuritis equi. (A)</p> Signup and view all the answers

Sabulous urolithiasis, characterized by sandy sediment in the bladder, is often associated with urinary incontinence in horses, particularly males. What is the MOST likely underlying mechanism linking urinary incontinence to the development of sabulous urolithiasis?

<p>Urinary stasis and incomplete bladder emptying associated with incontinence promote sediment accumulation. (C)</p> Signup and view all the answers

When evaluating proteinuria in equine urinalysis, particularly in alkaline urine, which of the following is the MOST appropriate next step to confirm true proteinuria and differentiate it from a false positive dipstick result?

<p>Order a urine protein:creatinine ratio to assess the magnitude of protein loss relative to urine concentration. (B)</p> Signup and view all the answers

In equine acute kidney injury (AKI), oliguria and anuria are considered poor prognostic indicators. Which of the following BEST explains WHY these clinical signs are associated with a worse prognosis compared to polyuria in AKI?

<p>Reduced urine output in oliguria/anuria indicates more severe nephron damage and decreased capacity for renal recovery. (C)</p> Signup and view all the answers

The use of dopamine in the treatment of acute kidney injury (AKI) in horses is mentioned in the text but with a caveat regarding recent studies. What is the PRIMARY intended pharmacological effect of dopamine in AKI, and why is its clinical efficacy now questioned?

<p>To improve renal blood flow and glomerular filtration rate; questioned due to limited proven clinical benefit and potential side effects. (C)</p> Signup and view all the answers

Compared to acute renal failure, chronic renal failure in horses presents with a distinct set of clinical signs reflecting the progressive nature of the disease. Which of the following clinical signs is MORE characteristic of CHRONIC renal failure than acute renal failure in horses?

<p>Chronic weight loss and poor haircoat. (D)</p> Signup and view all the answers

While cystitis is considered relatively rare as a primary condition in horses, certain factors can predispose them to developing this lower urinary tract infection. Which of the following is considered a PREDISPOSING FACTOR for cystitis in horses, as mentioned in the provided text?

<p>Bladder atony. (B)</p> Signup and view all the answers

Urolithiasis is a common cause of lower urinary tract disease in horses. Which of the following diagnostic methods is MOST reliable for definitively diagnosing urolithiasis in a horse suspected of having bladder stones?

<p>Rectal and/or transcutaneous ultrasonography of the bladder. (D)</p> Signup and view all the answers

Following surgical removal of a large calcium carbonate bladder stone in a horse, what is the MOST important long-term management strategy to prevent recurrence of urolithiasis, based on the information provided?

<p>Avoiding alfalfa hay and supplementing with salt to increase water intake and dilute urine. (B)</p> Signup and view all the answers

Myogenic or 'non-neurogenic' bladder dysfunction, often associated with sabulous urolithiasis, develops slowly and is linked to prolonged bladder distention. What is the MOST likely pathophysiological mechanism by which chronic bladder distention leads to myogenic bladder atony in these cases?

<p>Stretch-induced damage and decreased contractility of the detrusor muscle fibers themselves. (B)</p> Signup and view all the answers

A horse with glomerulonephritis presents with weight loss and ventral edema, but initial bloodwork reveals normal BUN and creatinine. According to the pathophysiology of glomerulonephritis in horses, what is the MOST likely explanation for the LACK of azotemia in this early stage of the disease?

<p>Compensatory hyperfiltration by remaining nephrons is masking the reduced glomerular filtration rate. (A)</p> Signup and view all the answers

Flashcards

Pollakiuria

Frequent urination in small volumes, often indicating lower urinary tract issues or non-urinary causes like estrus or colic.

Polyuria

Increased volume of urine production, stemming from renal issues like acute or chronic renal failure, endocrine problems, or non-renal causes such as psychogenic water drinking or salt consumption.

Stranguria

Difficulty or straining during urination.

Dysuria

Difficult urination.

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Oliguria

Decreased urine production.

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Anuria

Total lack of urine production.

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Azotemia

Increase in BUN and creatinine levels in the blood.

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Renal

USG is isosthenuric (1.008-1.012) or inappropriately concentrated in the face of dehydration; azotemia not completely corrected following rehydration.

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Acute Kidney Injury (AKI)

Increase in serum creatinine > 50% from baseline.

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Rectal palpation

Bladder (thick wall/stones) and caudal pole of left kidney.

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Rectal and transcutaneous ultrasonography

Evaluate kidneys, (stones, renal size, dilated pelvis), foals- assess bladder.

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Water deprivation testing

Differentiate diabetes insipidus from psychogenic.

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Renal biopsy

Confirm diagnosis and prognosis under ultrasound guidance.

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Acute Kidney Injury/Acute Renal Failure

Depression, anorexia, dehydration.

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Etiology

Toxin is most common; dehydration exacerbates. Includes aminoglycosides, oxytetracycline; NSAIDS; Pigmenturia, heavy metals, Vit D, Vit K3; Prolonged dehydration.

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Acute Renal Failure – Treatment

Intravenous fluid therapy improves perfusion, corrects electrolyte and acid/base disturbances, and induces diuresis.

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Diuretics and vasodilators

Administration of furosemide or dopamine.

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Chronic Renal Failure - Clinicopathology

Elevated Cr and BUN. Hypercalcemia.

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Lower Urinary Tract Disease - Clinical signs

Hematuria, pyuria, dysuria, stranguria, or pollakiuria. Urine dribbling, abdominal discomfort. Urine scalding in perineal area (mares) or dorsal surface of rear legs (males).

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Cystitis Treatments

Antibiotics based on culture, sensitivity and concentration in urine. Address underlying cause.

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Study Notes

Changes in Urination

  • Pollakiuria is frequent urination with small volume
    • Indicates lower urinary tract disease
    • Non-urinary causes: estrus or colic
  • Polyuria is increased urine volume
    • Renal causes: acute, chronic renal failure and endocrine issues
    • Non-renal causes: psychogenic water drinking, salt consumption
  • Stranguria is difficulty or straining during urination
  • Dysuria is difficult urination
  • Oliguria is decreased urine production
  • Anuria is a total lack of urine production

Laboratory Evaluation of Renal Disease

  • Azotemia indicates increased BUN and creatinine levels

Older Classification of Renal Issues

  • Pre-renal issues involve dehydration with appropriately concentrated urine
    • USG is greater than 1.020 or there is a correction of azotemia after rehydration
  • Renal issues involve urine that is isosthenuric (1.008-1.012)
    • Urine may not be appropriately concentrated despite dehydration
    • Azotemia is not completely corrected by rehydration
  • Post-renal issues have normal concentrating ability
    • Related to obstruction or a ruptured bladder, electrolyte abnormalities may be present

Acute Kidney Injury (AKI)

  • Current terminology favors defining AKI as an increase in serum creatinine exceeding 50% from baseline
    • Includes horses that have pre-renal and renal failure

Urinalysis

  • Equine urine is pale yellow to dark tan and turbid
    • Calcium carbonate crystals and mucus are normal
    • Calcium phosphate and calcium oxalate crystals can also be normal
    • Crystals are typically normal in equine urine
  • Alkaline pH (7.5-9.0) can cause false positives for protein on urine strips
    • High concentrate diets produce less alkaline urine
  • Protein is normally present at 1+ or trace amounts due to alkaline urine
  • Glucose threshold is 150-180 mg/dl, lower than dogs and humans
  • Blood in urine can be hematuria, hemoglobin, or myoglobin
    • Hematuria involves more than 5-10 cells/hpf
    • Hemoglobinuria arises from intravascular hemolysis, resulting in pink plasma and anemia
    • Myoglobinuria is linked to high muscle enzyme levels
  • Equine urine samples get examined for casts, WBC, RBC, and bacteria
    • Calcium carbonate and calcium oxalate crystals are normal
    • Urine collection is usually via free catch or catheterization
    • Sediment exams should be done soon after collection because casts are unstable in alkaline urine

Examination of the Urinary System

  • Rectal palpation can assess the bladder (thick wall/stones) and the caudal pole of the left kidney
  • Rectal and transcutaneous ultrasonography help evaluate kidneys (stones, renal size, dilated pelvis), and assess foal bladders
  • Endoscopy can identify urethritis and stones, and facilitates lavage to observe ureters
  • Water deprivation testing differentiates diabetes insipidous from psychogenic causes
  • Renal biopsy is ultrasound-guided and confirms diagnosis and prognosis

Acute Kidney Injury/Acute Renal Failure:

  • Clinical signs:
    • Depression, anorexia, and dehydration
    • Polyuria is most common
    • Oliguria/anuria means poor prognosis
    • Electrolyte imbalances may occur along with azotemia
      • This is hyponatremia, hypochloremia, potentially hyperkalemia and acidosis in severe and oliguric horses
  • Etiology
    • Toxins are the most common cause, dehydration exacerbates this
    • Aminoglycosides and oxytetracycline
    • NSAIDs cause ischemic renal damage due to PGE controlling renal blood flow
    • Pigmenturia, heavy metals, Vit D, and Vit K3
    • Prolonged dehydration where pre-renal conditions progress to renal
    • Acute bacterial nephritis is rare
      • Actinobacillus equuli in septic foals causes glomerular nephritis
      • Leptospirosis in adults causes interstitial nephritis
  • Treatment
    • Intravenous fluid therapy improves perfusion, corrects electrolyte and acid/base imbalances, and induces diuresis
      • Fluid therapy is the most important treatment for acute renal failure
      • A 50% reduction in creatinine after 24 hours of aggressive fluid therapy is a good sign
    • Diuretics and vasodilators:
      • Furosemide (1-2 mg/kg up to 4-6 mg/kg IV) improves anuria/oliguria
      • Dopamine infusion (3-5 ug/kg/min) improves renal blood flow but recent studies suggest that this may not be helpful
        • Fendoldopam offers less side effects
      • Mannitol may be used
    • Address the inciting cause and other clinical abnormalities

Chronic Renal Failure

  • Clinical Signs:
    • Chronic weight loss
    • Rough haircoat
    • Lethargy and inappetance
    • PU/PD
    • Ventral edema
    • Oral ulcers and dental tartar
  • Etiology
    • Often undiagnosed
    • Diagnostic aids include CBC, chemistry, UA, US, and biopsy
    • Most cases are unknown
    • Pyelonephritis and/or nephrolithiasis
    • Glomerulonephritis
  • Clinicopathology
    • Elevated Cr and BUN are seen
      • Cr of 10-12 indicates marked renal failure
      • Cr of 15 or greater indicates a grave prognosis
      • Monitor azotemia and electrolytes to monitor disease progression
        • A doubling of the Cr indicates a halving of renal function
    • Hypercalcemia contributes to disease progression
      • Calcium may exceed 15 mg/dl, which leads to calcification of tissues
    • Normocytic, normochromic anemia
    • Hypoalbuminemia in glomerulonephritis cases only
    • Mild hyponatremia, hypochloremia; some cases show acidosis and hyperkalemia
  • Treatment
    • Progressive disease with a poor long-term prognosis
    • Low calcium diet, avoid alfalfa
    • Less than 10% dietary protein
    • Grass hay or pasture and oats/corn
    • Supplement with NaCl or NaHCO3 as needed
    • Fresh water always available, IV fluids for acute exacerbations
    • Anabolic steroids maintain weight, packed cell volume, and appetite
  • Pathophysiology of Glomerulonephritis
    • Antigen-Antibody Complex Deposition (Type III Hypersensitivity Reaction)
    • Anti-Basement Membrane Antibody, this is only other species besides man
    • Weight loss and ventral edema without azotemia may be present
      • Tubular disease and azotemia may eventually develop

Lower Urinary Tract Disease

  • Clinical Signs
    • Hematuria, pyuria
    • Dysuria, stranguria, or pollakiuria
    • Urine dribbling
    • Abdominal discomfort
    • Urine scalding in the perineal area (mares) or dorsal surface of rear legs (males)
  • Cystitis
    • Primary cystitis is rare in horses
    • Predisposing factors: bladder atony, cystic calculi, cantharidin, and sorghum
    • U/A reveals pyuria > 5 WBCs/hpf, many bacteria
      • Gram-negative enteric bacteria
    • Treat with antibiotics based on culture, sensitivity, and concentration in urine
    • Address underlying cause
  • Urinary Incontinence
    • Upper motor neuron ("spastic") bladder: spinal cord disease and WNV
    • Lower motor neuron ("paralytic") bladder: polyneuritis equi, sorghum/sudan grass toxicity, EHV-1 myelitis, and sacral trauma
    • Myogenic ("non-neurogenic") bladder: develops slowly, usually with accumulation of sabulous sediment or secondary to prolonged obstruction
    • Treatment
      • Catheterization (intermittent or indwelling) until primary cause is resolved
      • Prophylactic antibiotics
      • Phenoxybenzamine relaxes urethral resistance
      • Bethanecol stimulates detrusor muscle tone
  • Urolithiasis
    • Bladder is most common, but can occur in kidneys, ureters causing a dilated pelvis and obstructive nephropathy
      • Small stones may attempt to pass from the bladder and cause a urethral obstruction
    • Hematuria, secondary cystitis, and pollakiuria present
    • Most often seen in middle-aged to aged horses
    • Large, single calcium carbonate stone is most common
    • Diagnosed by rectal palpation, ultrasound, and/or endoscopy
    • Treat with surgical excision or endoscopic lavage
    • Prevent recurrence by avoiding alfalfa and adding salt to feed to increase water consumption and urine dilution
      • Trying to acidify urine is difficult
  • Sabulous Urolithiasis
    • Accumulation of sandy material in the bladder
    • Likely secondary to urinary incontinence and most common in males
    • Cause of urinary incontinence is not usually apparent
    • Secondary accumulation further contributes to bladder incontinence and cystitis
    • Treatment
      • Identify underlying cause of bladder paralysis (if apparent)
      • Bladder lavage to remove material
      • Antibiotics, NSAIDs, bladder decompression, and bethanecol
      • Poor prognosis for return to function

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